7 research outputs found

    Antioxidant supplementation enhances erythrocyte antioxidant status and attenuates cyclosporine-induced vascular dysfunction

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    The aim of this study was to determine the effects of dietary antioxidant supplementation with a-tocopherol and a-lipoic acid on cyclosporine induced alterations to erythrocyte and plasma redox balance, and cyclosporine-induced endothelial and smooth muscle dysfunction. Rats were randomly assignedto either control, antioxidant, cyclosporine or cyclosporine + antioxidant treatments. Cyclosporine A was administered for 10 days after an 8-week feeding period. Plasma was analyzed for a-tocopherol, total antioxidant capacity, malondialdehyde and creatinine. Erythrocytes were analyzed for glutathione, methemoglobin, superoxide dismutase, catalase, glutathione peroxidase, glucose-6-phosphate dehydrogenase, a-tocopherol and malondialdehye. Vascular endothelial and smooth muscle function was determined in vitro. Antioxidant supplementation resulted in significant increases in erythrocyte a-tocopherol concentration and glutathione peroxidase activity in both of the antioxidant-supplemented groups. Cyclosporine administration caused significant decreases in glutathione concentration, methemoglobin concentration and superoxide dismutase activity. Antioxidant supplementation attenuated the cyclosporine-induced decrease in superoxide dismutase activity. Cyclosporine therapy impaired both endothelium-independent and -dependent relaxation of the thoracic aorta, and this was attenuated by antioxidant supplementation. In summary, dietary supplementation with a-tocopherol and a -lipoic acid attenuated the cyclosporine-induced decrease in erythrocyte superoxide dismutase activity and attenuated cyclosporine-induced vascular dysfunction

    Smoking in Schizophrenia: Diagnostic Specificity, Symptom Correlates, and Illness Severity

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    Background: Cigarette smoking was consistently found to be more prevalent in individuals with schizophrenia than in other psychiatric groups and the general population. These findings have been interpreted as evidence of a specific association between schizophrenia and smoking. However, the supporting data come primarily from cross-sectional studies, which are susceptible to confounding. Our aim was to test specificity of this link longitudinally in an epidemiologic sample. Methods: A cohort of 542 inpatients with psychosis was followed for 10 years after first hospitalization, completing 5 face-to-face interviews. Assessments included ratings of specific symptoms (psychotic, negative, disorganized, and depressive), Global Assessment of Functioning, and a categorical measure of cigarette consumption. All participants were assigned longitudinal consensus diagnoses by study psychiatrists, and 229 were diagnosed with schizophrenia spectrum disorders (SZ). Results: At baseline, 52.4% of participants were current smokers and 69.3% were lifetime smokers. Smoking rates did not differ among the diagnostic groups (schizophrenia spectrum, major depressive, bipolar, or other psychotic disorder) at any assessment point. Smokers were more severely ill than nonsmokers but did not differ in specific symptoms either cross-sectionally or longitudinally. Among smokers, changes in cigarette consumption were linked only with changes in depression (ÎČ = .16, P < .001). Conclusions: Rates of smoking were elevated in subjects with schizophrenia but were just as high with other psychotic disorders. Smoking was not associated with psychotic symptoms, but cigarette consumption covaried with depression over time. Given the devastating health consequences of cigarette use, smoking cessation interventions are urgently needed in this population and should specifically address depression
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