Alteration of antioxidant status in diabetic rats by chronic exposure to psychological stressors.

Antioxidant status was measured in heart, liver, kidney, lung, and erythrocytes of 2-week streptozotocin-diabetic male Wistar rats exposed to chronic intermittent psychological stress consisting of 1 h of restraint twice daily for 14 days. Diabetes reduced erythrocyte and heart and liver susceptibility to hydrogen peroxide-induced glutathione depletion. Susceptibility to peroxide-induced thiobarbituric acid reactive substance (TBARS) formation increased in erythrocytes, liver, kidney, and lung but decreased in heart. Significant changes also occurred in glutathione levels (increased in heart and decreased in liver) and in the activities of catalase (reduced in liver and kidney), glutathione reductase (elevated in heart and liver), and glutathione peroxidase (decreased in liver and lung), but not Cu,Zn-superoxide dismutase. Stress potentiated diabetes-associated hyperglycemia and attenuated diabetes-induced hyperlipidemia. In addition, the reduction in peroxide-induced glutathione depletion in heart and liver and the increased TBARS formation in kidney and lung were reversed. Similarly, the diabetes-induced induced increase in liver glutathione reductase and decreases in liver and lung glutathione peroxidase activities were abolished by stress. Thus, the relative resistance of antioxidant systems to stress can be modified under pathologic conditions in which antioxidant alterations are present.