Effect of Acute Paraquat Toxicity on Ascorbic Acid Levels of Liver and Plasma in Mice

The administration of paraquat (PQ to mice (oral administration of 200 mg/kg body weight and intraperitoneal injection of 100 mg/kg body weight resulted in a significant increase of ascorbic acid (AsA levels in the liver and plasma. The hepatic level of thiobarbituric acid reac‑ tive substances was significantly elevated after the treatment with PQ. We examined whether the metabolism of PQ and the oxidative stress by PQ influence the biosynthesis of AsA in mice. The activities of AsA‑synthesizing enzymes uridine diphosphate glucuronosyltransferase β ‑glucuronidase and L‑gulono‑γ‑lactone oxidase were measured in the mouse liver. These enzyme activities were not stimulated by the administration of PQ presumably due to the hy‑ drophilic property of PQ. Reduced glutathione (GSH level in the mouse liver was significantly decreased by the administration of PQ. The depletion of GSH in hepatocyte causes an increased AsA production via increased glycogenolysis. The increase of glucose concentration induced by glycogenolysis was not observed in blood. These data suggest that neither the metabolism of PQ nor the oxidative stress by PQ activate the AsA biosynthesis in mouse liver. It is likely that AsA level increased by the acute toxicity of PQ may be dependent upon the reduction of dehy‑ droascorbic acid by GSH rather than de novo biosynthesis of AsA in mouse liver.