Evaluation of selenium on kidney function following ischemic injury in rats; protective effects and antioxidant activity
Renal dysfunction is caused by ischemia-reperfusion (I/R) injury, which is a common problem in kidney surgery or kidney transplantation. The human body consists of enormous complex antioxidant systems, which inquires adequate selenium (Se) absorption for normal physiologic function. It is known that...
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Veröffentlicht in: | Journal of renal injury prevention 2017, Vol.6 (2), p.93-98 |
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Sprache: | eng |
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Zusammenfassung: | Renal dysfunction is caused by ischemia-reperfusion (I/R) injury, which is a common problem in kidney surgery or kidney transplantation. The human body consists of enormous complex antioxidant systems, which inquires adequate selenium (Se) absorption for normal physiologic function. It is known that Se has some antioxidant effects.
In the present research, effects of the Se on damages caused by I/R injury investigated.
In this experimental research, four groups of rats (weighing 220±10 g) used, include control group, I/R group, healthy group treated with Se for two weeks, and I/R group with two-week Se treatment. On the test day, I/R was treated in both right and left renal arteries for 45 minutes and the reperfusion was done for 24 hours.
In I/R group, the amount of urea and serum creatinine (Cr) was an injury indicator of the kidney cells which showed a significant increase compared with the control group. When the treatment with Se significantly reduced these indicators, glutathione (GSH) enzyme levels reduced significantly in the second group and the enzyme levels increased due to Se treatment in the fourth group. Furthermore, malondialdehyde (MDA) enzyme levels increased in I/R group due to the Se treatment in the fourth group which was significantly reduced. In addition, the tissue damage was reduced in the fourth group compared with I/R group.
Se has a protective effect against the I/R injury. This effect might be due to the antioxidant properties of Se. |
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ISSN: | 2345-2781 2345-2781 |
DOI: | 10.15171/jrip.2017.18 |