Demonstrates lethal toxicity effects of monochloroacetic acid exposure in rats, highlighting significant metabolic disruptions.
This study aimed to clarify the lethal toxicity in acute monochloroacetic acid (MCA) poisoning. MCA was subcutaneously injected in rats and blood was collected. We measured metabolites and hormones related to gluconeogenesis. The blood glucose level in the MCA-treated group was signifi- cantly reduced. Serum concentrations of acetoacetate and 3-hydroxybutyric acid were decreased and serum free fatty acid levels were increased in the MCA-treated group, whereas serum concen- trations of carnitine were reduced. Concentrations of plasma ammonia in the treated group were more than 5 times higher than those in the control group. Serum concentrations of hyperglycemic hormones (catecholamine, ACTH, cortisol, glucagon) were significantly increased in the MCA-treat- ed group. Serum concentrations of insulin were within the reference value in both groups. It was concluded that hypoglycemia caused by exposure to MCA is not due to the resultant hormonal dis- turbance, but might be partly induced by impaired beta-oxidation of fatty acid owing to the inade- quate biosynthesis of carnitine. Hypoglycemia, hypoketonemia and hyperammonemia may play roles in MCA poisoning deaths.
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Tominaga et al. (2003) studied this question.
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