Information

Relation between a compound's toxicity and it's concentration level

Relation between a compound's toxicity and it's concentration level


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

I know that ammonia is toxic for the body since it disturbs enzymes of mitochondria. I want to know that why the ammonotelic animals don't get affected by it? I mean that even if there is plenty of water to remove ammonia from their body, does ammonia not cause any damage till it's inside body? Does toxicity depends on concentration level? Can anyone tell me its evolutionary significance?

Sorry for the previous question… Actually it was a easy one and I got the answer. Sorry for the unclarity.;)


The article at linked at the bottom says that the marine organisms keep the concentration of Ammonia under very strict control.

  1. pH of the ECF (Extra Cellular Fluid) is said to play a very important role.
  2. The concentration of ammonia in the environment (ambient ammonia levels) also plays an important role.
  3. Less importantly temperature also plays a role.
  4. Ionic strength of water also is involved.

The NH3:NH4+ ratio seems to be more important than the abosolute value of ammonia.


Ammonia is more toxic than ammonium ion. The lipophilic (ammonia is amphiphilic - soluble in both water and lipid) nature of ammonia allows it to easily cross the cell membrane and the blood brain barrier (in organisms where BBB exist) and affect the physiologic functions. The ammonium ion on the other hand can't enter the cell as easily, as it is not as soluble in lipid as ammonia.


  1. For ammonia and marine organisms see http://www.sciencedirect.com/science/article/pii/S1546509801200053
  2. For more on ammonium toxicity see: http://www.ucl.ac.uk/~ucbcdab/urea/amtox.htm


Plasma Level of a Drug | Pharmacokinetics

The plasma level time curve is plotted after measured drug concentration in plasma of an animal at different time intervals. The concentrations of drug in each plasma sample are plotted on an ordinary graph paper against the corresponding time at which the plasma samples were collected.

As the drug reaches in systemic circulation, plasma drug concentration will rise to a maximum. The absorption of a drug is more rapid than its elimination. As the drug is being absorbed into systemic circulation, the drug is distributed to all the tissues in the body and is also simultaneously being eliminated.

Elimination of a drug can proceed by excretion or metabolism or combination of both. The relationship of the drug level time-curve and pharmacological parameters for a drug is given in figure 2.2. Minimum effective concentration (MEC) of a drug is the concentration of drug in plasma that is required for producing an effect.

For antibiotics, it is minimum inhibitory concentration (MIC) for preventing the growth of microorganism. The MIC of an antibiotic differs for different microorganism.

MTC is the minimum toxic concentration of a drug. The onset time is the time required for the drug to reach the MEC or MIC. The intensity of the pharmacological effect is proportional to the number of drug receptors occupied which is reflected in observation that high plasma drug concentrations produce a greater pharmacological response, up to a maximum.

The duration of a drug action is the difference between the onset time and the time for the drug to decline back to the MEC or MIC.


Background

Toxic species displaying bright colour patterns that advertise their unpalatability to predators are said to be aposematic [1, 2]. Although the association between warning coloration and distastefulness can rely on predators’ innate biases [3], they usually need several sampling events to learn it [4–7]. This predation pressure promotes evolutionary convergence in colour patterns between chemically protected species living in sympatry, because species that share a common warning signal share the cost of predator learning. This association is known as Müllerian mimicry [8], and different species that exhibit the same warning signal are said to form “mimicry rings”. Müllerian mimicry has been observed in various unpalatable organisms such as insects [9, 10] and amphibians [11]. Similar protection between Müllerian co-mimics has been classically assumed in theoretical approaches as it is modelled as a strictly mutualistic interaction. However, when co-mimetic species exhibit differences in defence levels, less protected mimics might dilute the protection of a given warning signal, acting in a semi-parasitic manner (i.e., quasi-batesian mimicry [12]). Uneven defences within mimicry ring can then promote warning signal shift in the most toxic species toward better-protected mimicry rings [13]. Such processes might homogenize defence levels among Müllerian mimics but empirical studies estimating defence variations within natural communities are still lacking. Species that are considered Müllerian co-mimics can rely on drastically different chemical compounds [14], and chemical defences can be either sequestered from diet [15–18] or neo-synthesized [19, 20]. Consequently, co-mimics are not always equally unpalatable, with levels of chemical protection varying from very similar to very uneven, as reported in some mimetic butterflies [21, 22] and frogs [23, 24]. Even within species, individuals are not equally protected. In extreme cases, this intraspecific variation includes palatable individuals within protected species an interaction known as automimicry [25]. Automimics thus benefit from the unpalatability of their co-mimics, without investing in chemical protection themselves. This variation in defence levels between mimics can be linked to several ecological factors.

Factors associated to the amount of prey encountered by predators (abundance) and how memorable such encounters are (enhanced by behaviours such as aggregation, for instance [4, 26] but for contrasting evidence see [27]) might be correlated with different defence levels. Moreover, when defences are sequestered, the efficiency in the use of the available resources (larger for specialist than for generalist feeders, for example [20, 28]) is also likely to play an important role in the evolution of chemical defences. Additionally, differences in the resource use between sexes associated to their relative vulnerability intrinsic to their specific ecological roles [23], need also to be considered when studying differences in chemical protection. All these factors are correlated, and might have a joint effect on defence level variation and warning signal convergence. Here we investigate the effect of those multifarious ecological traits in chemical protection variation.

Here, we focus on Neotropical Heliconius butterflies, which exhibit several outstanding examples of mimetic convergence between distantly related species both within [29] and outside the genus [30]. Heliconius butterflies contain toxic cyanogenic glucosides obtained from their Passiflora host plants during larval feeding [30, 31], and also through de novo synthesis as larvae and adults [16, 20]. Although all Heliconius have similar chemical compounds, they participate in a number of different sympatric mimicry rings, allowing investigation of variations in toxicity both within and between mimicry rings in a single community. Several previous studies have investigated toxicity (i.e., chemical compounds) and unpalatability (i.e., predators behaviour) variations in Heliconius butterflies. Studies of natural and experienced predators found differences in rejection behaviour towards several Heliconius species [32, 33]. However, no attempts were made to disentangle the visual and chemical components of aposematic prey. Chemical analyses have also revealed differences in the concentration of cyanogenic compounds in Heliconius butterflies, highlighting in particular the apparent association between the specialisation of Heliconius sara on the larval host-plant Passiflora auriculata and a significant increase in toxicity compared to generalist species [20, 34, 35]. However, most butterflies used in these studies were captive-bred, and in several cases were not reared on their natural host plant species. The variations in toxicity in natural populations, which are the products of multifarious ecological factors, have yet to be investigated.

By comparing toxicity in Heliconius species sharing warning signals but with contrasting abundances, and distinct behavioural (i.e., larval aggregation, communal roosting) and physiological traits (i.e., host-plant specialisation, capacity to synthesise cyanogenic glucosides), we test for associations between those different traits and chemical defence levels. We measured cyanide levels in wild caught individuals belonging to eight different sympatric Heliconius species, aiming to 1) quantify the variation of cyanide concentration within and between sympatric protected species. We also aim to test whether 2) co-mimetic species have similar levels of toxicity, 3) coexisting mimicry rings have different toxicity levels, and 4) differences in toxicity are correlated with a) the local abundance of the mimicry ring, b) sex, and c) life history traits such as communal roosting, larvae gregariousness and dietary specialisation.


Toxicokinetics

In the late 1800s, lithia water was first introduced as a mania and gout treatment [17]. Afterward, lithium tablets with higher lithium concentration largely replaced lithia water. However, the higher lithium concentration found in the tablets was associated with tremors and weakness, and in 1898 lithium toxicity was first described. To determine the extent of lithium toxicity, one must determine the ingested amount, time of ingestion, whether there are co-ingestants, and if the ingestion was intentional or unintentional. It is worth noting that lithium toxicity signs do not often conform to the measured lithium level[18].

Neurologic effects

Symptoms of intoxication include coarse tremor, hyperreflexia, nystagmus, and ataxia. Patients often show varying consciousness levels, ranging from mild confusion to delirium. Although the neurological symptoms are mostly reversible, some reports indicate that symptoms might persist for 12 months never resolve[9].

Renal toxicity is more common in patients on chronic lithium treatment. Toxicity includes impaired urinary concentrating ability, nephrogenic diabetes insipidus (the most common cause of drug-induced NDI), sodium-losing nephritis, nephrotic syndrome along with other manifestations is prescribed[19].

Cardiovascular effects

These are usually mild and non-specific. Almost all patients treated with lithium will develop T wave flattening. Sinus node dysfunction is the most common reported conduction defect followed by QT prolongation, intraventricular conduction defects, and U waves. These findings are reversible[20].

Gastrointestinal effects

Symptoms typically occur within 1 hour of ingestion and are more common in the acute overdose setting [15].

Endocrine effects

Lithium administration leads to the inhibition of thyroid hormone synthesis and subsequent release, resulting in hypothyroidism. Hyperthyroidism is less commonly manifested, which can mask symptoms of lithium toxicity and boost its toxicity by prompting cellular unresponsiveness and altered renal tubular handling of lithium [21].


Differences in exposure to toxic and/or carcinogenic volatile organic compounds between Black and White cigarette smokers

It is unclear why Black smokers in the United States have elevated risk of some tobacco-related diseases compared to White smokers. One possible causal mechanism is differential intake of tobacco toxicants, but results across studies are inconsistent. Thus, we examined racial differences in biomarkers of toxic volatile organic compounds (VOCs) present in tobacco smoke.

Method

We analyzed baseline data collected from 182 Black and 184 White adult smokers who participated in a randomized clinical trial in 2013–2014 at 10 sites across the United States. We examined differences in urinary levels of ten VOC metabolites, total nicotine equivalents (TNE), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), controlling for covariates such as cigarettes per day (CPD), as well as differences in VOCs per TNE to assess the extent to which tobacco exposure, and not metabolic factors, accounted for racial differences.

Results

Concentration of metabolites of acrolein, acrylonitrile, ethylene oxide, and methylating agents were significantly higher in Blacks compared to Whites when controlled for covariates. Other than the metabolite of methylating agents, VOCs per TNE did not differ between Blacks and Whites. Concentrations of TNE/CPD and VOCs/CPD were significantly higher in Blacks. Menthol did not contribute to racial differences in VOC levels.

Conclusions

For a given level of CPD, Black smokers likely take in higher levels of acrolein, acrylonitrile, and ethylene oxide than White smokers. Our findings are consistent with Blacks taking in more nicotine and toxicants per cigarette smoked, which may explain their elevated disease risk relative to other racial groups.


What Factors Impact a Chemical's Safety?

Why are some chemicals more harmful than other? Many factors are considered when evaluating a chemical's safety including potency, persistence, solubility, bioaccumulation and biomagnification. Potency refers to the amount of a chemical needed to cause harm. The more potent a toxin, the lower the concentration needed to cause harm. Persistencerefers to how long a substance takes to break down. Persistent chemicals are of greater concern because they remain in the environment (or even in organisms) for long time periods. Solubilityrefers to whether the chemical dissolves in certain solvents, such as water or fat. Generally, fat-soluble (lipid-soluble) toxins are more dangerous because they can accumulate in fatty tissues (see below) whereas water-soluble toxins could be more easily flushed out of the body. Furthermore, fat-soluble toxins are more easily absorbed by the body.

Bioaccumulation

Bioaccumulationis the buildup of chemicals in an organism&rsquos tissues over its lifetime. While bioaccumulated toxins are commonly fat soluble, such as DDT and PCBs, water-soluble toxins, such as inorganic forms of heavy metals can also bioaccumulate. For example, lead accumulates in the teeth and bone, and mercury can accumulate in the kidneys and brain.

Biomagnification

Biomagnificationis the increasing concentration of toxins in organisms at each successive trophic level. When organisms with bioaccumulated toxins are consumed, the toxins are transferred to their predators (figure (PageIndex)). Biomagnification explains why some fish species high on the food chain contain high concentrations of mercury and cadmium, another heavy metal.

Figure (PageIndex): Biomagnification. The biomagnified toxin becomes concentrated in the tissues of organisms representing four successive trophic levels in a food chain. Most of the toxin absorbed by primary producers remains in their bodies at that first trophic level. Through biomagnification, the concentration of the toxin (crosses) increases higher up the food chain. (Black dots represent other molecules.) Organisms at the top thus have a higher tissue concentration of toxins than lower levels. Trophic level I represents the primary producers trophic level II represents the primary consumers trophic level III represents the secondary consumers and trophic level IV represents the tertiary consumers. Image by Sballesteros15 (CC-BY-SA).

In addition to high persistence, fat solubility, and bioaccumulation, biomagnification explains why the now-banned insecticide dichlorodiphenyltrichloroethane (DDT) caused so much damage. Producers absorbed DDT and passed it on to successive levels of consumers at increasingly higher rates. For example, spraying a marsh to control mosquitoes will cause trace amounts of DDT to accumulate in the cells of microscopic aquatic organisms, the plankton, in the marsh. In feeding on the plankton, filter-feeders, like clams and some fish, harvest DDT as well as food. (Concentrations of DDT 10 times greater than those in the plankton have been measured in clams.) The process of concentration goes right on up the food chain from one trophic level to the next. Gulls, which feed on clams, may accumulate DDT to 40 or more times the concentration in their prey. This represents a 400-fold increase in concentration along the length of this short food chain. Ultimately, apex predators at the top of the food chain such as Bald Eagles, pelicans, falcons, and ospreys fed on contaminated fish, reaching dangerous DDT levels.

Another substances that biomagnifies is polychlorinated biphenyl (PCB). The National Atmospheric and Oceanic Administration (NOAA) studied biomagnification of PCB in the Saginaw Bay of Lake Huron of the North American Great Lakes (figure (PageIndex)). Concentrations of PCB increased from the producers of the ecosystem (phytoplankton) through the different trophic levels of fish species. The apex predator, the walleye, had more than four times the amount of PCBs compared to phytoplankton. Also, research found that birds that eat these fish may have PCB levels that are at least ten times higher than those found in the lake fish. This aquatic ecosystem offered an ideal opportunity to study biomagnification because PCB generally exists at low concentrations in this environment, but apex predators accumulated very high concentrations of the toxin.

Figure (PageIndex): Polychlorinated biphenyl (PCB) concentrations found at the various trophic levels in the Saginaw Bay ecosystem of Lake Huron. Numbers on the x-axis reflect enrichment with heavy isotopes of nitrogen ( 15 N), which is a marker for increasing trophic level. Notice that the fish in the higher trophic levels accumulate more PCBs than those in lower trophic levels. The organisms in order of 15 nitrogen enrichment are phytoplankton, zebra mussel, amphipod, white sucker, alewife, yellow perch, rainbow smelt, and walleye. (credit: Patricia Van Hoof, NOAA, GLERL)

Persistent Organic Pollutants (POPs)

Persistent organic pollutants (POPs) are a group of organic chemicals that pose risks to human health and ecosystems. Examples include the pesticide dichlorodiphenyltrichloroethane (DDT) and the industrial chemicals polychlorinated biphenyls (PCBs) and per- and polyfluoroalkyl substances (PFAS). The contaminant in Agent Orange (2,3,7,8-tetrachlorodibenzo-p-dioxin TCDD) is another POP (see The Scientific Method). Persistent organic pollutants have the following three characteristics:

  • Persistent: POPs are chemicals that last a long time in the environment. Some may resist breakdown for years and even decades while others could potentially break down into other toxic substances.
  • Bioaccumulative: POPs can accumulate in animals and humans, usually in fatty tissues and largely from the food they consume. As these compounds move up the food chain, they concentrate to levels that could be thousands of times higher than acceptable limits.
  • Toxic: POPs can cause a wide range of health effects in humans, wildlife and fish. They have been linked to effects on the nervous system, reproductive and developmental problems, suppression of the immune system, cancer, and endocrine disruption. The deliberate production and use of most POPs has been banned around the world, with some exemptions made for human health considerations (for example, DDT for malaria control) and/or in very specific cases where alternative chemicals have not been identified. However, the unintended production and/or the current use of some POPs continue to be an issue of global concern. Even though most POPs have not been manufactured or used for decades, they continue to be present in the environment and thus potentially harmful. The same properties that originally made them so effective, particularly their stability, make them difficult to eradicate from the environment.

The relationship between exposure to environmental contaminants such as POPs and human health is complex. There is mounting evidence that these persistent, bioaccumulative and toxic chemicals (PBTs) cause long-term harm to human health and the environment. Drawing a direct link, however, between exposure to these chemicals and health effects is complicated, particularly since humans are exposed on a daily basis to many different environmental contaminants through the air they breathe, the water they drink, and the food they eat. Numerous studies link POPs with a number of adverse effects in humans. These include effects on the nervous system, problems related to reproduction and development, cancer, and genetic impacts. Moreover, there is mounting public concern over the environmental contaminants that mimic hormones in the human body (endocrine disruptors).

Through atmospheric processes, they are deposited onto land or into water ecosystems where they accumulate and potentially cause damage. From these ecosystems, they evaporate, again entering the atmosphere, typically traveling from warmer temperatures toward cooler regions. They condense out of the atmosphere whenever the temperature drops, eventually reaching highest concentrations in circumpolar countries. Through these processes, POPs can move thousands of kilometers from their original source of release in a cycle that may last decades.

As with humans, animals are exposed to POPs in the environment through air, water and food. POPs can remain in sediments for years, where bottom-dwelling creatures consume them and who are then eaten by larger fish. Because tissue concentrations can biomagnify at each level of the food chain, top predators, including whales, seals, polar bears, birds of prey, tuna, swordfish and bass may have a million times greater concentrations of POPs than the water itself. Once POPs are released into the environment, they may be transported within a specific region and across international boundaries transferring among air, water, and land.

While generally banned or restricted (figure (PageIndex)), POPs make their way into and throughout the environment on a daily basis through a cycle of long-range air transport and deposition called the &ldquograsshopper effect.&rdquoThe &ldquograsshopper&rdquo processes begin with the release of POPs into the environment. When POPs enter the atmosphere, they can be carried with wind currents, sometimes for long distances.

Figure (PageIndex): Emissions of several persistent organic pollutants (POPs) by European Union countries has decreased over the years. These include hexchlorobenze (HCB), polychlorinated biphenyls (PCBs), dioxins (such TCDD), and total polycyclic aromatic hydrocarbons (PAHs), However, these compounds remain in the environment for long periods of time. Image modified from European Environment Agency of the European Union (CC-BY)


Related Biology Terms

  • Hypotonic – When one solution contains more water and less solutes than another solution.
  • Hypertonic – A solution of higher concentration that the solution it is being compared to.
  • Isotonic – Two solutions that exist with the same solute concentration.
  • Osmolarity – The concentration of a solution in parts of solute divided by volume of water.

1. A plant cell is placed in an aqueous solution. Water floods the cell, and the cell becomes rigid with pressure. What is the tonicity of the solution compared to the cell?
A. Isotonic
B. Hypertonic
C. Hypotonic

2. Two identical solutions contained in narrow beakers are separated by a semi-permeable membrane. If salt is added to one beaker, increasing its tonicity, what will happen to the volume of water in the beaker?
A. It will increase
B. It will decrease
C. It will stay the same


References

Becker RA, Borgert CJ, Webb S, Ansell J, Amundson S, Portier CJ, Goldberg A, Bruner LH, Rowan A, Curren RD, et al. Report of an ISRTP workshop: progress and barriers to incorporating alternative toxicological methods in the U.S. Regul Toxicol Pharmacol. 200646(1):18–22.

Boyd WA, McBride SJ, Freedman JH. Effects of genetic mutations and chemical exposures on Caenorhabditis elegans feeding: evaluation of a novel, high-throughput screening assay. PLoS One. 20072(12):e1259.

Anderson GL, Cole RD, Williams PL. Assessing behavioral toxicity with Caenorhabditis elegans. Environ Toxicol Chem. 200423(5):1235–40.

Boyd WA, McBride SJ, Rice JR, Snyder DW, Freedman JH. A high-throughput method for assessing chemical toxicity using a Caenorhabditis elegans reproduction assay. Toxicol Appl Pharmacol. 2010245(2):153–9.

Yang R, Rui Q, Kong L, Zhang N, Li Y, Wang X, Tao J, Tian P, Ma Y, Wei J, et al. Metallothioneins act downstream of insulin signaling to regulate toxicity of outdoor fine particulate matter (PM2.5) during spring festival in Beijing in nematode Caenorhabditis elegans. Toxicol Res. 20165(4):1097–105.

Boyd WA, Williams PL. Comparison of the sensitivity of three nematode species to copper and their utility in aquatic and soil toxicity tests. Environ Toxicol Chem. 200322(11):2768–74.

Dengg M, van Meel JC. Caenorhabditis elegans as model system for rapid toxicity assessment of pharmaceutical compounds. J Pharmacol Toxicol Methods. 200450(3):209–14.

Schouest K, Zitova A, Spillane C, Papkovsky D. Toxicological assessment of chemicals using Caenorhabditis elegans and optical oxygen respirometry. Environ Toxicol Chem. 200928(4):791–9.

Sprando RL, Olejnik N, Cinar HN, Ferguson M. A method to rank order water soluble compounds according to their toxicity using Caenorhabditis elegans, a complex object parametric analyzer and sorter, and axenic liquid media. Food Chem Toxicol. 200947(4):722–8.

Wang D, Xing X. Assessment of locomotion behavioral defects induced by acute toxicity from heavy metal exposure in nematode Caenorhabditis elegans. J Environ Sci (China). 200820(9):1132–7.

Brenner S. The genetics of Caenorhabditis elegans. Genetics. 197477(1):71–94.

Xian B, Shen J, Chen W, Sun N, Qiao N, Jiang D, Yu T, Men Y, Han Z, Pang Y, et al. WormFarm: a quantitative control and measurement device toward automated Caenorhabditis elegans aging analysis. Aging sCell. 201312(3):398–409.

Jin C, Li J, Green CD, Yu X, Tang X, Han D, Xian B, Wang D, Huang X, Cao X, et al. Histone demethylase UTX-1 regulates C. elegans life span by targeting the insulin/IGF-1 signaling pathway. Cell Metab. 201114(2):161–72.

Sternberg PW. Working in the post-genomic C. elegans world. Cell. 2001105(2):173–6.

Li Y, Gao S, Jing H, Qi L, Ning J, Tan Z, Yang K, Zhao C, Ma L, Li G. Correlation of chemical acute toxicity between the nematode and the rodent. Toxicol Res. 20132(6):403–12.

Jung SK, Aleman-Meza B, Riepe C, Zhong W. QuantWorm: a comprehensive software package for Caenorhabditis elegans phenotypic assays. PLoS One. 20149(1):e84830.

Mathew MD, Mathew ND, Ebert PR. WormScan: a technique for high-throughput phenotypic analysis of Caenorhabditis elegans. PLoS One. 20127(3):e33483.

Zhang W, Liu Y, Sun N, Wang D, Boyd-Kirkup J, Dou X, Han JD. Integrating genomic, epigenomic, and transcriptomic features reveals modular signatures underlying poor prognosis in ovarian cancer. Cell Rep. 20134(3):542–53.

Wahlby C, Kamentsky L, Liu ZH, Riklin-Raviv T, Conery AL, O'Rourke EJ, Sokolnicki KL, Visvikis O, Ljosa V, Irazoqui JE, et al. An image analysis toolbox for high-throughput C. Elegans assays. Nat Methods. 20129(7):714–6.

Gomes P, Cassanas G, Bingham C, Halberg F, Lakatua D, Haus E, Uezono K, Ueno M, Matsuoka M, Kawasaki T, et al. Individualized principal component analysis of endocrine circannual variability. Prog Clin Biol Res. 1987227B:521–32.

Chih-Chung Chang C-JL. LIBSVM: a library for support vector machines. ACM Trans Intell Syst Technol. 20112:1–27.

Funding

This work was supported by “National Natural Science Foundation of China” Grant (# 31401025, 81273108, 81641184), “The capital health research and development of special” Project in Beijing (# 2011–1013-03), Opening fund of “Beijing Key Laboratory of Enviromental Toxicology” (# 2015HJDL03), grants from the Chinese Academy of Sciences (CAS YZ201243 to J.-D.J.H), and Natural Science Foundation of Shandong Province, China (ZR2017BF041).

Availability of data and materials

The datasets used and analysed during the current study are available from the corresponding author on reasonable request.


REACTIVE OXYGEN SPECIES: Metabolism, Oxidative Stress, and Signal Transduction

Klaus Apel and Heribert Hirt
Vol. 55, 2004

Abstract

▪ Abstract Several reactive oxygen species (ROS) are continuously produced in plants as byproducts of aerobic metabolism. Depending on the nature of the ROS species, some are highly toxic and rapidly detoxified by various cellular enzymatic and . Read More

Figure 1: Generation of different ROS by energy transfer or sequential univalent reduction of ground state triplet oxygen.

Figure 2: The principal features of photosynthetic electron transport under high light stress that lead to the production of ROS in chloroplasts and peroxisomes. Two electron sinks can be used to alle.

Figure 3: The principal modes of enzymatic ROS scavenging by superoxide dismutase (SOD), catalase (CAT), the ascorbate-glutathione cycle, and the glutathione peroxidase (GPX) cycle. SOD converts hydro.

Figure 4: Schematic depiction of cellular ROS sensing and signaling mechanisms. ROS sensors such as membrane-localized histidine kinases can sense extracellular and intracellular ROS. Intracellular RO.

Figure 5: Different roles of ROS under conditions of (a) pathogen attack or (b) abiotic stress. Upon pathogen attack, receptor-induced signaling activates plasma membrane or apoplast-localized oxidase.


Module 5 / Inquiry Question 4

Last week, we briefly touched on Ksp alongside other equilibrium constants. In this week’s note we will explore Ksp further.

We will first look at mechanisms of which ionic compounds dissolve in water and what are the conditions required for the solute to successfully dissolve in water.

Then, we will explore how Aboriginal People use the principle of solubility of toxins in water to remove them from their food before consumption.

Following this, we will explore general solubility rules to allow us to predict if a compound produced will appear as a precipitate or in aqueous state.

After that, we will determine the precipitate that will form when we mix two ionic solutions together. This is done using two methods. One is that we use the solubility rules to determine if the reaction between reactants are capable of forming precipitates using general solubility rules. Also, we compare the reaction quotient (Q) to the Ksp value to predict if a precipitate will form.

Towards the end of this week’s notes, we will go over the mathematical derivation of the Ksp formula and other Keq in general.

Lastly, we will go through a question to calculate the solubility of an ionic compound.

Brief recap of ionic compounds from Preliminary HSC Chemistry

Let’s do a quick revision of ionic compounds as this week’s material puts them under the spotlight

Ionic compounds are substances that are formed where their atoms are joined via ionic bonds. When one atom completely transfers its valence electron(s) to another atom, an ionic bond is formed between the two.

The atom that donated its valence electron(s) becomes a charged atom called an ion.

More specifically, it is an cation as it is positively charged by having fewer electron(s) than its neutral atomic state.

The atom that accepted the valence electron(s) is called the anion as it has more electrons than its neutral atomic state.

So, anions are negatively charged atoms (ions).

The magnitude of their charge is proportional on the number of electrons that it has donated or accepted.

The charge of the cation and anion are equal but differ in their signs (positive or negative). This essentially creates electrostatic attraction which is the ionic bond.

Relationship between ionic compounds and salts

There are many definitions for the term ‘salt’ which differ depending on the level of chemistry you are studying.

One possible definition for salt is a product (compound) of an acid-base reaction. The formation of a salt is illustrated in diagram below, where the salt is a product of the reaction between a Bronsted-Lowry Acid and a Bronsted-Lowry Base.

A Bronsted-Lowry acid is a substance that donates a proton (hydrogen ion) in a chemical reaction

A Bronsted-Lowry base is a substance that accepts a proton (hydrogen ion) in a chemical reaction.

Please do note the difference in definitions between a Bronsted-Lowry Acid/Base and an Arrhenius Acid/Base which we explored in last week’s notes.

The effect of their differing definitions will have consequences on how you write out the chemical equilibrium reaction for the dissolution of acids and bases.

Also note that weak Bronsted-Lowry acids and bases will result in the above equation having a two-way arrow to indicate equilibrium. The above diagram shows a single way arrow, depicting a strong acid under Bronsted-Lowry definition where all strong acid molecules (H-X) donates its proton (H+ ion) to the base, “C”.

Strong acids and bases do not form equilibrium reactions, their dissociation into ions is depicted as one way arrow only as such above.

However, like we said last week, we will formally introduced strong/weak acids and bases in Module 6. We just felt like talking about them here as we were here already and saw some relevance to start building some first impressions on acids & bases.

Learning Objective #1 - Describe and analyse the processes involved in the dissolution of ionic compounds in water

The dissolution of ionic compounds in water can be separated into three processes:

The interaction between solvent molecules (the water)

The interaction between solute molecules (the ionic compound)

The interaction between the molecules of the solute and solvent

The reason to this is because that, prior to the dissolution process, there is interaction between water molecules via hydrogen bonding which must be broken for ions to dissolve in water. Also, there is electrostatic attraction interactions between the ions of an ionic compound, forming their ionic bonds. These bonds also need to be broken for ions to dissolve in water.

When the solute is added to the solvent, it is the interaction between the water molecules and the ionic compounds that allows the compound to dissolve in water.

Water is a polar molecule due to the electronegativity differences between hydrogen and oxygen. Oxygen is more electronegative than hydrogen which results in the oxygen atom ‘pulling/attracting’ more electrons towards oxygen atom and away from two hydrogen atoms.

This results in the hydrogen atoms being partially positively charged and the oxygen atom being partially negatively charge. Moreover, the lone pair of electrons in water molecules repels the electrons between the electrons in the two O-H bonds, giving water a bent shape which enhances its polarity. Collectively, this result in the polar nature of water molecules.

As ionic compounds comprise of cations and anions, when an ionic compound interacts water, the cations will be attracted to the partially negatively charged oxygen atom of water molecules. Vice versa, the anions will be attracted to the partially positively hydrogen ions of water molecules. This attraction between ions and water molecules is called ion-dipole force.

The ion-dipole force weakens the strength of the electrostatic attraction and breaks the ionic bonds between the cation and anions holding the ionic compound together. Also, this force also breaks the hydrogen bonds between water. Hydration is the process whereby the ion-dipole force causes ions to be separated and be surrounded by water molecules. This process gives off energy known as hydration energy.

Hydration energy is the energy that is given off when an ion of an ionic compound are hydrated, or surrounded by water.

For an ionic compound to successfully dissolve in water, the hydration energy must be greater than the lattice energy of the ionic compound as well as the energy required to break the hydrogen bonding between water molecules. Lattice energy is the energy that was released when the ionic bond was formed between cation and anions via electrostatic attraction to make the ionic compound).

Also, the hydration energy released due to the formation of the ion-dipole bond or force must be large enough to break the hydrogen bonding between water molecules as well. If not, the ions of the ionic compound will not be hydrated or dissolve.

Beyond Syllabus Information:

The water molecules surrounding the ions effectively minimises the electrostatic attraction between the cation and anions, disallowing formation the ionic bonds by creating a ‘shield’ of water molecules.

Due to the significantly smaller size of individual ions compared to its undissolved form as an ionic compound, when the ions are hydrated, the ionic bonds are broken and ions separated evenly throughout the water molecules (solvent). This decrease in size from ionic compound crystals to individual ions is what we see as the physical change when dissolving ionic compounds.

The amount of water molecules that an ion can attract will depend on the ratio between the ion’s charge to its surface area.

So, an ion with a small surface area but a high charge (e.g. 5+) will attract more molecules than an ion with high surface area but equal charge (e.g. 5+) which we explored in Preliminary HSC Chemistry course.

Recall from earlier, the charge of an ion will depend on how many electrons it accepted or donated. For instance, a neutral atom that donated 5 electrons will have a charge of 5+.

Vice versa, a neutral atom that accepted 5 electrons will have a charge of -5.

Establishing equilibrium when dissolving ionic compounds in water

Equilibrium occurs when a solution is saturated by an ionic compound.

This means that there will not be enough water molecules to be shield every ions away from each other, i.e. when water molecules are attracted to a new ion and, form ion-dipole forces, they will move away and dehydrated another ion which they were previously attracted to.

Therefore, in an aqueous ionic solution, there is a continuous breaking of ion-dipole bonds, hydrogen bonds and ionic bonds.

Since this process will repeats back-and-forth, an dynamic equilibrium is formed which can be expressed as:

NaCl(s) + H2O(l) <-> Na+ (aq) + Cl– (aq) + H2O(l)

We could can leave out water as it is a spectator molecule but we are putting it here for illustration purposes.

Having explored dynamic equilibrium in the first week, we know that the rate of the forward reaction is equal to the rate of the reverse reaction.

Hence the rate at which the water molecules surround an ion is equal to the rate at which water molecules are removed from the ion as they attracted to another ion (dehydrating the ion.).

Learning Objective #2 - Investigate the use of solubility equilbria by Aboriginal and Torres Strait Islander Peoples when removing toxicity from foods

Macrozamia is a type of cycad plant as per learning objective.

Let’s explore how Aboriginal People and Torres Strait Islander People are able to remove toxins from macrozamia seeds so they can consume it harmlessly.

Cycads such as Macrozamia have a large, high density seed that is surrounded by a layer of flesh called sarcotesta. The pigments in the sarcotesta gave the cycads’ seeds their colourful colours.

Prior to the colonisation of Australia by the European in the white settlement, there were Dutch explorers that consumed the seeds of Macrozamia plants. It was documented by James Drummond, a botanist who was a early settler in Australia, that eating the fruit without prior processing resulted in many symptoms such as vomiting and unconsciousness.

The Aboriginal people are able to use a variety of food processing methods to detoxify Macrozamia. According to sources from Grey and Moore, the aboriginal people used anaerobic fermentation techniques to process and detoxify the seeds of Macrozamia.

The detoxification process involved cutting the sarcotesta of the seed and submerging the food directly in shallow lakes for leaching. There are toxic substances such as cycasin and macrozamin in macrozamia’s sarcotesta. The slicing of the sacrotesta increased the surface area whereby toxins can be leached out. Sometimes the cycad was grounded down to further increase the surface area for leaching.

The washing process was done delicately to prevent toxic substances of the fruit to pollute nearby water channels which was used as potable water.

Following this, the seeds were buried in holes and concealed the hole from sunlight using a blanket of leaves. The fermentation process for the fruits was approximately two weeks until the sarcotesta became mouldy. The holes had a depth of approximately a woman’s arm length (50 to 60 centimetres deep) with a diameter of 30 centimetres.

Overall, these deep holes provided an environment that was deprived of oxygen (anaerobic), absent of sunlight and at a temperature suitable for fermentation to occur. Moreover, this minimised the risk of other organisms such as bugs and marsupials with the capacity to burrow from eating the seeds.

As time was forwarded to the late nineteenth century, bags were used submerge seeds in salt water which was usually attached to trees in the nearby lakes. A rope was used to close off the bag’s opening to prevent the water and endosperm of the food (see diagram below) from escaping.

It is important to note that the Noongar People, aboriginal people from southwest Australia, did not eat the endosperm of the Macrozamia. Instead, they only ate the sarcotesta (outermost flesh section).

On the other hand, Aboriginal people from the eastern board of Australia took a different approach in consuming the Macrozamia.

Rather than discarding the endosperm, they consumed it. However, unlike the Noongar People, they did not consume the sarcotesta. It is still not clear to why this is the case.

Below is a diagram of the fruit, Macrozamia.

There are toxic substances such as cycasin and macrozamin in the sarcotesta and endosperm. Aboriginal people removed most of such toxins from by leaching them out in water of shallow lakes (‘soak pools’).

Cycasin is soluble in water so it can be dissolved leached out from the fruit and into the water. It is important to note that since the leaching was opened in an open system (flowing water in the shallow lakes), the solubility equilibrium, Cycasin(s) <-> Cycasin(aq), was never allowed to be reached to reach equilibrium. However, while the solubility equilibrium could exist in nature, it was never reached equilibrium. Either way, the removal of cycasin and macrozamin through leaching was successful as it is soluble in water.

Other methods that were used included leaving the fruits out to age where sunlight help breakdown the chemical structure of the toxin, effectively reducing the toxins in the food.

Sometimes the fruits and its seeds were roasted prior to leaching which also helps breakdown the toxins’ chemical structure and reduce their levels.

The overall fermentation process allowed Aboriginal People to make the taste of the sarcotesta more potent, elevate texture, increase nutritional value (Vitamin A and D) and facilitate the remove the endosperm from the sarcotesta for consumption (Aboriginal people on eastern Australia) or disposal (Noongar People).

Another food source that was consumed by Aboriginal People and Torres Strait Islanders People (specifically the Tiwi People living from the Tiwi islands) in Northern Territory was bitter yam.

The process was similar to the detoxification process of cycads where they were roasted using earth ovens and leached prior to consumption. This process of leaching removed toxic oxalates from the yam.

Learning Objective #4 - Derive equilibrium expressions for saturated solutions in terms of Ksp and calculate the solubility of an ionic substance from its Ksp value

Notice in the learning objective, the term ‘saturated solutions’ is used instead of unsaturated solutions.

This is because for an equilibrium to be established in the event of the dissolution of an ionic substance, the ionic compound must saturate the solution. This is because unsaturated solutions do not have enough ions dissolved to form trace quantities of precipitate and hence cannot form an equilibrium between the ionic compound and its ions.

Recall the concept of reaction quotient (Q) that we touched on last week. It was used to compare to the Keq value. By comparing the Q and Keq value, it is possible to determine which way the equilibrium position will shift in order to make Q equal to Keq, which is happens at equilibrium.

Recall that there many types of Keq including Ka, Kb, Kc, Kp and Ksp.

Let’s take a closer look into the relationship between Qsp and Ksp here.

The generic formula for the dissolution of an ionic compound such as Calcium Fluoride is:

As we have talked about in last week’s note, to calculate the reaction quotient, Q, you just take the initial or current concentrations of the calcium ions and fluoride ions and multiply them together (after taking into account mole ratio). There is no fractions so we don’t need to divide by the reactants because we exclude solids and pure liquids from equilibrium expressions where the reasons have already been discussed in the prior weeks’ notes.

There are questions for you to practice at the end of this week’s notes. You can check solutions after you do em’.

If Q is greater than Ksp, it would mean that the equilibrium must shift to the left so that Q equals to Ksp (Please refer to previous week’s note if you are unfamiliar with the reaction quotient and Keq relationship). This would mean that more CaF2 solid, or precipitate, will form. The precipitate will stop forming when the value of Q is equal to Ksp. At this point, the solution will be saturated, i.e. at equilibrium. Solutions with Q greater than Ksp are called supersaturated solutions – precipitate will form as long as Q is greater than Ksp or until Qsp = Ksp.

If Q is equal to Ksp, it would mean that the dissolved ionic compound is at equilibrium and the solution is completely saturated. In this situation, addition of more solute (ionic compound) will not dissolved. Solutions with Q equal to Ksp are called saturated solutions. These solution contains the maximum amount of ions, in terms of concentration, that can be dissolved or exist in solution. In this situation of saturated solutions, the rate of precipitation is equal to rate of dissolution so no precipitate will form and no more solid will dissolve. This is because as precipitate are formed, they are immediately dissolved, i.e. no precipitate is formed as there is no shift in equilibrium position as system is at equilibrium.

NOTE: For HSC purposes, trace (very small quantities) quantities of precipitates are formed when Qsp = Ksp. This is because the concentration of ions is just enough to make a saturated solution, allowing trace quantities of precipitates to be formed. However, if the question only says ‘precipitate’ and NOT ‘trace precipitate’ then no precipitate will form when Qsp = Ksp.

If Qsp is less than Ksp, it means that the equilibrium will shift to the right so that Q equals to Ksp. When Q is less than Ksp, it means that the solution is unsaturated and no precipitate will form from the aqueous ions. In this situation, if you add more of the ionic compound, more of it will dissolve to form its ions. So, the concentration of the ionic compound will not increase as no precipitate (ionic compound) will form. This will continue to happen as you add more ionic compound and dissolution will only stop you have added enough so that Q is equal to Ksp. Solutions with Q less than Ksp are called unsaturated solutions and precipitate will not form as long as Q is less than Ksp.