Hui J Y, Beery J T, Higley N A, Taylor S L
Food Research Institute, University of Wisconsin, Madison 53706.
Food Chem Toxicol. 1989 Jun;27(6):349-59. doi: 10.1016/0278-6915(89)90140-3.
A subchronic oral toxicity study of sodium metabisulphite and acetaldehyde hydroxysulphonate was conducted in normal and sulphite oxidase-deficient rats. At the highest dose level (350 mg SO2 equiv./kg body weight/day for 3 wk followed by 175 mg SO2 equiv./kg body weight/day for 5 wk of either compound), gastric lesions were noted histologically in both normal and sulphite oxidase-deficient rats. The lesions were more severe and more frequently encountered in the sulphite oxidase-deficient rats. The no-effect level for Na2S2O5 was 70 mg SO2 equiv./kg body weight/day in both normal and sulphite oxidase-deficient rats. Liver lesions were noted in rats treated with acetaldehyde hydroxysulphonate. These lesions may possibly be attributable to the effects of free acetaldehyde. The no-effect level for acetaldehyde hydroxysulphonate was 7 mg SO2 equiv./kg body weight/day for sulphite oxidase-deficient rats and 70 mg SO2 equiv./kg body weight/day for normal rats. Increased urinary excretion of sulphite was noted in sulphite oxidase-deficient rats whether or not they were given exogenous sulphites. An increase in urinary sulphite levels in sulphite oxidase-deficient rats was observed after dosing with acetaldehyde hydroxy-sulphonate. These findings suggest that acetaldehyde hydroxysulphonate is metabolized to acetaldehyde and free sulphite.
在正常大鼠和亚硫酸盐氧化酶缺乏的大鼠中进行了焦亚硫酸钠和乙醛羟基磺酸盐的亚慢性经口毒性研究。在最高剂量水平(两种化合物均为350毫克二氧化硫当量/千克体重/天,持续3周,随后为175毫克二氧化硫当量/千克体重/天,持续5周)时,正常大鼠和亚硫酸盐氧化酶缺乏的大鼠在组织学上均出现胃部病变。亚硫酸盐氧化酶缺乏的大鼠病变更严重且更频繁出现。在正常大鼠和亚硫酸盐氧化酶缺乏的大鼠中,焦亚硫酸钠的无作用剂量均为70毫克二氧化硫当量/千克体重/天。用乙醛羟基磺酸盐处理的大鼠出现肝脏病变。这些病变可能归因于游离乙醛的作用。对于亚硫酸盐氧化酶缺乏的大鼠,乙醛羟基磺酸盐的无作用剂量为7毫克二氧化硫当量/千克体重/天,对于正常大鼠为70毫克二氧化硫当量/千克体重/天。无论是否给予外源性亚硫酸盐,亚硫酸盐氧化酶缺乏的大鼠尿中亚硫酸盐排泄均增加。在用乙醛羟基磺酸盐给药后,观察到亚硫酸盐氧化酶缺乏的大鼠尿中亚硫酸盐水平升高。这些发现表明乙醛羟基磺酸盐代谢为乙醛和游离亚硫酸盐。