OXIDATIVE STRESS IN RODENT CLOSED DUODENAL LOOP PANCREATITIS

Citation
J. Peralta et al., OXIDATIVE STRESS IN RODENT CLOSED DUODENAL LOOP PANCREATITIS, International journal of pancreatology, 19(1), 1996, pp. 61-69
Citations number
39
Categorie Soggetti
Endocrynology & Metabolism",Physiology
ISSN journal
01694197
Volume
19
Issue
1
Year of publication
1996
Pages
61 - 69
Database
ISI
SICI code
0169-4197(1996)19:1<61:OSIRCD>2.0.ZU;2-F
Abstract
Conclusions. Production of excited oxygen species is earlier in the li ver than in the pancreas and could contribute to damage in a reflux mo del. Treatment with SOD could attenuate 59% light emission in pancreas , but did not modify serum enzyme levels or pancreatic edema, resultin g as an insufficient isolated therapy, Unexpectedly, it was found an i ncreased plasma antioxidant capacity that was related to total bilirub in levels, and declined at late stages probably denoting other circula ting antioxidant consumption. Background. Oxidative stress has been sh own to play a role in different models of acute pancreatitis, although it has not been studied in the severe necrohemorrhagic model produced by closed duodenal loop pancreatitis. Methods. We studied Sprague Daw ley female rats in two groups: a closed duodenal loop pancreatitis gro up and a control, sham-operated group. In order to evidence the oxygen excited species production, in situ spontaneous chemiluminescence fro m living and naturally perfused pancreas and liver was measured at 0, 0.5, 1.5, 3, 6, 12, and 24 h after the duodenal ligature. Blood pancre atic amylase and aminotransferases levels were determined as expressio n of tissue damage in pancreas and liver. At the same time, plasma ant ioxidant capacity was measured by the peroxyl radical trapping capabil ity of plasma samples compared to that of Trolox (synthetic analog of vitamin E), and results are expressed as Trolox equivalence. Bovine su peroxide dismutase (SOD) was administered to attenuate oxygen free rad icals activity at the beginning of the peroxidation chain and also as a therapeutic tool. Results. The experimental procedure induced a seve re pancreatitis, as evidenced by pancreatic enzymes that rose markedly in the early hours of disease and remained heightened throughout the experiment. The results show early light emission from the liver at 3 h and peak levels at 12 h, whereas in the pancreas, luminescence incre ased at 6 h and doubled later at 12 h, both returning to control level s at 24 h.