Akademik Veri Yönetim Sistemi
Turkish Journal of Gastroenterology, cilt.8, sa.2, ss.171-174, 1997 (Scopus)
In the etiology of pancreatitis, the causative role of chronic alcohol ingestion is well established, however, there are also rare studies indicating pancreatitis due to acute large doses of ethanol. Oxygen free radicals are shown to have an important role in the pathogenesis of experimental pancreatitis. Our aim was to investigate whether a single dose of ethanol causes malondialdehyde (MDA) formation and glutathione (GSH) depletion which are indirect indicators of free radical-mediated oxidative stress. And in the case that this occurred, we wanted to assess histopathologic damage after alcohol. In the study, rats were used and divided into two groups. Control group (5 rats) did not receive any chemicals. After a single dose of ethanol (0,5 gr/kg bw. of ethanol, % 40 vol/vol, intraperitoneally) had been infused to the study group (10 rats) of animals, no significant change was observed in protein (0.54 ± 0.10 vs. 0.54 ± 0.13), MDA (6.52 ± 1.04 vs. 5.34 ± 0.55) and GSH levels (0.14 ± 0.06 vs. 0.14 ± 0.08) in pancreas. Also, there was no histopathologic change after ethanol by light microscopy. In conclusion, a high single dose of ethanol given with parenteral route does not cause oxidative stress and histopathological damage in pancreas.