تاثیر الکل و دخانیات بر روی گلوتاتیون داخل بدن در جوانان مبتلا به اختلال دوقطبی: مطالعه اکتشافی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|73030||2014||9 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Psychiatric Research, Volume 55, August 2014, Pages 59–67
Risky alcohol consumption and tobacco smoking is highly prevalent in bipolar disorder (BD) and is associated with increased formation of neural reactive oxygen species. Proton magnetic resonance spectroscopy (1H-MRS) is an in vivo imaging modality that allows quantification of glutathione (GSH) concentration, the brains primary antioxidant. Sixty-four patients with BD and 49 controls (18–30 years) completed self-report questionnaires regarding alcohol and tobacco use and underwent 1H-MRS. Levels of GSH in the hippocampus and anterior cingulate cortex (ACC) were determined. Within-group Pearson's correlations were used to explore the relationship between alcohol use and GSH concentration for BD and controls, covarying for age, gender, family history of alcohol dependence and smoking status. Relationships between GSH and presence/severity of alcohol-induced blackouts were determined using Spearman's correlations. In BD, reduced hippocampal-GSH associated with higher alcohol use (R = −0.489, p < 0.021). Reduction of ACC-GSH with increased drinking was non-significant when controlling for tobacco use. Independent samples t-test revealed a significantly decreased ACC-GSH in smokers with BD (t (53) = 4.162, p < 0.001). In controls, alcohol use was not correlated to GSH in either region. In both patients and controls, reduced hippocampal-GSH was associated with blackout presence/severity, supporting a role for the hippocampus in the continuum of alcohol-induced memory impairments. Our preliminary findings suggest that in youth with BD reduced hippocampal-GSH is associated with risky alcohol use and alcohol and tobacco use is associated with reduced ACC-GSH, highlighting the role of these substances as modifiable risk factors for decreased anti-oxidant capacity in BD.