Effect of acrylamide intoxication on pyridine nucleotide concentrations and functions in rat cerebral cortex

Abstract

Male rats were given cumulative doses of 428 mg/kg (low dose) and 668 mg/kg (high dose) of acrylamide. Concentrations of oxidized pyridine nucleotides were determined in samples of cerebral cortex from treated and control rats. The concentration of NAD + was significantly increased (P < 0.01) in brains from the high dose animals. The function of pyridine nucleotides was evaluated by measuring substrates of pyridine nucleotide-dependent enzymes both in immediately frozen cerebral cortex and in cortices subjected to ischemia, by measuring total high-energy phosphate and the rate of its use during ischemia, and by determining the cytoplasmic redox state of pyridine nucleotides from enzyme equilibrium constants and measured substrate levels. α-Glycerophosphate was significantly elevated in the brains from the high dose animals (P < 0.05), while other measured substrates were unchanged. Changes in substrate concentrations during ischemia were similar in cerebral cortices from controls and treated rats and did not suggest interference by acrylamide with coenzyme function. Total highenergy phosphate sources were unchanged in treated animals and the rate of their use during ischemia was the same as that of controls. Calculation of the redox state of cytoplasmic pyridine nucleotides suggested that both NAD and NADP may be more in the reduced form in cerebral cortices of treated animals than in controls; however, these changes were small compared to redox changes under other conditions. While acrylamide increased the concentration of NAD + in cerebral cortices from treated rats, there was little suggestion of an interference with pyridine nucleotide function.