Antioxidant effect of zinc chloride against ethanol-induced gastrointestinal lesions in rats

• Published in: Food and chemical toxicology 2013-08, Vol.58, p.522-529
• Main Authors: Ineu, Rafael Porto, Oliveira, Cláudia Sirlene, Oliveira, Vitor Antunes, Moraes-Silva, Lucélia, da Luz, Sônia Cristina Almeida, Pereira, Maria Ester
• Format: Article
• Language: English
• Subjects: Animals; antioxidant activity; Antioxidants - pharmacology; ascorbic acid; Ascorbic Acid - metabolism; Biological and medical sciences; catalase; Catalase - metabolism; Chemical and industrial products toxicology. Toxic occupational diseases; Chlorides - pharmacology; ethanol; Ethanol - toxicity; Gastric Mucosa - drug effects; Gastric Mucosa - enzymology; Gastric Mucosa - metabolism; Histopathology; Intestine; intestines; Lipid Peroxidation; Male; Medical sciences; Metals and various inorganic compounds; oral administration; Oxidative stress; protective effect; Rats; Rats, Wistar; Reactive Oxygen Species - metabolism; Stomach; Sulfhydryl Compounds - metabolism; superoxide dismutase; Superoxide Dismutase - metabolism; thiobarbituric acid-reactive substances; tissues; Toxicology; zinc; Zinc Compounds - pharmacology; Zinc content
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/j.fct.2013.05.022

•Ethanol consistently induced damage in the rat glandular stomach and intestine.•Zinc content in stomach was raised by treatment with ZnCl2.•Renal and hepatic metabolic parameters are not altered by ethanol-induced gastric damage in rats.•Zn did not demonstrate effect per se but reduced gastrointestinal lesions when administered before or after lesions induction.•Oral administration of zinc chloride protects against gastrointestinal mucosa damage induced by ethanol. 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% (2mL/kg) was administered by gavage in 36h fasted rats. Zinc chloride (27mg/kg, ∼13mg/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.