Biological paralysis

Enzyme Inhibition. Some materials produce toxic effects by inhibition of biologically vital enzyme systems, leading to an impairment of normal biochemical pathways. The toxic organophosphates, for example, inhibit the cholinesterase group of enzymes. An important factor in thek acute toxicity is the inhibition of acetylocholinesterase at neuromuscular junctions, resulting in an accumulation of the neurotransmitter material acetylcholine and causing muscle paralysis (29) (see Neuroregulators). 

The biological effect of the quinolizidine alkaloids is on the nervous system. Tremors, convulsions and pulmonary arrest have been noted in laboratory animals. Quinolizidine alkaloids cause depression, laboured breathing, trembling, convulsions and respiratory paralysis in sheep . 

Unlike the nonspecific effects and uncommon occurrence of direct mortality observed in wildlife exposed to chlorinated hydrocarbon pesticides, several studies have documented direct mortality from exposure to OP and carbamate insecticides. The method by which the OPs and carbamate insecticides affect wildlife is quite different from the method by which the chlorinated hydrocarbon insecticides effect wildlife. The OPs and carbamates inhibit cholinesterase, primarily acetylcholinesterase (AChE), which is an enzyme that functions in the breakdown of the neurotransmitter acetylcholine. Acetylcholine functions in the transmission of nerve impulses. Therefore, when AChE is inhibited by an OP or carbamate insecticide, it can no longer breakdown acetylcholine and there is continued transmission of nerve impulses that eventually leads to nerve and muscle exhaustion. The respiratory muscles are a critical muscle group that is affected, often leading to respiratory paralysis as the immediate cause of death. A major difference in the mode of action between OPs and carbamates is that the inhibition of AChE by OPs is, from a biological standpoint, irreversible, while the inhibition from exposure to carbamates is reversible in a biologically relevant time frame. There... 

Major alkaloid extracted from seeds of Colchicum autumnale common meadow saffron. Nausea, vomiting, convulsions, paralysis, death. Used as a treatment for gout and in experimental biology as an arrestor of mitosis to facilitate examination of chromosomes. 

The biological action of azides is caused by HN, formed by hydrolysis (Bradbury et al.. 1957 Parochetti and Warren, 1970). The biochemical mode of action is based, according to Keilin (1936), on the paralysis of cell respiration and on the inhibition of the oxidative enzyme system of the cell. 

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