ESOPHAGITIS IN SPRAGUE-DAWLEY RATS IS MEDIATED BY FREE-RADICALS

被引:98
作者
WETSCHER, GJ
PERDIKIS, G
KRETCHMAR, DH
STINSON, RG
BAGCHI, D
REDMOND, EJ
ADRIAN, TE
HINDER, RA
机构
[1] CREIGHTON UNIV, SCH MED, DEPT SURG, OMAHA, NE 68131 USA
[2] CREIGHTON UNIV, DEPT PHARMACOL, OMAHA, NE 68131 USA
[3] CREIGHTON UNIV, DEPT BIOMED SCI, OMAHA, NE 68131 USA
[4] UNIV INNSBRUCK, DEPT SURG 2, A-6020 INNSBRUCK, AUSTRIA
关键词
ESOPHAGITIS; FREE RADICALS; GLUTATHIONE; SUPEROXIDE DISMUTASE; BUTHIONINE SULFOXIMINE;
D O I
10.1007/BF02065542
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Free radical-mediated esophagitis was studied during duodenogastroesophageal reflux (mixed reflux) or acid reflux in rats. The influence of reflux on esophageal glutathione levels was also examined. Mixed reflux caused more gross mucosal injury than acid reflux. Gross mucosal injury occurred in the mid-esophagus. Total glutathione (GSH) in the esophageal mucosa of control rats was highest in the distal esophagus. The time course of esophageal GSH in rats treated by mixed reflux showed a significant decrease 4 hr after initiation of reflux, followed by a significant increase from the 12th hour on. Mucosal GSH was increased in both reflux groups after 24 hr but significantly more so in the mixed than in the acid reflux group. The free radical scavenger superoxide dismutase (SOD) prevented esophagitis and was associated with decreased GSH levels. GSH depletion by buthionine sulfoximine (BSO) prevented esophagitis and stimulated SOD production in the esophageal mucosa. It is concluded that gastroesophageal reflux is associated with oxidative stress in the esophageal mucosa. The lower GSH levels in the mid-esophagus may predispose to damage in this area. Duodenogastroesophageal reflux causes more damage than pure acid reflux. Oxidative stress leads to GSH depletion of the esophageal mucosa in the first few hours following damage but then stimulates GSH production. GSH depletion by BSO does not worsen esophagitis since it increases the esophageal SOD concentration.
引用
收藏
页码:1297 / 1305
页数:9
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