کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739796 | 1046889 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lipid peroxidation during ischemia depends on ischemia time in warm ischemia and reperfusion of rat liver
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کلمات کلیدی
4-HNEPC-OOHPLPC-OOHMDAPHGPxGSHALTGSSG4-hydroxy-2-nonenal - 4-هیدروکسی-2 غیرنالROS - ROSAlanine aminotransferase - آلانین آمینوترانسفرازIschemia - ایسکمیOxidative stress - تنش اکسیداتیوFree radicals - رادیکال آزادReperfusion - رپرفیوژنcopper zinc superoxide dismutase - سوکسوید دیسموتاز روی مسphosphatidylcholine - فسفاتیدیل کولینphosphatidylethanolamine - فسفاتیدیلتانولامینmalondialdehyde - مالون دی آلدهیدCu/Zn-SOD - مس / روی-SODChemiluminescence - نورتابی شیمیایی یا کمی لومی نسانسPhosphatidylcholine hydroperoxide - هیدروپراکسید فسفاتیدیل کولینLipid peroxidation - پراکسیداسیون لیپیدLiver - کبدtotal bilirubin - کل بیلی روبینGlutathione - گلوتاتیونglutathione disulfide - گلوتاتیون دی سولفیدcytosolic glutathione peroxidase - گلوتاتیون پراکسیداز سیتوزولReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Prolonged hepatic warm ischemia has been incriminated in oxidative stress after reperfusion. However, the magnitude of oxidative stress during ischemia has been controversial. The aims of the present study were to elucidate whether lipid peroxidation progressed during ischemia and to clarify whether oxidative stress during ischemia aggravated the oxidative damage after reperfusion. Rats were subjected to 30 to 120 min of 70% warm ischemia alone or followed by reperfusion for 60 min. Lipid peroxidation (LPO) was evaluated by amounts of phosphatidylcholine hydroperoxide (PC-OOH) and phosphatidylethanolamine hydroperoxide (PE-OOH) as primary LPO products. Total amounts of malondialdehyde and 4-hydroxy-2-nonenal (MDA + 4-HNE), degraded from hydroperoxides, were also determined. PC-OOH and PE-OOH significantly increased at 60 and 120 min ischemia with concomitant increase of oxidized glutathione. These hydroperoxides did not increase at 60 min reperfusion after 60 min ischemia, whereas they did increase at 60 min reperfusion after 120 min ischemia with deactivation of phospholipid hydroperoxide glutathione peroxidase and superoxide dismutase. The amount of MDA + 4-HNE exhibited similar changes, but the velocity of production dropped with ischemic time longer than 60 min. In conclusion, oxidative stress progressed during ischemia and triggered the oxidative injury after reperfusion. Secondary LPO products are less sensitive, especially during ischemia, which may cause possible underestimation and discrepancy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 38, Issue 10, 15 May 2005, Pages 1372-1381
Journal: Free Radical Biology and Medicine - Volume 38, Issue 10, 15 May 2005, Pages 1372-1381
نویسندگان
Moto Fukai, Takaaki Hayashi, Ryoichi Yokota, Tsuyoshi Shimamura, Tomomi Suzuki, Masahiko Taniguchi, Michiaki Matsushita, Hiroyuki Furukawa, Satoru Todo,