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Information Seminar Paper

Title

DECREASING THE OXIDANT STRESS FROM NITROFURANTOIN IN ISOLATED PERFUSED RAT LUNG USING CAPTOPRIL

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Abstract

 Introduction: Nitrofurantoin is an antibiotic used for the treatment of urinary tract infections, has been shown to cause pulmonary fibrosis in humans and experimental animals. The exact mechanism(s) by which nitrofurantoin damages the lung remains unclear. Results from in vitro studies have shown that a cyclic single electron reduction / oxidation (redox cycling) of the parent molecule is a critical mechanistic event. The purpose of this study was to evaluate the biochemical changes due to lung toxicity of nitrofurantoin and its inhibition by Captopril in isolated rat lung.Methods: Male Wistar rats weighting 220-300 g were used in this experiment. Animals were divided into five groups. In groups 1-4, lung were perfuse by Krebs-Ringer buffer alone (control), nitrofurantoin (600 µM), dimethylformamide, captopril (10 µM), group 5, after 5 min of stabilization with Krebs-Ringer buffer, captopril (10 µM) was added to perfusion for 20min. Then, nitrofurantoin (600 µM) was added to perfusion fluid and biochemical changes in isolated rat lung were examined within 1 hr and compared to nitrofurantoin alone.Results: There was no significant difference in tissue glutathione level of pretreatment compared to nitrofurantoin alone group (p>0.05). The levels of tissue MDA were found to be significantly lower in pretreatment compared to nitrofurantoin alone group (p<0.05).Conclusion: Lung toxicity due to nitrofurantoin may be reduced through prevention of lipid peroxidation. The exact mechanism of this finding need to be more elucidated in the future.

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