@article {Addolorato:May 2001:0163-2116:1057, author = "Addolorato G.", author = "Campli C.D.", author = "Simoncini M.", author = "Pasini P.", author = "Nardo B.", author = "Cavallari A.", author = "Pola P.", author = "Roda A.", author = "Gasbarrini G.", author = "Gasbarrini A.", title = "Oxygen Free Radical Production in Rat Liver", journal = "Digestive Diseases and Sciences", volume = "46", year = "May 2001", 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.

", pages = "1057-1066(10)", url = "http://www.ingentaconnect.com/content/klu/ddas/2001/00000046/00000005/00302640" }