Mechanisms of toxic action and structure-activity relationships for organochlorine and synthetic pyrethroid insecticides.

Abstract

The mechanisms and sites of action of organochlorine (DDT-types and chlorinated alicyclics) and synthetic pyrethroid insecticides are presented with discussion of symptoms, physiological effects, and selectivity. The structural requirements for toxicity are assessed, and structure-activity relationships are considered for each subclass. Lipophilicity is important for all the groups because it facilitates delivery of these neurotoxicants to the site of action in the nerve. Steric factors including molecular volume, shape, and isomeric configuration greatly influence toxicity. Electronic parameters also have been demonstrated to affect biological activity in some of the groups of insecticides, e.g., Hammett's sigma and Taft's sigma * as indicators of electronegativity. New synthetic pyrethroids continue to be developed, with varied structures and different physicochemical and biological properties. Environmental Health Perepectives Vol. 87, pp. 255-262, 1990 Mechanisms of Toxic Action and StructureActivity Relationships for Organochiorine and Synthetic Pyrethroid Insecticides by Joel R. Coats* The mechanisms and sites of action of organochlorine (DDT-types and chlorinated alicyclics) and synthetic pyrethroid insecticides are presented with discussion of symptoms, physiological effects, and selectivity. The structural requirements for toxicity are assessed, and structure-activity relationships are considered for each subclass. Lipophilicity is important for all the groups because it facilitates delivery of these neurotoxicants to the site of action in the nerve. Steric factors including molecular volume, shape, and isomeric configuration greatly influence toxicity. Electronic parameters also have been demonstrated to affect biological activity in some of the groups of insecticides, e.g., Hammett's a and Taft's a* as indicators of electronegativity. New synthetic pyrethroids continue to be developed, with varied structures and different physicochemical and biological properties.

Accumulation of Endosulfan in Wild Rat, Rattus norvegious as a Result of Application to Soya Bean in Mazoe (Zimbabwe)

“…Endosulfan has a half-life of three to seven days in plants so since the first samples were collected a week after spraying, then no appreciable levels of endosulfan sulphate was expected (Matsumura, 1975). Degradation of endosulfan sulphate is also faster than that of endosulfan in the body, so as levels of endosulfan decrease then those of endosulfan sulphate should also decrease, but the decrease should be greater (Coats, 1990). As expected, the levels of endosulfan sulphate were lower than those of endosulfan and followed a similar trend to those of endosulfan.…”

“…Cyclodienes like endosulfan are thought to act on the central nervous system by binding at the picrotoxinin site in the g-aminobutyric acid (GABA) chloride ionophore complex (Coats, 1990). GABA is an inhibitory neurotransmitter that operates through membrane hyperpolarization as mediated by increased chloride flux into nerve cells.…”

“…External symptoms include depressed activity a few hours after exposure followed by hyper excitability, tremors and convulsions. Convulsions can lead to death by interfering with pulmonary gas exchange and by generating severe metabolic acidosis (Coats, 1990;Kiran & Varma, 1988;Nath & Dikshith, 1979).…”

Developmental neurotoxic effects of two pesticides: Behavior and neuroprotein studies on endosulfan and cypermethrin

“…Depending on their structural class, these pesticides exert their neurotoxic effect by different mechanisms. In short, they disrupt the signal transduction in the nervous system by affecting the ion transport across the cell membrane (Coats, 1990). Endosulfan is a restricted OC-classed pesticide and is being voluntary phased-out and scheduled for cancellation in 2016 (EPA, 2010).…”

Molecular response of Drosophila melanogaster tyramine receptor cascade to plant essential oils

“…They have been shown to inhibit both the GABA receptor in marine algi (Coats, 1990), and inhibit acetylcholinesterase (AChE) isolated from different insect species (Grundy and Still, 1985;Ryan and Byrne, 1988), and bovine erythrocytes (Miyazawa et al, 1997). However, no correlation was found between in vivo inhibition of AChE and the toxicity of monoterpenoids.…”