Investigation of lipid peroxidation and antiapoptotic effects of zinc aganist liver damage in diabetic rats

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Tunçdemir M. , Ertürküner S. P. , Özcelik D.

HUMAN & EXPERIMENTAL TOXICOLOGY, cilt.36, ss.813-822, 2017 (SCI İndekslerine Giren Dergi)

  • Cilt numarası: 36
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1177/0960327116666619
  • Sayfa Sayısı: ss.813-822



Several mechanisms for the pathogenesis of diabetic complications have been proposed, one of which is abnormal zinc (Zn) homeostasis. Zn is necessary for proper liver function since it has important antioxidant, anti-inflammatory, and antiapoptotic properties. We aimed to investigate whether or not Zn has morphologically protective effect on diabetes-induced liver damage in rats. In addition, we have investigated the role of Zn supplementation on apoptosis, lipid peroxidation levels, and the distribution of metallothionein (MT) in diabetic liver tissue. Wistar albino rats were divided into four groups: control, Zn, diabetic, and Zn-diabetic group. Experimental diabetes was induced by a single-dose streptozotocin intraperitoneally and Zn was administrated via gastric gavage tube for 6 weeks. MT expressions were showed with immunohistochemical staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay was used for apoptosis. Also, Zn, MT, and malondialdehyde (MDA) levels were determined in liver of rats. MDA levels of the Zn-supplemented diabetic group was less than the diabetic group though MT levels were increased. The number of apoptotic cells per unit area was found to be significantly decreased in this group. In the Zn-supplemented diabetic group, fibrotic tissue density and the collagen tissue density were observed less than the diabetic group. MT immunoreactivity was observed less in Zn-supplemented diabetic group. In conculusion, the present study indicated that Zn has a potential in preventing or even repairing effect against diabetic damage of the liver cells by increasing expression of MT and by reducing the apoptotic cell death and the oxidative stress.