Lipid Peroxidation is Key to Neuronal Cell Death in the Inferior Colliculus of STZ-Induced Diabetic Rats

Neuropathy is one prominent complication yet to be separated from diabetes mellitus and various mechanisms have been identified for this complication. In this study, lipid peroxidation was investigated as a possible neuropathic agent in the inferior colliculus (IC) of Streptozotocin-induced diabetic rats.

A total of 29 adult Wistar rats of both sexes and average weight 220 ± 15.3 g were used in the study The rats were randomly divided into one control group and three experimental groups as group 1 (control – 5 rats), group 2 (P4 – 8 rats), group 3 (P7 – 8 rats) and group 4 (P10 – 8 rats). Each experimental rat was given 1ml of the equivalence of a single large dose of 70mg per kg body weight of Streptozotocin dissolved in citrate buffer (pH 4.5) by intraperitoneal injection. The control rats received 1ml of the Citrate buffer only also intraperitoneally. Enzymatic activities of LP, CAT, and SOD were estimated at post-induction periods P4, P7 and P10 in weeks. The morphology of the IC was also assessed at histological and histochemical levels.

The major findings in this study include a sustained over four-fold elevation in blood glucose levels in experimental rats, significant body and neuronal density reductions in experimental rats compared with the control animals. Light microscopic observations revealed the dissolution of Nissl substance (chromatolysis), the swelling up of nuclei (karyolysis) and subsequent necrosis with degeneration of the neurons of IC (treated) which were more pronounced at P7 and 10 than at P4. At P10 especially, many neurophagic cells were seen in the vicinity engulfing the degenerating neurons and leaving lots of vacuolation. Significant increases were observed in Lipid Peroxidation in the Inferior Colliculus showing significantly different (P≤0.05) values between the control and treatment groups of the same period in the Inferior Colliculus. Data obtained from estimation of enzyme activities also revealed significant decreases (P≤0.05) in CAT and SOD in experimental animals when compared to those of the control animals.

In conclusion, this study offers evidence that diabetes mellitus induced by STZ is implicated in hearing impairment probably due to the destruction of membrane lipids and accumulation of the end-products of lipid peroxidation reactions which are especially dangerous for the viability of cells, in this case the neurons in the inferior colliculus.