Improved serotonergic neurotransmission by genistein pretreatment regulates symptoms of obsessive-compulsive disorder in streptozotocin-induced diabetic mice.

Background Initial evidences have shown that diabetes mellitus occurs concomitantly with obsessive-compulsive disorder (OCD) symptomatology. Serotonergic psychiatric therapy posits that serotonin is a central character in the management of OCD. Hence, it is worth investigating novel chemical entities affecting the serotonergic system for targeting OCD. An isoflavonoid phytoestrogen, genistein, has been recognized as of great pharmacological value especially for protecting neurodegeneration, depression (serotonin regulation), and diabetes. The effectiveness of genistein pretreatment on the symptoms of OCD in streptozotocin-induced diabetic mice is investigated in this study. We also evaluate the probable involvement of the serotonergic system. Methods Groups of diabetic mice were treated with genistein at the dose of 5.0 and 10.0 mg/kg (intraperitoneal, twice daily, 14 days), and symptoms of OCD were assessed by the marble-burying behavior, in comparison with the standard drug fluoxetine. Neurochemical assessment of the serotonergic ratio 5-hydroxyindole-3-methoxyphenylacetic acid/5-hydroxytryptamine (5-HIAA/5-HT) in the cortical region of the brain was performed using HPLC (high-pressure liquid chromatography). Results Chronic treatment with genistein significantly recovered [F(6, 35)=53.00, p<0.0001, R2=0.9008] the symptoms of OCD as assessed by marble burying behavior in normal and diabetic mice. Locomotor performance was not influenced by the diabetic condition or any associated treatment. The turnover of serotonin neurotransmission (5-HIAA/5-HT) was significantly boosted in the diabetic condition; genistein treatment dragged it [F(6, 35)=35.75, p<0.0001, R2=0.8597] toward the respective control. Conclusions Genistein supplementation might be a potential therapeutic line for the management and/or prevention of diabetes-associated OCD symptomatology.

Study of oxidative stress and trace element levels in patients with alcoholic and non-alcoholic coronary artery disease.

Alcohol consumption induces oxidative stress, and leads to lipid peroxidation. These effects have been linked to alcohol-related toxicity and diseases are considered relevant to alcohol-atherosclerosis interrelationship. Deficiency of many antioxidants and trace elements may impair the antioxidant defense leading to ethanol induced oxidative stress. In the present study, our aim was to investigate the lipid peroxidation, lipid profile, antioxidant enzymes and trace elements in patients with and without alcoholic coronary artery disease (CAD). Our study included 61 patients suffering from CAD, 124 patients suffering from alcoholic CAD with high to moderate alcohol intake, 75 controls were randomly selected for our study. Increased serum lipid peroxidation, total cholesterol, triglycerides, LDL cholesterol and copper levels were high while levels of HDL cholesterol, glutathione peroxdiase, superoxide dismutase, trace elements like Selenium and Zinc were low in high alcoholic CAD patients compared with moderate and non alcoholic CAD patients. The results obtained from present study indicate that high alcohol intake predicts low antioxidant enzyme and that trace element may contribute to the increased susceptibility for the development of CAD.