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An Peng,¹ Wen-Hua Wang,¹ Chun-Xia Wang,¹ Zi-Jian Wang,¹ Hai-Feng Rui,¹ Wai-Zhe Wang,² and Zi-Wei Yang²

¹SKLEAC, Research Center for Eco-environmental Sciences, Chinese Academy of Sciences, Beijing 100085, P. R. China
²Department of Pathophysiology, Liaoning Institute of Basic Medicine, Shenyang, 110005 P. R. China

Abstract

We conducted in vitro and in vivo assays in a selenium-deficient system to determine if organic matter (mainly fulvic acid ; FA) is involved in a free radical mechanism of action for Kashin-Beck disease. Cartilage cell culture experiments indicated that the oxy or hydroxy functional groups in FA may interfere with the cell membrane and result in enhancement of lipid peroxidation. Experiments with rats demonstrated that toxicity from FA was reduced when the hydroxy group was blocked. Induction of lipid peroxidation by FA in liver and blood of rats was similar to that exhibited by acetyl phenyl hydrazine. FA accumulated in bone and cartilage, where selenium rarely concentrates. In addition, selenium supplementation in rats' drinking water inhibited the generation of oxy-free radicals in bone. We hypothesized that FA in drinking water is an etiological factor of Kashin-Beck disease and that the mechanism of action involves the oxy and hydroxy groups in FA for the generation of free radicals. Selenium was confirmed to be a preventive factor for Kashin-Beck disease. Key words: free radical, fulvic acid, Kashin-Beck disease, humic substances, selenium. Environ Health Perspect 107:293-296 (1999) . [Online 11 March 1999]

http://ehpnet1.niehs.nih.gov/docs/1999/107p293-296peng/ abstract.html

Address correspondence to A. Peng, Research Center for Eco-environmental Science, Chinese Academy of Sciences (KZ951-B,-204) , P.O. BOX 2871, Beijing, 100085, P. R. China.

This work was supported by the Chinese National Sciences Foundation (no. 39570640) and the Chinese Academy of Sciences. We thank S.Z. Zhen, Hai Dian Hospital, for his help with the animal experiments.

Received 28 November 1997 ; accepted 24 November 1998.