Heffernan W P, Guion C, Bull R J
J Environ Pathol Toxicol. 1979 Jul-Aug;2(6):1487-99.
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.
研究发现，大鼠在饮用水中接触高达500 ppm的亚氯酸钠90天后，会出现轻微但可代偿的贫血。接触30天后出现的血红蛋白、红细胞计数和血细胞比容下降，在治疗90天时已基本恢复。适应性的迹象表现为，在接触50 ppm和100 ppm ClO2- 90天后，红细胞中的2,3 - 二磷酸甘油酸浓度仍保持升高。然而，在低至50 ppm的亚氯酸盐水平下检测到的红细胞谷胱甘肽水平与剂量相关的下降，在接触90天后仍未恢复。虽然未观察到其他明显的毒性迹象，但接触ClO2- 的猫红细胞周转率增加，证实了溶血性贫血的存在。亚氯酸盐在体内引起的谷胱甘肽减少，在体外进一步用亚氯酸盐处理时，被证明会增强过氧化氢的形成。因此，在全面确定水中亚氯酸盐的危害之前，必须特别关注对溶血性贫血敏感的个体。
