IngentaConnect Oxygen Free Radical Production in Rat Liver

Authors: Addolorato G.¹; Campli C.D.¹; Simoncini M.¹; Pasini P.¹; Nardo B.¹; Cavallari A.¹; Pola P.¹; Roda A.¹; Gasbarrini G.¹; Gasbarrini A.¹

Source: Digestive Diseases and Sciences, Volume 46, Number 5, May 2001 , pp. 1057-1066(10)

Publisher: Springer

Abstract:

Ethanol is known to have a deleterious effect on liver ischemia–reperfusion injury, but recent reports suggest that light ethanol consumption may produce a protective effect in several organs. We aimed to investigate effects of different doses of ethanol on liver oxidative injury. Rats were fed with ethanol-containing diets (24, 30, 36, 40% for groups A, B, C, D, respectively). After four weeks, livers were exposed to ischemia–reperfusion. Chemiluminescence was recorded; total lipids, adenosine triphosphate, malondialdehyde, reduced glutathione and lactic dehydrogenase were assessed. In all groups, ischemia resulted in the disappearance of O_2^•−, a decrease in glutathione and adenosine triphosphate, and stable malondialdehyde values. During the reperfusion phase, O_2^•− production, malondialdehyde and lactic dehydrogenase increased, reaching significantly higher values in groups C and D and significantly lower values in group B. The effect of ethanol on ischemia–reperfusion injury seems to be a dose-related response, with an additional toxic effect only at high doses of ethanol.

Keywords: ethanol; ischemia–reperfusion; liver injury; chemiluminescence

Language: English

Document Type: Regular paper

Affiliations: 1: Patologia Medica and Medicina Interna, Catholic University of Rome, Rome, Italy; and Scienze Farmaceutiche and Clinica Chirurgica II, University of Bologna, Bologna, Italy.

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