Sodium selenite (Na₂SeO₃) is the selenium form used in the composition of dietary supplements, and diphenyl diselenide (PhSe)₂ is an important intermediate in organic synthesis, which increases the risk of human exposure to this chemical in the workplace. These compounds have been reported to inhibit the cerebral and hepatic aminolevulinic acid dehydratase (ALA‐D) in vitro, and now we show that ascorbic acid can reverse some alterations caused by in vivo selenium exposure, but not ALA‐D inhibition. The effect of Na₂SeO₃ or (PhSe)₂ and ascorbic acid on selenium distribution, total non‐protein thiol, ascorbic acid content (liver and brain) and haemoglobin was also examined. Mice were exposed to 250 μmol/kg (PhSe)₂, or 18.75 μmol/kg Na₂SeO₃ subcutaneously, and to ascorbic acid, twice a day, 1 mmol/kg intraperitonially, for 10 days. Hepatic ALA‐D of mice treated with (PhSe)₂ was inhibited about 58% and similar results were observed in the animals that received ascorbic acid supplementation (P<0.01, for (PhSe)₂‐treated and (PhSe)₂+ascorbic acid‐treated mice). The haemoglobin content decreased after treatment with (PhSe)₂ (P<0.01). However, the haemoglobin content of the (PhSe)₂+ascorbic acid group was significantly higher than in the (PhSe)₂‐treated mice (P0.10). Ascorbic acid treatment decreased significantly the hepatic and cerebral deposition of Se in (PhSe)₂‐exposed mice (P<0.01). Hepatic non‐protein thiol content was not changed by treatment with (PhSe)₂, ascorbic acid or (PhSe)₂+ascorbic acid. Hepatic content of ascorbic acid was twice that in mice that received (PhSe)₂, independent of ascorbic acid treatment (P<0.001). The results of this study suggest that vitamin C may have a protective role in organodiselenide intoxication.