Effect of dietary fluoride on selenite toxicity in the rat |
| |
Authors: | Qing Yu Florian L Cerklewski Philip D Whanger Olaf Hedstrom James W Ridlington |
| |
Institution: | (1) Department of Nutrition and Food Management, Oregon State University, 97331 Corvallis, OR;(2) Department of Agricultural Chemistry, Oregon State University, 97331 Corvallis, OR;(3) College of Veterinary Medicine, Oregon State University, 97331 Corvallis, OR |
| |
Abstract: | Three factorial experiments were conducted to determine if high dietary fluoride (F) would inhibit selenite toxicity in rats.
Initially, three levels of selenite (0.05, 3, and 5 mg/kg diet) were matched against three levels of F (2, 75, and 150 mg/kg
diet). Fluoride failed to prevent the depressive effect of selenite on 8-wk food intake and body wt gain. Selenium (Se) concentration
of plasma and kidney and enzymatic activity of whole blood glutathione peroxidase (GSH-Px) were also unaffected by F. Liver
Se concentration, however, was slightly (12%) but significantly (p<0.025) reduced when the highest F and Se levels were combined. Fluoride (150 mg/kg) appeared to reduce liver selenite toxicity
(5 mg/kg). Therefore, further study focused on liver histology with treatments that eliminated the middle levels of selenite
and F. Fluoride prevented the hepatic necrosis seen in selenite-toxic rats. Similar histological lesions were not observed
for kidney or heart. Fluoride partially (26%) but significantly (p<0.025) reduced thiobarbituric-reactive substances in selenite-toxic rats, but there was no F effect on intracellular distribution
of liver Se, glutathione levels in liver and kidney, or on liver xanthine oxidase activity. Overall, the protective effect
of F on selenite toxicity appears to be confined to liver pathology. The exact mechanism for this effect, however, remains
unclear.
Oregon Agricultural Experiment Station Technical Paper No. 9728. |
| |
Keywords: | Selenite toxicity fluoride liver necrosis glutathione peroxidase reduced glutathione xanthine oxidase |
本文献已被 SpringerLink 等数据库收录! |
|