Abstract

Male rats were given vitamin A acetate orally either daily in a dose of 0, 0.83 or 10.0 mg/kg or every third day at three times this dose, 2 wk before and continuing after daily administration of 50 or 75 mg hexachlorophene (HCP)/kg. At certain levels and regimens, vitamin A offered partial protection against HCP toxicity, in that it retarded the rate at which deaths occurred but not the eventual outcome. The highest level of vitamin A (30 mg/kg) given every third day for 2 wk did not alter significantly the single-dose LD 50 of HCP. Vitamin A deficiency produced by omission of the vitamin from the diet considerably increased the toxicity of HCP after daily dosing at various levels. Cerebrospinal-fluid pressure in vitamin A-deficient control rats was 88 mm saline compared with 251 mm in HCP-treated normal rats. These quantitative differences suggest that these two factors exert independent and possibly additive effects rather than that vitamin A plays a primary role in the genesis of HCP neurotoxicity. Results do indicate, however, that the nutritional status of the animal affects its susceptibility to toxic halogenated hydrocarbons.

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