(1) Previous studies showed that acute administration of O,O,S trimethyl phosphorothioate (OOS-TMP), a contaminant in malathion, acephate and fenitrothion, led to increases in metabolic activities, such as, secretion of interleukin 1 and nonspecific esterase, of splenic and peritoneal macrophages.
(2) High correlation (r = 0.78) was found between skin exposure level and urine acephate elimination.
(3) Reports that near-lethal doses of the pesticide methamidophos (O,S-dimethyl phosphoramidothioate) caused a delayed neurotoxicity (OPIDN) in humans and that another phosphoramidate, isofenphos, caused OPIDN in the hen at high doses, prompted a study of the abilities of acephate (O,S-dimethyl acetylphosphoramidothioate) to inhibit brain acetylcholinesterase (AChE) and neuropathy target esterase (NTE) in vivo.
(4) The toxicity of acephate to four species of aquatic insects, as well as the metabolism and cholinesterase-inhibiting properties of the chemical in the rat were studied.
(5) The first batch was treated with chronic (50 mg.Kg-1.day-1 for 7 weeks) and second batch was treated with acute (600 mg.Kg-1.day-1 for one day) doses of acephate, third group was served as control which received vehicle only.
(6) Acephate residue levels in rind were less than 3.0 ppm 14 days after treatment; acephate residues in pulp were less than 3.0 ppm throughout the experiment.
(7) These observations suggest that chronic exposure to acephate altered the activity of the noncholinergic system without altering the cholinergic activity, and that low-level chronic exposure to organophosphorous compounds cannot be predicted by measuring the ChE or AChE enzyme activities.
(8) However, solubilization did not alter the kinetics of inhibition of rat AChE by methamidophos or the kinetics of inhibition of cockroach AChE by acephate or methamidophos.
(9) Acephate is a water-soluble organophosphate insecticide whose action on insects has been related to its conversion to methamidophos, a very potent anticholinesterase agent which has caused delayed neuropathy in man.
(10) In this investigation of two insecticides, methamidophos was at least 75 to 100 times more potent an inhibitor of acetylcholinesterase (AChE) and cholinesterase (ChE) than was acephate.
(11) Based on these values, daily workers' absorption of acephate was estimated to be in the order of 10-20 mg. Urinary excretion of unchanged acephate followed a pattern consistent with exposure, showing peak values of excretion during the workshift or in the eight hr after the end of the workshift.
(12) Others (methyl-parathion, acephate, phosphamidon, monocrotophos) have no such effects, even if they have a very high intrinsic toxicity.
(13) Neither acephate, methamidophos, nor carbaryl could be shown to escape from water into the atmosphere.
(14) The mechanism of acephate-cockroach AChE interaction was different than the mechanism of acephate-rat AChE interaction.
(15) Unlike acephate, methamidophos was a potent inhibitor of both cockroach and rat enzymes.
(16) It is proposed that both the rat and cockroach enzyme may contain, along with the anionic and esteratic sites, an "electron deficient" (ED) binding site which may exhibit selectivity for acephate and nefopam.
(17) When acephate was added to the enzyme after methamidophos, its protective effect decreased with increasing time between the additions.
(18) The genotoxic potential of acephate technical (AT) in vitro and in vivo has been studied in bioassays detecting primary DNA damage, chromosomal alterations, and gene mutation.
(19) Under the same conditions, carbaryl was less persistent than acephate in the natural waters: 18 to 20% were recovered from pond water after 42 days, and 37 to 40% from creek water after 50 days.
(20) The decreased oxidative potential and reduced flux of ketoacids into TCA cycle through transamination reactions indicate that acephate caused energy crisis in the brain during chronic treatment.