In vivo toxicity, and glutathione, ascorbic acid and copper level changes induced in mouse liver and kidney by copper(II) gluconate, a nutrient supplement

While copper(II) gluconate (CuGL) is generally used as a nutrient supplemen t for infant foods and as an oral deodorant, little information is availabl e regarding a toxic effect of CuGL on mammals. In this article, we examined in vivo induction of toxicity and change of level of glutathione and ascor bic acid, major biological antioxidants, lipid peroxide and copper (Cu) in liver and kidney 4 h after single intraperitoneal administration of CuGL at 0.05 and 0.10 mmol/kg to mice. Serum glutamic pyruvic transaminase (SGPT) activity, an indicator of hepatotoxicity, significantly increased compared to control in proportion to doses of CuGL. Hepatic level of glutathione mea sured as nonprotein sulfhydryl was not proportional to CuGL doses, but enha nced after dosing of 0.05 mmol/kg and lowered by 0.10 mmol/kg. Like SGPT ac tivity, serum urea nitrogen (SUN) concentration, an indicator of nephrotoxi city, significantly increased in proportion to doses of CuGL. Renal glutath ione level was not different from control after dosing of 0.05 mmol/kg and lowered by 0.10 mmol/kg. In both organs, relative organ weight and lipid pe roxide level were not affected by the treatment with CuGL; ascorbic acid le vel was elevated after dosing of 0.05 mmol/kg and was not different from co ntrol after treatment with 0.10 mmol/kg; like SGPT activity and SUN concent ration, Cu level significantly increased in proportion to doses of CuGL. Th ese results suggest that in the liver and kidney after the treatment with C uGL Cu accumulated may induce toxicity, leading to level changes of glutath ione and ascorbic acid and to no induction of oxidative damage.