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.
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Authors | A Peng, W H Wang, C X Wang, Z J Wang, H F Rui, W Z Wang, Z W Yang |
Journal | Environmental health perspectives
(Environ Health Perspect)
Vol. 107
Issue 4
Pg. 293-6
(Apr 1999)
ISSN: 0091-6765 [Print] United States |
PMID | 10090708
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Benzopyrans
- Free Radicals
- Water Pollutants
- Malondialdehyde
- Selenium
- fulvic acid
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Topics |
- Animals
- Benzopyrans
(adverse effects, pharmacology)
- Bone and Bones
(drug effects, metabolism)
- Cartilage
(drug effects, metabolism)
- Chick Embryo
- Endemic Diseases
- Female
- Free Radicals
(metabolism)
- Humans
- Lipid Peroxidation
(drug effects)
- Male
- Malondialdehyde
(analysis)
- Osteoarthritis
(chemically induced)
- Rats
- Rats, Inbred Strains
- Selenium
(administration & dosage, deficiency)
- Water Pollutants
(adverse effects, pharmacology)
- Water Supply
(analysis)
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