Effect of astaxanthin on kidney function impairment and oxidative stress induced by mercuric chloride in rats

被引:60
|
作者
Augusti, P. R.
Conterato, G. M. M.
Somacal, A.
Sobieski, R.
Spohr, P. R.
Torres, J. V.
Charao, M. F.
Moro, A. M.
Rocha, M. P.
Garcia, S. C.
Emanuelli, T. [1 ]
机构
[1] Univ Fed Santa Maria, Ctr Rural Sci, Dept Aliment Technol Sci, Integrat Ctr Lab Anal Dev NIDAL, BR-9715900 Santa Maria, RS, Brazil
[2] Univ Fed Santa Maria, Ctr Nat & Exact Sci, BR-9715900 Santa Maria, RS, Brazil
[3] Univ Fed Santa Maria, Ctr Hlth Sci, Dept Pathol, BR-9715900 Santa Maria, RS, Brazil
[4] Univ Fed Santa Maria, Ctr Hlth Sci, Dept Clin Toxicol Anal, BR-9715900 Santa Maria, RS, Brazil
关键词
antioxidant enzymes; delta-aminolevulinate dehydratase; creatinine; kidney tubular necrosis; thiobarbituric acid reactive substances;
D O I
10.1016/j.fct.2007.08.001
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Reactive oxygen species are implicated as mediators of tissue damage in the acute renal failure induced by inorganic mercury. Astaxanthin (ASX), a carotenoid with potent antioxidant properties, exists naturally in various plants, algae, and seafoods. This paper evaluated the ability of ASX to prevent HgCl2 nephrotoxicity. Rats were injected with HgCl2 (0 or 5 mg/kg b.w., sc) 6 It after ASX had been administered (0, 10, 25, or 50 mg/kg, by gavage) and were killed 12 h after HgCl2 exposure. Although ASX prevented the increase of lipid and protein oxidation and attenuated histopathological changes caused by HgCl2 in kidney, it did not prevent creatinine increase in plasma and 6-aminolevulinic acid dehydratase inhibition induced by HgCl2. Glutathione peroxidase and catalase activities were enhanced, while superoxide dismutase activity was depressed in HgCl2-treated rats when compared to control and these effects were prevented by ASK Our results indicate that ASX could have a beneficial role against HgCl2 toxicity by preventing lipid and protein oxidation, changes in the activity of antioxidant enzymes and histopathological changes. (c) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:212 / 219
页数:8
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