Carnosine is a dipeptide having strong antioxidant effects. Oxidative stress plays an important role in pathogenesis of alcohol-induced liver injury. In this study, we investigated the effect of carnosine pretreatment on ethanol-induced oxidative stress and hepatotoxicity. Rats were given carnosine (2 g/L in drinking water) for 4 weeks and then ethanol was administered orally to rats at a dose of 5 g/kg every 12 hours for 3 doses totally (binge model). All rats were killed 6 hours after last ethanol injection. Plasma alanine (ALT) and aspartate (AST) transaminase activities and liver triglyceride, malondialdehyde (MDA), diene conjugate (DC), glutathione (GSH), vitamin E and vitamin C levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities were determined. Binge ethanol administration resulted in significant increases in plasma transaminase activities, hepatic triglyceride and lipid peroxide levels. However, GSH, vitamin E, vitamin C levels and GSH-Px and GST activities were found to be decreased following ethanol administration. Macromicrovesicular steatosis was also seen. Carnosine pretreatment appeared to prevent the increase of plasma ALT and AST activities and hepatic MDA and DC levels following ethanol treatment. In addition, hepatic GSH levels increased, but there were no changes in triglyceride, vitamin E, vitamin C levels and SOD, GSH-Px and GST activities, following ethanol treatment in carnosine-pretreated rats. There was also no change in liver histopathological appearance. In conclusion, carnosine prevented the increases in serum transaminase activities and lipid peroxides in liver of ethanol-treated rats, without any change on steatosis in liver.

Endogen malondialdehyde (MDA), diene conjugate levels, the susceptibility to copper-induced lipid peroxidation and antioxidant activity of serum were determined In patients with atherosclerotic diseases such as diabetes mellitus and myocard infarction. Lipid peroxidation susceptibility and antioxidant activity did not change, however, an increase in endogen MDA and diene conjugate levels was observed in serum of these patients, These results indicate the presence of oxidative stress in diabetes meHitus and myocard infarction.

In this study, prooxidant and antioxidant status in liver homogenates and their mitochondrial fractions were investigated in both chronic and chronic plus acute ethanol-treated rats. Increases in serum transaminase activities, as well as increases in total lipid, triglyceride, malondialdehyde (MDA) and diene conjugate (DC) levels and decreases in glutathione (GSH), vitamin E and vitamin C levels, have been observed in liver homogenates following chronic ethanol treatment (20% ethanol, v/v as drinking water for 3 months), but CuZn-superoxide dismutase (CuZnSOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities remained unchanged in postmitochondrial fractions. When an acute dose of ethanol (5 g/kg, i.p.) was given rats which had received ethanol chronically, serum transaminase activities and hepatic lipid and MDA and DC levels increased further, but GSH levels and antioxidant enzymes decreased more compared to the chronic ethanol-treated rats. There were no significant differences in the levels of MDA, DC and protein carbonyl and the activities of GSH-Px and GST in the hepatic mitochondrial fraction of rats following both chronic and chronic plus acute treatments. Mn-superoxide dismutase (MnSOD) activities increased in both groups, but mitochondrial GSH levels decreased only after chronic plus acute treatment. Therefore, we suggest that the increase in MnSOD activity may play an important role in the regulation of mitochondrial susceptibility against ethanol-induced oxidative stress.

Insulin-secreting pancreatic tumors and insulin-like growth hormone-secreting non-islet cell tumors can cause hypoglycemia. However, insulin-releasing paraganglioma or pheochromocytoma has almost never been reported. A 67-year-old female patient was admitted to our hospital because of headache, palpitation, perspiration, faintness, frequent sense of hunger and absent-mindedness. These intermittent symptoms had begun approximately a year before admission. On physical examination, she had high blood pressure of 150/90 mm Hg. Hormonal studies demonstrated increased urinary norepinephrine levels, and hyperinsulinemic hypoglycemia was confirmed while the patient was symptomatic. Abdominal MRI revealed a retroperitoneal mass measuring 4.5 cm in the pancreatic region. She was treated with an alpha-blocking agent to control blood pressure preceding the removal of the mass. Histopathological diagnosis was paraganglioma, and immunohistochemically insulin staining in the neoplastic cells was demonstrated. Her blood pressure normalized and hypoglycemia relieved after the operation. The patient did not have recurrence of hypoglycemia after a year of follow-up. Paraganglioma is a rare tumor of the neural crest, and co-secretion of insulin and catecholamines has been reported only by a single case report in the literature. The present patient is another case with this co-secretion.

No abstract