Toxicological effects of sodium selenite in swiss mice

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Abstract
Se as sodium selenite was administered by gavage (three consecutive times) and as drinking water supplements for 46 d to male and female Swiss mice. With respect to survival in 7‐wk‐old mice, Se was less toxic in males than in females when gavaged. Drinking water supplements of 1–64 ppm Se resulted in 1 male and 1 female death in mice first given Se at 7 wk of age. Se supplements to the drinking water of adult (18‐wk‐old) mice was less toxic in females. All young (7‐wk‐old) and adult (18‐wk‐old) mice provided 7–16 ppm Se in the drinking water survived the 46‐d treatment, but in adult mice 64 ppm Se significantly reduced survival. Only 64 ppm Se supplements caused a sharp reduction in body weight in young and adult mice of both sexes. Supplements of 1–8 ppm Se in all mice elicited growth responses similar to those of untreated controls. Occasional liver and kidney congestion, liver necrosis, parenchymal cell degeneration, and bile duct proliferation were observed in control and treatment groups. Serum alkaline phosphatase and glutamic‐oxaloacetic transaminase (SGOT) increased with 32 ppm Se and higher supplements. Survival, growth, serum enzymes, and pathology were normal in untreated controls and in mice of both ages and sexes given 1, 4, and 8 ppm Se supplements. A chronic toxicity study was conducted in female Swiss mice given 1, 4, and 8 ppm Se supplements for 50 wk. The survival of Se‐treated groups was more than 90% and that of controls was only 72% after 50 wk. All mice gained weight, but the group treated with 8 ppm Se gained half as much as other groups. Both liver Se and glutathione peroxidase activity increased in Se‐treated mice compared to controls at 25 and 50 wk. A reduced white blood cell count and increased alkaline phosphatase and SGOT suggested a mild toxic effect of the 8 ppm Se supplement in the chronic study.