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These abnormalities became more marked with time, even on constant dosing. Spike potentials were recorded between the direct response and reflex responses with latency similar to the repetitive activity potential. These electrophysiological abnormalities may be attributable to acetylcholinesterase inhibition at neuromuscular junctions (Maxwell and LeQuesne 1982). CHLORFENVINPHOS 2. 4, 8, or 24 mg/kg/day (females) mg/kg/day in the diet for 104 weeks. 8 mg/kg/day for females). No gross or microscopic histopathology was evident in the brain tissue examined (Ambrose et al.

Similarly, the change in plasma pseudocholinesterase was not used to derive an intermediate MRL because while the inhibition of plasma pseudocholinesterase may have some physiological significance, alteration in the levels of this enzyme is generally regarded more as a biomarker of exposure to organophosphate compounds than as an adverse neurological effect. 5% CHLORFENVINPHOS 2. HEALTH EFFECTS of casein (low-protein diet), 26% of casein (optimal-protein diet), or standard (Murigran) diet for 30 days exhibited depressed cholinesterase activities following oral exposure to chlorfenvinphos.

4, 8, or 24 mg/kg/day (females), no consistent difference in body weight gains in males was evident at any dose level tested, as compared to undosed controls. However, chlorfenvinphos exposure caused a significant decrease in body weight gain in females in the 8 and 24 mg/kg/day dose groups from the 26th week until near the end of the study. The decreased body weight gain became statistically insignificant at the end of the study (Ambrose et al. 1970). 8 mg/kg/day in the diet for 30 days (Barna and Simon 1973).

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