Effect of Recurrent Hypoglycemia on SOD Activity and Neurexin – 1 Gene Expression in Streptozotocin Induced Diabetic Rats

Abstract

Administration of insulin beyond the recommended dose in diabetes causes hypoglycemia. During diabetes, generation of oxidative stress increases reactive oxygen species and is known to damage the normal cellular assembly of kidney thereby causing diabetic nephropathy. Diabetes was induced in adult male Wistar rats by using Streptozotocin (50 mg/kg body weight – i.v.) and Hypoglycemia in Control and Diabetic rats by injecting Human Insulin (1.5 IU and 10 IU/kg body weight respectively – s.c.). Generation of ROS causes an alteration in anti-oxidant enzyme levels, of which superoxide dismutase enzyme serves as the first-line of defense against oxidative stress. SOD levels in kidney and spleen of control and experimental group of rats were assessed. Generation of ROS might act as a causative agent to induce morphological alterations in kidneys. These alterations in kidneys of diabetic and experimental group of rats were observed by staining kidney sections by H&E staining procedure. Podocytes, present in kidney are reported to be damaged in diabetic nephropathy. These podocytes have CAMs which are important for cell-cell cross talk. Neurexin-1, a CAM present on podocytes cells is important for maintaining intracellular trafficking within podocytes. To scrutinize this crosstalk, gene expression studies of Neurexin-1 gene was carried out following total RNA isolation and c-DNA synthesis from kidneys of control and experimental group of rats. Further, in spleen due to presence of glycated RBCs in diabetes, recycling of ROS is reported to be altered. To study the status of ROS in diabetic and hypoglycemic conditions, SOD enzyme activity was assessed from spleen also.