Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica, Universidade Federal de Santa Maria - UFSM, 97105-900 Santa Maria, RS, Brazil.
Food Chem Toxicol. 2013 Aug;58:522-9. doi: 10.1016/j.fct.2013.05.022. Epub 2013 May 29.
The aim of the present study was to evaluate the possible effects of zinc chloride against the gastrointestinal lesions caused by oral administration of ethanol in rats. Rats were divided into five groups, namely, saline, ethanol, zn, zn+ethanol and ethanol+zn. Ethanol 70% (2 mL/kg) was administered by gavage in 36 h fasted rats. Zinc chloride (27 mg/kg, ~13 mg/kg of zinc) was given by gavage 1h before or 1h after the administration of ethanol. Oral administration of ethanol consistently induced damage in the rat glandular stomach and intestine. Zinc did not demonstrate effect per se and significantly reduced gastrointestinal lesions when administered either before or after lesion induction. Ethanol induced enhancement of thiobarbituric acid reactive substance and reactive species levels, diminished the ascorbic acid and total protein SH content as well as superoxide dismutase and catalase activity in stomach and intestine of rats. Zinc treatment prevented and reversed these alterations induced by ethanol. Stomach and intestine of rats treated with zinc presented higher zinc content than the tissues of rats treated only with ethanol. Non-protein SH content was not altered by any treatment. Results suggested that the gastrointestinal protective effect of zinc in this experimental model could be due to its antioxidant effect.
本研究旨在评估氯化锌对乙醇灌胃引起的大鼠胃肠道损伤的可能作用。大鼠分为 5 组，即生理盐水、乙醇、zn、zn+乙醇和乙醇+zn。禁食 36 小时后，通过灌胃给予 70%乙醇（2 mL/kg）。在给予乙醇前 1 小时或后 1 小时，通过灌胃给予氯化锌（27mg/kg，~13mg/kg 的锌）。乙醇口服给药可持续引起大鼠胃和肠的损伤。锌本身没有作用，当在损伤诱导前或后给予时，可显著减少胃肠道损伤。乙醇诱导胃和肠中硫代巴比妥酸反应物质和活性物质水平升高，降低抗坏血酸和总蛋白质 SH 含量以及超氧化物歧化酶和过氧化氢酶活性。锌处理可预防和逆转乙醇引起的这些改变。用锌处理的大鼠胃和肠的锌含量高于仅用乙醇处理的大鼠组织的锌含量。任何处理都没有改变非蛋白 SH 含量。结果表明，在这种实验模型中，锌对胃肠道的保护作用可能与其抗氧化作用有关。
