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Cholinesterase inhibitors acute effects

CHRONIC HEALTH RISKS cholinesterase inhibitor cumulative effect of acute hazards is possible. [Pg.420]

CHRONIC HEALTH RISKS repeated or prolonged contact may cause allergic sensitization of skin an organic phosphate cholinesterase inhibitor cumulative effect of acute haz-ards/symptoms is possible may possibly cause reproductive effects in humans human mutation data has been reported. [Pg.708]

Nathan, P.J., Baker, A., Carr, E., et ah Cholinergic modulation of cognitive function in healthy subjects acute effects of donepezil, a cholinesterase inhibitor. Hum. Ptychopharmacol. 16, 481-483, 2001. [Pg.356]

An example of absolutely cumulative toxicity is afforded by tri-o-cresyl phosphate or TOCP (Fig. 2.13). This compound is a cholinesterase inhibitor and neurotoxin. In chickens, an acute dose of 30 mg /kg has a severe toxic effect, which is produced to the same extent by a dose of 1 (mg/kg)/day given for 30 days. This effect may of course be produced by accumulation of the compound in vivo to a threshold toxic level, or it may result from the accumulation of the effect, as it probably does in the case of TOCP. [Pg.32]

The acute toxic effects of the cholinesterase inhibitors, like those of the direct-acting agents, are direct extensions of their pharmacologic actions. The major source of such intoxications is pesticide use in agriculture and in the home. Approximately 100 organophosphate and 20 carbamate cholinesterase inhibitors are available in pesticides and veterinary vermifuges used in the USA. [Pg.146]

Exposure to some organophosphate cholinesterase inhibitors results in a delayed neuropathy characterized by degeneration of axons and myelin. This effect is not associated with the inhibition of acetylcholinesterase, but rather with the inhibition of an enzyme described as neuropathy target esterase (NTE) however, the exact mechanism of toxicity is not yet fully understood (Munro et al., 1994). For some organophosphate compounds, delayed neuropathy can be induced in experimental animals at relatively low exposure levels, whereas for others the effect is only seen following exposure to supralethal doses when the animal is protected from the acute toxic effects caused by cholinesterase inhibition. [Pg.123]

The wide use of cholinesterase inhibitors in various spheres of human activities and the risk of acute and chronic intoxications associated with this process prompted investigation of the role of acetylcholinesterase (AChE) and nonspecific esterases in the immunotropic effects of these chemicals. They irreversibly bind to AChE that normally catalyzes the hydrolysis of acetylcholine (ACh) at the... [Pg.600]

Moser, V.C. (1995). Comparisons of the acute effects of cholinesterase inhibitors using a neurobehavioral screening battery in rats. Neurotoxicol. Teratol. 17 617-25. [Pg.857]

Benomyl is a synthetic, organic fungistat having little or no acute toxic effect in mammals. No systemic poisonings have been reported in humans. Although the molecule contains a carbamate grouping, benomyl is not a cholinesterase inhibitor. It is poorly absorbed across skin that which is absorbed is promptly metabolized and excreted. [Pg.200]

O-ethyl O-4-nitrophenyl phenylphosphonothionate (EPN) is a cholinesterase inhibitor. Combined exposure to both EPN and MBK resulted in a neurotoxic effect in hens that was twice than expected from an additive effect of the two chemicals, l102 and treatment of hens with a combination of EPN, MIBK, and 72-hexane produced acute cholinergic and delayed neurotoxic symptomsJ103l... [Pg.310]

Its excellent pesticidal properties are vitiated by its high toxicity to mammals. Its acute oral lDj, for rats is S.4 mg/kg. In chronic oral toxicity tests the no lTect level for rats was found to be SO ppm. Atropine sulfate appeared to be an antidote of oxamil, but pyridine-2-aldoxime methiodide (PAM), a well-known antidote to cholinesterase inhibitors, does not appear to be effective in this respect. [Pg.258]

CHRONIC HEALTH RISKS prolonged contact may cause dermatitis and skin sensitization cholinesterase inhibitor low blood pressure anorexia cumulative effect of acute hazards is possible. [Pg.577]

CHRONIC HEALTH RISKS cholinesterase inhibitor anorexia low blood pressure cardiac irregularities paralysis cumulative effects of acute hazards/symptoms is possible. [Pg.599]

CHRONIC HEALTH RISKS cholinesterase inhibitor (i.e., causes depressed levels of cholinesterase activity in the serum and erythrocytes) anorexia cardiac irregularities repeated exposure to this chemical may result in cumulative effect of acute hazards/symptoms. [Pg.931]

In Section III, we review studies on persistent effects of exposure to cholinesterase inhibitors. The human epidemiological literature is examined for evidence that persistent behavioral effects of exposure can be measured in populations with histories of acute poisoning and/or chronic ongoing exposure. We then review behavioral data from animal models designed to characterize the behavioral changes caused by experimental treatments with cholinesterase-inhibiting pesticides and identify similarities with the literature on human.s exposed occupationally to these compounds. [Pg.348]


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See also in sourсe #XX -- [ Pg.348 , Pg.349 , Pg.350 ]




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