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Original Articles

Dietary selenium protects against acute toxicity of T‐2 toxin in rats

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Pages 821-827 | Accepted 18 Jun 1990, Published online: 10 Jan 2009
 

Abstract

The efficacy of dietary selenium (Se) supplementation on acute toxicity of T‐2 toxin was investigated. Wistar male rats were divided into six groups with 15 rats in each and fed for 6 weeks ad libitum a semi‐synthetic diet containing either 0.03 (groups 1 and 2), 0.5 (groups 3 and 4) or 2.5 mg Se/kg (groups 5 and 6). By the end of the experiment the rats in groups 2, 4 and 6 were administered once per os 3.8 mg/kg body weight T‐2 toxin, while the animals in groups 1, 3 and 5 received the solvent. Twenty‐four hours after administration of the toxin the surviving rats were sacrificed and the liver microsomes isolated and determined for activities of enzymes relating to xenobiotics metabolism and Se. The results showed that feeding the rats 2·5 mg Se/kg diet increased the deethylation rate of 7‐ethoxycoumarin by 42% and slightly decreased (20%) glutathione‐S‐transferase activity. Twenty‐four hours after the administration of T‐2 toxin the lethality percentages in groups 2, 4 and 6 were 47%, 27% and 20%, respectively. Furthermore, administration of T‐2 toxin to group 6 rats resulted in a significant decrease in the level of cytochrome P‐450 and 7‐ethoxycoumarin deethylase activity (to 78% and 51%, respectively) compared to the control group. At the same time a 72% increase in the UDP‐glucuronosyltransferase activity and of 61% in epoxide hydrolase activity compared to the control group was found. Similarly, although somewhat smaller, changes were seen in the group 4 rats receiving 0.5 mgSe/kg diet. These data demonstrate that 2.5 mgSe/kg diet is effective in protecting rats against acute toxicity by T‐2 toxin shown by a decrease in the lethality and by the extent of seventy of intoxication symptoms. Moreover, the observed decrease in T‐2 toxin intoxication in the animals receiving a Se‐rich diet was accompanied by a suppression of functional activity of the monooxygenase system of the liver and a significant intensification of the glucuronidation process.

Notes

To whom correspondence should be addressed.

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