Responses Of Living Organisms When Exposed To Toxins.docx

Responses of living organisms when exposed to toxins 1. covalent bonding- modifications of normal biological effects mediated by the cell receptor When most small-molecule drugs meet a protein target, they nestle close to their intended. But the flirtatious relationship between drug and target is often fleeting, with the drug repeatedly drifting away and coming back. Like a teenager with no interest in settling down, the drug forms no permanent bond with its target. Some small molecules, however, do forge lasting ties. Their irreversible covalent bonds with proteins link compound and protein for good. 2. Genotoxic interaction Chemical interaction with DNA possibly leading to heritage change  Clastogenic (chromosal ) effects  Mutagenic (base pair) effects  Development and reproductive toxicity – adverse effects on conception and structure and function of the conception  In genetics, genotoxicity describes the property of chemical agents that damages the genetic information within a cell causing mutations, which may lead to cancer. While genotoxicity is often confused with mutagenicity, all mutagens are genotoxic, whereas not all genotoxic substances are mutagenic. The alteration can have direct or indirect effects on the DNA: the induction of mutations, mistimed event activation, and direct DNA damage leading to mutations. The permanent, heritable changes can affect either somatic cells of the organism or germ cells to be passed on to future generations. Cells prevent expression of the genotoxic mutation by either DNA repair or apoptosis; however, the damage may not always be fixed leading to mutagenesis. 3. Receptor interaction Toxicant at low concentrations modify or inhibit some biological process by binding at a specific site or molecule have a specific acting mode of toxic action. However, at high enough concentrations, toxicants with specific acting modes of toxic actions can produce narcosis that may or may not be reversible. Nevertheless, the specific action of the toxicant is always shown first because it requires lower concentrations. Uncouplers of oxidative phosphorylation. Involves toxicants that uncouple the two processes that occur in oxidative phosphorylation: electron transfer and adenosine triphosphate (ATP) production. Acetylcholinesterase (AChE) inhibitors. AChE is an enzyme associated with nerve synapses that it’s designed to regulate nerve impulses by breaking down the neurotransmitter Acetylcholine (ACh). When toxicants bind to AChE, they inhibit the breakdown of ACh. This results in continued nerve impulses across the synapses, which eventually cause nerve system damage. Examples of AChE inhibitors are organophosphates and carbamates, which are components found in pesticides (see Acetylcholinesterase inhibitors). Irritants. These are chemicals that cause an inflammatory effect on living tissue by chemical action at the site of contact. The resulting effect of irritants is an increase in the volume of cells due to a change in

size (hypertrophy) or an increase in the number of cells (hyperplasia). Examples of irritants are benzaldehyde, acrolein, zinc sulphate and chlorine. Central nervous system (CNS) seizure agents. CNS seizure agents inhibit cellular signaling by acting as receptor antagonists. They result in the inhibition of biological responses. Examples of CNS seizure agents are organochlorine pesticides. Respiratory blockers. These are toxicants that affect respiration by interfering with the electron transport chain in the mitochondria. Examples of respiratory blockers are rotenone and cyanide. 4. Immune mediated hypersensitive reactions –antigenic chemicals resulting to allergic reaction. Cell-mediated immunity is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. 5. Immune suppression- increased susceptibility to infectious agents and tumorigenesis. Immunosuppression is a reduction of the activation or efficacy of the immune system. Some portions of the immune system itself have immunosuppressive effects on other parts of the immune system, and immunosuppression may occur as an adverse reaction to treatment of other conditions 6. Necrosis – cell or tissue death Necrosis (from the Greek "death, the stage of dying, the act of killing" from dead") is a form of cell injury which results in the premature death of cells in living tissue by autolysis. Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma which result in the unregulated digestion of cell components. In contrast, apoptosis is a naturally occurring programmed and targeted cause of cellular death. While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.Cellular death due to necrosis does not follow the apoptotic signal transduction pathway, but rather various receptors are activated, and result in the loss of cell membrane integrity and an uncontrolled release of products of cell death into the extracellular space. 7. Enzyme inhibition – biochemical pathway interruption e.g interference with phosphate molecule synthesis An enzyme inhibitor is a molecule that binds to an enzyme and decreases its activity. Since blocking an enzyme's activity can kill a pathogen or correct a metabolic imbalance, many drugs are enzyme inhibitors. They are also used in pesticides. 8. Lethal synthesis- toxicant incorporation into biochemical pathway lethal synthesis. The metabolic conversion of a substance that has been taken up by a cell into another substance that results in the cell's death. It is colloquially called suicide metabolism

9. Neoplasmic Neoplasia is a type of abnormal and excessive growth of tissue. The growth of a neoplasia is uncoordinated with that of the normal surrounding tissue, and it persists growing abnormally, even if the original trigger is removed. This abnormal growth usually (but not always) forms a mass. When it forms a mass, it may be called a tumor.

10. Lipid peroxidation- free radical oxidation of fatty acids leading to death Lipid peroxidation is the oxidative degradation of lipids. It is the process in which free radicals "steal" electrons from the lipids in cell membranes, resulting in cell damage. This process proceeds by a free radical chain reaction mechanism. It most often affects polyunsaturated fatty acids, because they contain multiple double bonds in between which lie methylene bridges (-CH2-) that possess especially reactive hydrogen atoms. As with any radical reaction, the reaction consists of three major steps: initiation, propagation, and termination. The chemical products of this oxidation are known as lipid peroxides or lipid oxidation products (LOPs). 11. Inflammation -Local and systematic response Local effects Some substances have only a localized effect on one part of the body - where the hazardous agent comes into contact with or enters the body. For example, the local effect can be on the skin, such as an acid burn, or in the digestive tract when a hazardous agent is ingested. Some substances like ammonia, chlorine, welding fumes and exhaust fumes can cause local irritation to the lungs when they are inhaled. B. Systemic effects Systemic effects are problems caused inside the body once a hazardous agent has entered. Systemic effects can occur in the blood when the substance is absorbed into the bloodstream, and in the organs that either store the toxic material (such as the bones and the brain), neutralize it (such as the liver), or remove it from the body (such as the kidney and bladder). A typical systemic effect in the blood is anaemia (a shortage of red blood cells) which can be caused by a number of chemicals, including: lead, beryllium, cadmium, mercury compounds and benzene. Benzene can damage the cells that form blood, leading to leukaemia. The liver can be damaged by toxic substances because it tries to break down many of them once they have entered the body. Some chemicals known to damage the liver are: benzene, DDT, dioxane, phenol and trichloroethylene. Vinyl chloride monomer, used in the plastics industry, is known to cause a rare form of liver cancer.The kidneys and bladder also can be affected by many toxic substances because they are major routes of exit out of the body.