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What does Toxicology mean?
Toxicology seeks to characterize the potentially adverse effects of foreign chemicals and their dosage response relationships to protect public health. Toxicology is defined as the study of the adverse effects of chemicals on living organisms. The term toxicity is defined as the inherent capacity of a chemical to cause injury. Thus, all chemicals, including drugs, have some degree of toxicity. This was first documented by the physician Paracelsus (1493ac1541), who stated that All substances are poisons: There is none which is not a poison. The right dose differentiates a poison from a remedy.  

How do toxic chemicals work?
Toxic chemicals from the environment may contact the skin and/or be absorbed after ingestion or inhalation. These exogenous chemicals are distributed to various organs, where they may be metabolized to products that may be more or less toxic than the administered chemical. The parent compound or its metabolites interact with target macromolecules, resulting in a toxic effect.

A. Common target tissues
Any tissue or organ within the body can potentially be affected by a chemical toxin, and indeed, most chemicals adversely affect more than one tissue. However, the lungs (the portal of entry for gases, vapors, and particles that can be inhaled), liver (the portal of entry for ingested chemicals), and tissues with a high blood flow, such as brain and kidney, are particularly vulnerable to the toxic actions of chemicals. In addition the heart is sensitive to any toxin-induced disruption in ionic gradients.

B. Nonselective actions
Exposure to some chemicals, such as corrosive compounds, leads to a local irritation and/or caustic effects that are nonselective in nature and occur wherever the site of application or exposure is located. Examples include exposure to strongly alkaline or acidic substances, which cause injury by denaturation of macromolecules, such as proteins, and cleavage of chemical bonds essential to the function of biomolecules.

C. Selective actions
Many chemicals produce their toxic effects by interfering with the functions of specific biochemical pathways and/or macromolecules within a tissue. For example, the rodenticide warfarin inhibits the vitamin K dependent posttranslational modification of certain clotting factors by the liver. Selective toxic actions of chemicals are usually apparent only after the chemical has been absorbed and distributed within the body, in contrast to nonselective actions, which generally occur at the exposure site.

D. Immediate and delayed actions
Many compounds have toxic actions that will quickly lead to symptoms following exposure. For example, inhibition of acetylcholinesterase by an organophosphate insecticide like malathion will rapidly lead to symptoms of excess acetylcholine at synapses and neuroeffector junctions. However, many chemicals exert effects that have latency periods of as long as several decades for example, the carcinogen asbestos can lead to formation of significant pulmonary pathology, including cancer, 15 to 30 years after exposure.

How do antidotes work ?
Specific chemical antidotes for poisonings exist for only a small number of chemicals or classes of chemicals. The following are examples of strategies that form the basis for the use of specific chemical antidotes, with an example of how each can be applied.

A. Pharmacologically antagonize toxic action
Atropine is a muscarinic-receptor antagonist that is used as an antidote for intoxication by the anticholinesterases. It works by blocking access of excess acetylcholine to muscarinic receptors .

B. Accelerate detoxification of toxic agent
Acetaminophen at very high doses will produce liver necrosis as a result of its metabolic activation by cytochromes P450. Administration of N-acetylcysteine will serve as a substitute for glutathione by binding to and inactivating the reactive metabolites produced from acetaminophen. To be effective, N-acetylcysteine must be given as early as possible (within 8-10 hours of ingestion of acetaminophen).

C. Provide alternative target
Cyanide poisoning is treated with a two-step process. Sodium nitrite is administered to induce the oxidation of hemoglobin to methemoglobin, which has a high binding affinity for cyanide to produce cyanmethemoglobin. Amyl nitrite can also be used for this purpose. The second step in the antidotal treatment of cyanide intoxication is to accelerate its detoxification. Administration of sodium thiosulfate will accelerate the production of thiocyanate, which is much less toxic than cyanide and is also quickly excreted in the urine. In patients with smoke inhalation and cyanide toxicity, the induction of methemoglobin should be avoided unless the carboxyhemoglobin concentration is less than 10 percent. Otherwise, the oxygen-carrying capacity of blood becomes too low.

D. Reduce metabolic activation
The toxicity of methanol is thought to be mediated by formic acid, which is produced by the metabolism of methanol by alcohol dehydrogenase. Fomepizole is considered an antidote to methanol, because it inhibits alcohol dehydrogenase. Slowing the rate of methanol metabolism reduces the rate of rate formic acid production, thereby protecting the patient from the toxic effects of formic acid.

E. Restore altered target
Acetylcholinesterase that has been inhibited as a result of phosphorylation by organophosphorus compounds often can be reactivated by the antidote pralidoxime.

F. Chelators
Chelators are drugs that will form covalent bonds with cationic metals. The chelator-metal complex is then excreted in the urine, thereby greatly facilitating the excretion of the heavy metal. Unfortunately, chelators are not specific to heavy metals, and essential metals, such as zinc, often can also be chelated. Additionally, some chelators have potentially serious adverse effects themselves, and their use in treatment of heavy metal intoxication is undertaken only when the benefits of chelation therapy outweigh the associated risks.

• Dimercaprol: Dimercaprol, also known as British Anti-Lewisite, was the first chelator utilized, having been developed during World War II as a chelator for the arsenical war gas Lewisite. Dimercaprol is used by itself to chelate mercury and arsenic and in combination with edetate calcium disodium to treat lead intoxication. It is not effective after oral administration and is usually given intramuscularly. Use of dimercaprol is often limited by its capacity to increase blood pressure and heart rate.
• Succimer: Succimer (dimercaptosuccinic acid) is a derivative of dimercaprol that is effective upon oral administration. A second advantage of succimer over dimercaprol is the lack of increased blood pressure and heart rate during treatment. Some elevation of serum levels of hepatic enzymes can be observed with succimer treatment. Succimer is currently approved for treatment of lead intoxication, but may be effective in chelation of other metals as well.
• Edetate calcium disodium: Edetate calcium disodium is used primarily for treatment of lead intoxication, but it can also be used for poisoning by other metals. It is not effective after oral administration and is usually given intravenously or intramuscularly. The calcium disodium salt of EDTA must be the form utilized to prevent chelation of calcium and its depletion from the body. Edetate calcium disodium can cause renal damage that is reversible upon cessation of the drug.