The role of N-acetylcysteine (NAC), a glutathione (GSH) precursor, was investigated in protection against isoniazid-(INH) and rifampicin-(RIF) induced oxidative hepatic injury in young Wistar rats. The hepatotoxic dose of INH and RIF was 50 mg kg-1 day-1 each and the hepatoprotective dose of NAC was 100 mg kgday-. All drugs were administered intraperitoneally (i.p.) in sterile water (4.0 ml kg-1 day-1) over a period of 3 weeks. Status of oxidative/antioxidative profiles was the mechanistic approach to assess the hepatotoxicity and/or hepatoprotection. The oxidative injury in INH-RIF co-exposed animals was closely associated with significant decline of GSH and related thiols, as well as with compromised antioxidant enzyme system. The oxidative stress was further supported by increased lipid peroxidation observed in these animals. The co-administration of NAC prevented the induction of oxidative stress in INH-RIF co-exposed animals. The amelioration of oxidative stress by NAC was faithfully reflected as normal morphology in these animals, except the presence of mild degree of portal triaditis in one animal co-exposed to INH-RIF and NAC. In contrast, the animals co-exposed to INH-RIF alone showed histological lesions which ranged from intralobular inflammation to patchy necrosis. These results suggest that INH-RIF-induced oxidative injury can be prevented by supporting the cellular antioxidant defense mechanism by NAC.

The present study was conducted to evaluate some of the components of antioxidant defense system and oxidative damage in 20 male patients of alcoholic liver disease (ALD). The results were compared with 20 healthy male smokers and 20 healthy male non-smokers volunteers. Patients were subjected to detailed clinical examination and laboratory investigations. Blood samples were collected for estimating reduced glutathione (GSH), total thiols (T-SH) malondialdehyde (MDA), transaminases (AST, ALT), glutathione-S-transferease (GST) and gammaglutamyl transferase (GGT). Serum aspartate amino transferase (AST)/alanine amino transferase (ALT) ratio was significantly (p<0.01) reduced in ALD patients as compared to the controls. However, the core of utility of MDA and GST was found to be significantly (p<0.01) increased in ALD patients compared to controls. There was a significant negative correlation of MDA with both GSH and TSH. Plasma GGT levels were significantly (p<0.01) increased in alcoholics and the enzyme showed a significant positive correlation with MDA. These results give enough evidence of increased oxidative stress and compromised antioxidant defense system in patients with ALD.

For a long time, aluminium (Al) has been considered an indifferent element from a toxicological point of view. In recent years, however, Al has been implicated in the pathogenesis of several clinical disorders, such as dialysis dementia, the fulminant neurological disorder that can develop in patients on renal dialysis. In the present study, the effect of chronic oral administration of Al on certain biochemical parameters of brain homogenate has been investigated. The feeding of test diet for 6 wk resulted in a decrease of thiols, glutathione reductase (GR), and adenosine Triphosphatase (ATPase). A nonsignificant decrease in peroxidation and glutathione-S-transferase (GST) was also detected in the Al-treated rats. From this study, it can be concluded that oxidative stress is produced by the metal.

Rotavirus affects amino acid uptake in the small intestine at the time of peak infection.

1 Weaning rats were fed ad libitum isocaloric diets containing 5% and 20% casein based proteins. 5% protein diet was protein deficient diet. Pair fed rats with the 5% protein group were maintained simulta neously on 20% protein diet but the amount restricted to the amount taken up by PEM group. 2 Glutathione, antioxidative enzymes, lipid peroxida tion and histopathological studies in liver and only glutathione and antioxidative enzymes in blood were carried out. 3 Rats fed the 5% protein diet developed a severe protein energy malnutrition (PEM) whereas those on pair-fed diet developed mild to moderate PEM. 4 Glutathione related thiols, superoxide dismutase, glutathione peroxidase, catalase and glutathione-S- transferase with (1 Chloro 2,4-dinitro benzene (CDNB) substrate) were decreased in liver with concomitant increase of lipid peroxidation in severe PEM. In blood glutathione, glutathione peroxidase and catalase were decreased while superoxide dismutase was increased in severe PEM group. 5 Mild to moderate PEM (pair-fed group) also resulted in similar changes in liver except glutathione peroxidase, lipid peroxidation in liver and superoxide dismutase in blood. 6 Hepatic injury was detectable only in the severe PEM group. 7 Oxidative-stress and hepatic injury occurred in severe PEM and to a lesser degree in mild to moderate PEM.