science

Toxication

Toxication is a science topic covered in the lgStudy science library. This page brings together a partial reference excerpt, illustrations, worked examples, real-world applications and a short study plan, so you can understand Toxication rather than just read about it. In short: Toxication, toxification or toxicity exaltation is the conversion of a chemical compound into a more toxic form in living organisms or in substrates such as soil or water. The conversion can be caused by enzymatic metabolism in the organisms, as well as by abiotic chemical reactions.

Key takeaways

Toxication belongs to science; place it in that map before memorising details.
Learn the definition first, then one example that makes the definition concrete.
Connect Toxication to a quantity you can measure, compute or draw — that is where exam questions come from.
Reproduce the core statement of Toxication from memory before moving on to harder problems.

Reference excerpt

Toxication, toxification or toxicity exaltation is the conversion of a chemical compound into a more toxic form in living organisms or in substrates such as soil or water. The conversion can be caused by enzymatic metabolism in the organisms, as well as by abiotic chemical reactions. While the parent drug is usually less active, both the parent drug and its metabolite can be chemically active and cause toxicity, leading to mutagenesis, teratogenesis, and carcinogenesis. Different classes of enzymes, such as P450 monooxygenases, epoxide hydrolase, or acetyltransferases can catalyze the process in the cell, mostly in the liver. Parent non-toxic chemicals are generally referred to as protoxins. While toxication is generally undesirable, in certain cases it is required for the in vivo conversion of a prodrug to a metabolite with desired pharmacological or toxicological activity. Codeine is an example of a prodrug, metabolized in the body to the active compounds morphine and codeine-6-glucuronide.

Toxication by enzymatic metabolism

CYP450 enzymes

Phase I of drug metabolism are bioactivation pathways, which are catalyzed by CYP450 enzymes, produce toxic metabolites and thus have the potential to damage cells. The unusual level of activity CYP450 enzymes might lead to the changes in drug metabolism and convert drugs into their more toxic forms. Among Phase I CYP450 enzymes, the subfamilies CYP2D6 and CYP3A are responsible for hepatotoxicity during drug metabolism with a number of different drugs, including flucloxacillin, troleandomycin, and troglitazone. Hepatotoxicity indicates the drug's toxicity to liver. Paracetamol (acetaminophen, APAP) is converted into the hepatotoxic metabolite NAPQI via the cytochrome P450 oxidase system, mainly by the subfamily CYP2E1. Hepatic reduced glutathione (GSH) will detoxify this formed NAPQI quickly if APAP is taken at a proper level. In the case of overdoses, the storage of GSH will not be enough for NAPQI detoxication, thereby resulting in acute liver injury.

Other oxidoreductases Oxidoreductases are enzymes that catalyze the reactions that involve the transfer of electrons. Methanol in itself is toxic due to its central nervous system depression properties, but it can be converted to formaldehyde by alcohol dehydrogenase and then converted to formic acid by aldehyde dehydrogenase, which are significantly more toxic. Formic acid and formaldehyde can cause severe acidosis, damage to the optic nerve, and other life-threatening complications.

Ethylene glycol (common antifreeze) can be converted into toxic glycolic acid, glyoxylic acid and oxalic acid by aldehyde dehydrogenase, lactate dehydrogenase (LDH) and glycolate oxidase in mammalian organisms. The accumulation of the end product of the ethylene glycol mechanism, calcium oxalate, may cause malfunction in the kidney and lead to more severe consequences.

Other examples Other examples of toxication by enzymatic metabolism include:

Conversion of secondary amines in the stomach into carcinogenic nitrosamines via NO pathway. Nicotine into the nitrosated carcinogenic NNK (4-(methylnitrosamino)- 1-(3-pyridyl)-1-butanone) in the lung. Benzo[a]pyrene into the carcinogenic benzo[a]pyrene diol epoxide (BP-7,8-dihydrodiol-9,10-epoxide) Hypoglycin A into the highly toxic MCPA-CoA

Toxication by abiotic chemical reactions Increases in toxicity can also be caused by abiotic chemical reactions. Non-living elements affect the abiotic chemical reactions. Anthropogenic trace compounds (ATCs) have potential toxicity to the organisms in aquatic system. Arsenic contamination in drinking water can be chemically toxic. The uptake and metabolism of arsenic may result in damage to the body. When organic arsenic is converted into more toxic inorganic arsenic, it causes carcinogenesis, cytotoxicity (toxic to cells) and genotoxicity (causing mutations in genes).

See also Chelation therapy Detoxification

References

Illustrations

Worked examples

Example 1 — a first encounter with Toxication

Start with the simplest possible case. Write down what Toxication claims or describes in one sentence, then invent the smallest concrete situation in which that sentence is true. In science, the smallest case is usually a single object, a single equation or a single measurement. Check that every symbol or term in your sentence has a meaning in that case.

Example 2 — changing one variable

Take the situation from Example 1 and change exactly one quantity: double it, halve it, or set it to zero. Predict what should happen to Toxication before you calculate. Comparing your prediction with the result is the fastest way to find out whether you understand the idea or only the words.

Example 3 — an exam-style question

Typical questions about Toxication ask you to (a) state it precisely, (b) apply it to given data, and (c) explain a limitation. Practise writing all three answers in under five minutes; the third part is what separates a full-mark answer from an average one.

Applications of Toxication

In research: Toxication appears in science research whenever the underlying quantities have to be modelled precisely. Papers usually cite it as a starting assumption and then explore where it breaks down.
In technology and industry: Engineering practice reuses Toxication in design rules, simulations and safety margins. Knowing the idea lets you read a specification sheet and understand why the numbers look the way they do.
In the classroom: Toxication is common in secondary-school and first-year university syllabi. It links to neighbouring topics Biodegradation, Pharmacokinetics, so understanding it makes those chapters shorter.
In everyday life: Look for Toxication outside the textbook — in sport, cooking, traffic, electronics or the sky above you. An example you found yourself is remembered far longer than one you were given.

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How to study Toxication in 20 minutes

Read the reference excerpt below once, without taking notes.
Close the page and write down what Toxication means in your own words.
Compare your version with the excerpt and mark what you missed.
Work through the three examples above with pen and paper.
Explain Toxication out loud to somebody else — or to Teacher Smith in the lgStudy chat.

Frequently asked questions

What is Toxication in simple terms?

Why does Toxication matter?

Because it connects several science ideas at once: it gives you a definition you can apply, a quantity you can calculate, and a way to check whether a result is plausible.

How should I study Toxication?

Read the excerpt, restate it from memory, then work through the examples and applications listed on this page. The five-step study plan above takes about twenty minutes.

What does this page cover?

It gives you a compact reference excerpt plus original lgStudy explanations, examples, applications and study material on Toxication.