HYPEROXIC PRECONDITIONING FAILS TO CONFER ADDITIONAL PROTECTION AGAINST ISCHEMIA-REPERFUSION INJURY IN ACUTE DIABETIC RAT HEART

Experimental studies show that detrimental effects of ischemia-reperfusion (I/R) injury can be attenuated by hyperoxic preconditioning in normal hearts, however, there are few studies about hyperoxia effects in diseased myocardium. The present study was designed to assess the cardioprotective effects of hyperoxia pretreatment (≥ 95 % O2) in acute diabetic rat hearts. Normal and one week acute diabetic rats were either exposed to 60 (H60) and 180 (H180) min of hyperoxia or exposed to normal atmospheric air (21 % O2). Then hearts were isolated immediately and subjected to 30 min of regional ischemia followed by 120 min of reperfusion. Infarct size, cardiomyocyte apoptosis, enzymes release and ischemia induced arrhythmias were determined. Heart of diabetic control rats had less infarct size and decreased LDH and CK-MB release compared to normal hearts. 60 and 180 min of hyperoxia reduced myocardial infarct size and enzymes release in normal hearts. 180 min of hyperoxia also decreased cardiomyocytes apoptosis in normal state. On the other hand, protective values of hyperoxia were not significantly different in diabetic hearts. Moreover, hyperoxia reduced severity of ventricular arrhythmias in normal rat hearts whereas; it did not confer any additional antiarrhythmic protection in diabetic hearts. These findings suggest that diabetic hearts are less susceptible to ischemia-induced arrhythmias and infarction. Hyperoxia greatly protects rat hearts against I/R injury in normal hearts, however, it could not provide added cardioprotective effects in acute phase of diabetes

Effects of fumonisin B1 on the stomach and colon cell lines in vitro

Background: Fumonisins, a family of mycotoxins, are mainly found in wheat, corn and their products. Previous studies have shown that fumonisin B1 (FB1), the most abundant and toxic of known fumonisins, has been associated with many animal and human diseases including cancer. In the present study, the effects of FB1 were examined on the production of inflammatory cytokines in intestine and stomach cell lines. Methods: This study was performed in the Cancer Research Center of Tehran University of Medical Sciences in 2010. The cell lines of colon adenocarcinoma (SW742) and gastric epithelium (AGS) were purchased from the Pasteur Institute of Iran. The cells were pretreated with different concentrations of FB1 (0 to 100 µM) for 3 days. The cells were later stimulated by lipopolysaccharides. Twenty-four hours after cell induction, the cytokines including tumor necrosis factor-alpha (TNF-α), interlukin-1 beta (IL-1β) and interlukin-8 (IL-8) were measured by ELISA. Results: Treatment with FB1 induced a dose-dependent decrease in IL-8 production (P<0.05). This decrease was seen in both SW742 and AGS cell lines. Moreover, FB1 induced a dose-dependent increase in the production of TNF-α and IL-1β in both cell lines (P<0.05). Conclusion: The results of this study indicated that FB1 could increase the inflammatory cytokines including TNF-α and IL-1β in gastric and intestinal celllines. These effects might result in the development of inflammatory responses and subsequent mucosal atrophy in in-vivo conditions