Cholinesterase brain

M (44% decreased plasma and 25% decreased brain cholinesterase levels)... 

When methyl parathion was given orally to rats at doses of 1.5 mg/kg and to guinea pigs at 50 mg/kg, plasma, erythrocyte, and brain cholinesterase activity was maximally inhibited within 30 minutes after administration. In rodents of both species that died after acute intoxication, brain cholinesterase levels decreased to 20% of control values and often to 5-7% (Miyamoto et al. 1963b). The species difference in susceptibility to orally administered methyl parathion is noted in Section 3.2.2.1. 

Mean plasma, erythroc54e, and brain cholinesterase activities were significantly reduced by 67-88%, 9-20%, and 76-79%, respectively, in rats of both sexes following 2-year exposures to 2.5 mg/kg/day methyl parathion (Suba 1984). This effect did not occur in rats exposed to either 0.025 or 0.25 mg/kg/day methyl parathion. 

Permethrin, a pyrethrin pesticide, decreased the inhibition of brain cholinesterase activity by methyl parathion, but methyl parathion decreased the LD50 of permethrin when the two pesticides were simultaneously administered to rats (Ortiz et al. 1995). The potentiation of permethrin lethality may be due to the inhibition by methyl parathion of carboxylesterase, which metabolizes permethrin. 

The inhibition of brain cholinesterase is a biomarker assay for organophosphorous (OP) and carbamate insecticides (Chapter 10, Section 10.2.4). OPs inhibit the enzyme by forming covalent bonds with a serine residue at the active center. Inhibition is, at best, slowly reversible. The degree of toxic effect depends upon the extent of cholinesterase inhibition caused by one or more OP and/or carbamate insecticides. In the case of OPs administered to vertebrates, a typical scenario is as follows sublethal symptoms begin to appear at 40-50% inhibition of cholinesterase, lethal toxicity above 70% inhibition. 

Grue, C.E., Hart, A.D.M., andMineau, P. (1991). Biological consequences of depressed brain cholinesterase activity in wildlife. In Mineau, P. (Ed.) Cholinesterase Inhibiting Insecticides— Their Impact on Wildlife and the Environment, 151-210. Amsterdam Elsevier. 

Dieter MP, Ludke JL. 1975. Studies on the combined effects of organophosphates and heavy metals in birds. I. Plasma and brain cholinesterase in Cotumix quail fed methyl mercury and orally dosed with parathion. Bull Environ Contam Toxicol 13 257-262. 

Total bird numbers on treated plots decreased. Some of the decrease (2-3%) was due to death, but most represented movements of birds in reaction to a reduction in their arthropod food. Brain cholinesterase levels in several avian species were depressed 1 week posttreatment (Mullie and Keith 1993)... 

Horned larks (Eremophila alpestris) had brain cholinesterase activity levels depressed 22% at 3 days posttreatment, and 8% at 16 days. No sick or dead birds found however, no systematic searches were made for the small lark carcasses, nor were specific observations for toxic signs conducted (McEwen etal. 1986)... 

McEwen, L.C., L.R. DeWeese, and P. Schladweiler. 1986. Bird predation on cutworms (Lepidoptera Noctuidae) in wheat fields and chlorpyrifos effects on brain cholinesterase activity. Environ. Entomol. 15 147-151. 

Montz, W.E., Jr. and R.L. Kirkpatrick. 1985. Temporal patterns of brain cholinesterase activities of whitefooted mice (Peromyscus leucopus) following dosing with diazinon or parathion. Arch. Environ. Contam. Toxicol. 14 19-24. 

Owls had brain cholinesterase activity values intermediate between controls and those fed poisoned whole Coturnix... 

---