Pancreas is known to be vulnerable to ethanol (ETOH) at high doses, but little is known about the effect of lower doses. Therefore, in this study, the levels of glutathione (GSH), sulfhydryl proteins (P-SH), carbonyl proteins, malondialdehyde (MDA), and adenosine triphosphate (ATP) production were determined in the pancreatic tissue and mitochondria of rats fed for 8 weeks with 3\% ETOH. ETOH decreased the pancreatic pool of ATP, while GSH and P-SH also decreased in mitochondria. MDA concentrations increased both in the pancreas and mitochondria, while carbonyl proteins increased only in mitochondria. Pancreatic cells of ETOH-treated rats were frequently affected by cytoplasmic vacuolization and swelling; these alterations were often associated with ductular dilatation. In conclusion, ETOH produces oxidative and morphologic alterations in the pancreas of the rat, including impairment of mitochondria. These effects may represent basic mechanisms of ETOH-induced pancreatic injury.
Chronic ethanol administration induces oxidative alterations and functional impairment of pancreatic mitochondria in the rat.
VENDEMIALE, GIANLUIGI;
1999-01-01
Abstract
Pancreas is known to be vulnerable to ethanol (ETOH) at high doses, but little is known about the effect of lower doses. Therefore, in this study, the levels of glutathione (GSH), sulfhydryl proteins (P-SH), carbonyl proteins, malondialdehyde (MDA), and adenosine triphosphate (ATP) production were determined in the pancreatic tissue and mitochondria of rats fed for 8 weeks with 3\% ETOH. ETOH decreased the pancreatic pool of ATP, while GSH and P-SH also decreased in mitochondria. MDA concentrations increased both in the pancreas and mitochondria, while carbonyl proteins increased only in mitochondria. Pancreatic cells of ETOH-treated rats were frequently affected by cytoplasmic vacuolization and swelling; these alterations were often associated with ductular dilatation. In conclusion, ETOH produces oxidative and morphologic alterations in the pancreas of the rat, including impairment of mitochondria. These effects may represent basic mechanisms of ETOH-induced pancreatic injury.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
