Wetscher G J, Hinder P R, Bagchi D, Perdikis G, Redmond E J, Glaser K, Adrian T E, Hinder R A
Department of Surgery, Creighton University, Omaha, Nebraska 68131, USA.
Dig Dis Sci. 1995 Jun;40(6):1292-6. doi: 10.1007/BF02065541.
Free radical damage in reflux esophagitis of rats induced by 24-hr duodenojejunal ligation was studied. Oxygen free radicals were selectively blocked. Groups were: sham operation, reflux, reflux + superoxide dismutase (SOD), catalase, dimethylthiourea, allopurinol, and inactivated SOD or inactivated catalase alone or in the combination SOD + catalase or SOD + catalase + dimethylthiourea + allopurinol. Macroscopic esophagitis was inhibited only by SOD, alone or in combination with other agents. Esophageal mucosal lipid peroxidation was 10-fold increased in the reflux group compared to the sham group (P < 0.05). This response was damped by SOD > catalase (P < 0.05) but not by the inactivated enzymes, dimethylthiourea or allopurinol. SOD + catalase showed no significant improvement on SOD alone. Total inhibition of lipid peroxidation was achieved by combining all scavengers. Total glutathione (GSH) in the esophageal mucosa was stimulated by reflux. This response was inhibited by scavengers equivalent to their efficacy in preventing lipid peroxidation. It is concluded that reflux esophagitis is associated with free radical release with O2- being the main source. Free radicals appear to stimulate GSH production in this prolonged oxidative stress.
研究了24小时十二指肠空肠结扎诱导的大鼠反流性食管炎中的自由基损伤。选择性阻断氧自由基。分组如下:假手术组、反流组、反流+超氧化物歧化酶(SOD)组、过氧化氢酶组、二甲基硫脲组、别嘌呤醇组,以及单独使用失活的SOD或失活的过氧化氢酶组,或SOD+过氧化氢酶组合组,或SOD+过氧化氢酶+二甲基硫脲+别嘌呤醇组合组。仅SOD单独或与其他药物联合使用可抑制宏观食管炎。与假手术组相比,反流组食管黏膜脂质过氧化增加了10倍(P<0.05)。这种反应被SOD>过氧化氢酶抑制(P<0.05),但未被失活的酶、二甲基硫脲或别嘌呤醇抑制。SOD+过氧化氢酶组与单独使用SOD相比无显著改善。联合使用所有清除剂可实现脂质过氧化的完全抑制。反流刺激食管黏膜中的总谷胱甘肽(GSH)。这种反应被清除剂抑制,其抑制效果与其预防脂质过氧化的效果相当。结论是反流性食管炎与自由基释放有关,其中O2-是主要来源。在这种长期氧化应激中,自由基似乎刺激了GSH的产生。