Oxidative damage to the erythrocyte induced by sodium chlorite, in vivo.

Sodium chlorite in drinking water was found to produce a slight but compensated anemia in rats after exposure to up to 500 ppm for 90 days. Decreases in hemoglobin, red cell count, and packed cell volume seen after 30 days exposure had substantially recovered by 90 days of treatment. Signs of adaptation remained in that 2,3-diphosphoglyceric acid concentrations in the red cell remained elevated after 90 days exposure to 50 and 100 ppm CIO2-. However, dose-related decreases in erythrocyte glutathione levels, detected at chlorite levels as low as 50 ppm, remained decreased after 90 days exposure. While no other signs of overt toxicity were observed, the fact that hemolytic anemia was involved was confirmed by an increased turnover of red cells in cats exposed to CIO2-. Chlorite-induced decreases in glutathione in vivo were demonstrated to enhance formation of hydrogen peroxide when treated further with chlorite in vitro. Consequently, before a comprehensive determination of the hazards of chlorite in water can b: made, particular attention must be paid to individuals sensitive to hemolytic anemia.