The impact of experimental diabetes mellitus on the catalase immunoreactivity in the mice parotid gland

Diabetes mellitus is a metabolic disorder and has been considered as a chronic disease of oxidative stress-linked tissue dysfunction with persistent hyperglycemia. Oxidative stress is a key factor contributing to the pathogenesis of diabetic complications by imbalancing cellular homeostasis and antioxidant systems. The salivary glands, in particular, the parotid gland are more vulnerable to oxidative stress during diabetes. Catalase, which is a hallmark enzymatic antioxidant in cells has a fundamental role to scavenge hydrogen peroxide and redox status of tissue. The purpose of this study was to determine the influence of experimental diabetes mellitus on catalase immunoreactivity in the parotid gland. Eighteen male BALB/c mice were randomly assigned to the sham group and control group, diabetic group. The parotid gland of adult rats was collected 30 days after diabetes induction, and submitted to histological and immunohistochemistry analysis. The immunohistochemical analysis of catalase expression and localization was made. Histological analysis showed that the overall structure of the parotid glands in all groups was retained through and no marked tissue injury was observed in diabetic animals. Immunohistochemically, we observed positive catalase immunoreactivity in the connective tissue and epithelium found at the initial, secretory, and excretory level of parotid gland in all groups. Remarkably, catalase immunoreactivity was much higher in the diabetic group than that observed in control and sham groups. These results indicate that the experimental diabetes causes changes in the antioxidant defense system of parotid glands with a rise in catalase expression. The increase in catalase immunoreactivity may be a compensatory mechanism for an increased oxidative stress in diabetes.