Zinc Supplementation Attenuates Metallothionein and Oxidative Stress Changes in Kidney of Streptozotocin-Induced Diabetic Rats
- 739 Downloads
Zinc is an element that under physiological conditions preferentially binds to and is a potent inducer of metallothionein under physiological conditions. The present study was conducted to explore whether zinc supplementation morphologically and biochemically protects against diabetic nephropathy through modulation of kidney metallothionein induction and oxidative stress in streptozotocin-induced diabetic rats. Thirty-two Wistar albino male rats were equally divided into four groups. The first group was used as untreated controls and the second group was supplemented with 30 mg/kg/day zinc as zinc sulfate. The third group was treated with streptozotocin to induce diabetes and the fourth group was treated with streptozotocin and supplemented with zinc as described for group 2. The blood glucose and micro-albuminuria levels, body and kidney weights were measured during the 42-day experimental period. At the end of the experiment, the kidneys were removed from all animals from the four groups. Diabetes resulted in degenerative kidney morphological changes. The metallothionein immunoreactivity level was lower and the kidney lipid peroxidation levels were higher in the diabetes group than in the controls. The metallothionein immunoreactivity levels were higher in the tubules of the zinc-supplemented diabetic rats as compared to the non-supplemented diabetic group. The zinc and metallothionein concentrations in kidney tissue were higher in the supplemented diabetic group compared to the non-supplemented diabetes group. The activity of glutathione peroxidase did not change in any of the four groups. In conclusion, the present study shows that zinc has a protective effect against diabetic damage of kidney tissue through stimulation of metallothionein synthesis and regulation of the oxidative stress.
KeywordsExperimental diabetic nephropathy Oxidative stress Zinc Metallothionein Antioxidant
The authors thank the Scientific Research Projects Coordination Unit of Istanbul University for the support of the present study (project number 3987). DÖ formulated the present hypothesis. MÖ, ÖÇ and MT were responsible for analysis of the data. MN was responsible for writing the report. MFFA made critical revision for the manuscript. Abstract of the study was published in abstract book of 4th International Congress on Cell Membranes and Oxidative Stress: Focus on Calcium Signaling and TRP Channels, 26–29 June 2012, Isparta, Turkey.
Conflict of interest
The authors declare that there are no conflicts of interest arising from their study.
- 1.Nazıroğlu M, Dikici DM, Dursun S (2012) Role of oxidative stress and Ca(2+) signaling on molecular pathways of neuropathic pain in diabetes: focus on TRP channels. Neurochem Res. (ın press)Google Scholar
- 2.Özkaya D, Nazıroğlu M, Armağan A, Demirel A, Köroglu BK, Çolakoğlu N, Kükner A, Sönmez TT (2011) Dietary vitamin C and E modulates oxidative stress induced-kidney and lens injury in diabetic aged male rats through modulating glucose homeostasis and antioxidant systems. Cell Biochem Funct 29:287–293PubMedCrossRefGoogle Scholar
- 11.Zhou Z, SunX KYJ (2002) Metallothionein protection against alcoholic liver injury through inhibition of oxidative stress. Exp Biol Med 227:214–222Google Scholar
- 25.Kovacic P, Somanathan R (2008) Unifying mechanism for eye toxicity: electron transfer, reactive oxygen species, antioxidant benefits, cell signaling and cell membranes. Cell Membr Free Radic Res 2:56–69Google Scholar
- 32.Dinesh Kumar S, Vijaya M, Perumal Samy R, Thameem Dheen S, Ren M, Watt F, James Kang Y, Bay BH, Tay SS (2012) Zinc supplementation prevents cardiomyocyte apoptosis and congenital heart defects in embryos of diabetic mice. Free Radic Biol Med. http://dx.doi.org/ 10.1016/j.freeradbiomed.2012.07.008