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BRIEF REPORT
Year : 2016  |  Volume : 5  |  Issue : 1  |  Page : 96

The role of S-methylisothiourea hemisulfate as inducible nitric oxide synthase inhibitor against kidney iron deposition in iron overload rats


1 Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran
3 Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan; Department of Physiology, Isfahan University of Medical Sciences, Isfahan; Isfahan MN Institute of Basic and Applied Sciences Research, Isfahan, Iran

Correspondence Address:
Prof. Mehdi Nematbakhsh
Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2277-9175.183145

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Background: Iron dextran is in common use to maintain iron stores. However, it is potentially toxic and may lead to iron deposition (ID) and impair functions of organs. Iron overload can regulate the expression of inducible nitric oxide synthase (iNOS) in some cells that has an important role in tissue destruction. S-methylisothiourea hemisulfate (SMT) is a direct inhibitor of iNOS, and this study was designed to investigate the effect of SMT against kidney ID in iron overload rats. Materials and Methods: 24 Wistar rats (male and female) were randomly assigned to two groups. Iron overloading was performed by iron dextran 100 mg/kg/day every other day for 2 weeks. In addition, during the study, groups 1 and 2 received vehicle and SMT (10 mg/kg, ip), respectively. Finally, blood samples were obtained, and the kidneys were prepared for histopathological procedures. Results: SMT significantly reduced the serum levels of creatinine and blood urea nitrogen. However, SMT did not alter the serum levels of iron and nitrite, and the kidney tissue level of nitrite. Co-administration of SMT with iron dextran did not attenuate the ID in the kidney. Conclusion: SMT, as a specific iNOS inhibitor, could not protect the kidney from ID while it attenuated the serum levels of kidney function biomarkers.


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