Relationship between dietary protein level and enzymatic changes in acute poisoning of rats with chlorfenvinphos

Puzayńska, L.

doi:10.1002/food.19840280802

Cited by 2 publications

(1 citation statement)

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“…Reductions in dietary protein can impair protein synthesis in numerous tissues (Garlick et al, 1975) including brain (Yokogoshi et al, 1992;Hayase et al, 1998) and liver (Grant & Hoffenberg, 1977;Yoshizawa et al, 1998). Rats maintained on protein-deficient (4.5%) diets exhibited higher acute toxicity and brain AChE inhibition following exposure to the OP pesticide chlorfenvinphos (Puzynska, 1984). Availability of dietary factors could be critically limited during the first few days after PS exposure (Figures 1 and 2), at a time when demands for de novo protein synthesis would presumably be high.…”

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confidence: 98%

Glucose Feeding Exacerbates Parathion-Induced Neurotoxicity

Olivier

Liu

Karanth

et al. 2001

Journal of Toxicology and Environmental Health, Part A

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Excessive dietary intake of sugars could alter various biotransformation processes and the pharmacological and toxicological properties of numerous xenobiotics. In the present study, the effects of glucose supplementation were examined on the neurotoxicity of the organophosphorus (OP) pesticide parathion (PS) and its active metabolite, paraoxon (PO), a potent inhibitor of acetylcholinesterase (AChE). Rats (n = 6-12/treatment group) were given free access to tap water or 15% glucose (w/v) in tap water beginning 7 d prior to OP toxicant exposure. Food, caloric intake, and body weight were measured daily. Animals were challenged with either PS (4.5, 9, or 18 mg/kg, sc) or PO (0.3 0.5, or 0.7 mg/kg, sc) and clinical signs of neurotoxicity (i.e., autonomic dysfunction, involuntary movements) were recorded daily for the following 13 d. Glucose feeding was associated with a dramatic drop (approximately 50%) in feed intake and an increase (approximately 20% in total caloric consumption over the 7 d prior to OP exposure. Functional toxicity associated with PS exposure was increased in glucose-fed (GF) rats, but the glucose diet had no apparent effect on clinical signs of toxicity following PO treatment. Glucose feeding increased the magnitude of AChE inhibition in the frontal cortex and plasma at lower dosages (i.e., 4.5 and 9 mg/kg) 3 d following PS treatment. Time-course studies (3, 7, and 11 d after PS exposure, 18 mg/kg, sc) indicated significantly greater brain and plasma AChE inhibition in glucose-fed animals at later time points. In contrast, glucose feeding had no effect on the degree of AChE inhibition following PO exposure. Neither liver microsomal oxidative desulfuration of PS, nor liver or plasma paraoxonase, nor liver or plasma carboxylesterase activities were measurably affected by glucose feeding. Downregulation of muscarinic receptors 7 d after PS exposure (18 mg/kg, sc) was more extensive in GF rats. It is postulated that excessiveglucose consumption decreases the intake of other dietary components, in particular amino acids, limiting the de novo synthesis of AChE and consequent recovery of synaptic transmission. Due to the shorter duration of inhibition following PO exposure, sponta neous reactivation of AChE may be more important than de novo protein synthesis in recovery of function, and thus with the effects of glucose feeding on its toxicity. Individuals that derive a large proportion of their calories from sugars may be at higher risk of acute toxicity from organophosphorus pesticides such as PS.

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