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Year : 2019  |  Volume : 12  |  Issue : 2  |  Page : 65-71

Streptozotocin-induced molecular and metabolic targets in pancreatic beta-cell toxicity

Department of Biochemistry, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates

Correspondence Address:
Haider Raza
Department of Biochemistry, College of Medicine and Health Sciences, United Arab Emirates University, Po Box 17666, Al Ain
United Arab Emirates
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/HMJ.HMJ_54_18

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Background/Aim: The prevalence of diabetes is on the rise globally causing excessive burden on the health systems. Pancreatic beta-cell mass destruction/neogenesis/proliferation (seen in type1diabetes) and/or malfunction (type 2 diabetes) have been implicated in the aetiology, pathology, progression as well as in responses towards therapies and disease managements. Oxidative stress and alterations in mitochondrial energy metabolism play important roles in diabetes-induced cellular complications. Several studies, including our own, have suggested that Rin-5F pancreatic beta cells are extremely susceptible to oxidative stress due to excessive production of endogenous and exogenous reactive oxygen/nitrogen species (ROS/RNS) and low antioxidant defences, particularly, associated with GSH metabolism. Our aim was to investigate the molecular mechanism of streptozotocin (STZ), a beta cell-specific antibiotic, cytotoxicity in pancreatic cells. Methods: Rin-5F cells were treated with STZ under varying conditions to study oxidative stress-related changes. Results: Our studies have suggested that treatment of Rin-5F cells with STZ, inhibits cell survival and induces cytotoxicity by altering cellular survival and apoptotic signalling and gene expressions. Increased oxidative stress with increased DNA fragmentation and oxidative protein carbonylation were seen in STZ-treated cells. We also observed that beta cells treated with high glucose (up to 25mM) exhibited enhanced cytotoxicity. Cells exposed to conditions mimicking diabetes (hyperglycaemia) were under elevated oxidative stress and showed increased apoptosis and altered redox homeostasis leading to increased cytotoxicity. N-acetyl cysteine (NAC) treatment attenuated these changes in STZ-treated cells. Conclusion: These results may have implications in understanding the mechanism of beta cell survival/death in response to potential therapeutics/managements as well as in the aetiology and pathophysiology of diabetes.

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