Antioxidant defense potential of rabbit renal tissues after ESWL: protective effects of antioxidant vitamins.

Antioxidant defense potential, malondialdehyde (MDA) levels, and relative hydroxyl radical (OH.) concentrations were measured in order to establish the effects of extracorporeal shock wave lithotripsy (ESWL) on free radical production and antioxidant defense potential of the rabbit kidney tissues. Electron microscopic examination was also performed to observe ultrastructural changes. The antioxidant defense potential of the ESWL-treated tissues was found to be reduced, and the MDA levels increased as compared with controls. Vitamin (vitamin E plus C combination) pretreatment ameliorated antioxidant defense potential in part, prevented increases in MDA levels in the ESWL-treated tissues, and increased the antioxidant defense potential in the control kidney tissues. After ESWL, a significant amount of OH. radical was measured in the affected tissue. This revealed the source of oxidant stress and peroxidation reactions in the ESWL-treated kidney tissue. Vitamin pretreatment caused significant reduction in the OH. radical concentration. In the electron microscopic investigation, some significant subcellular changes, such as endothelial injury, loss of foot processes, damage of glomerular basal membrane, etc., were observed in the ESWL-treated renal tissue slices. Vitamin pretreatment to a great extent prevented formation of these subcellular changes. Our results suggest that the antioxidant capacity of the kidney tissue was reduced after ESWL treatment and that the tissue was exposed to oxidant stress. Vitamin pretreatment exerted significant protection against the radical damage.

Impaired antioxidant defence in guinea pig heart tissues treated with halothane.

PURPOSE: To investigate the effects of halothane and halothane plus vitamin E treatment on myocardial free radical metabolism in guinea pigs. METHODS: Four groups of seven animals were studied: control, halothane, halothane plus vitamin E and vitamin E groups. In the halothane group, halothane 1.5% in oxygen was given for 90 min over three days. In the halothane plus vitamin E group, 300 mg.kg-1.day-1 vitamin E im was started three days before the first halothane treatment and continued for three days. Following sacrifice, the hearts were assayed for superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) and malondialdehyde (MDA) level was determined. Electron spin resonance (ESR) analysis and electron microscopy (EM) were also performed. RESULTS: In the halothane group, SOD activities and MDA concentrations were increased compared with control and GSH-Px and CAT activities were decreased. In the halothane plus vitamin E group, there were no differences in enzyme activity compared with halothane alone but the MDA level was decreased. In the vitamin E group, enzyme activities were increased compared with control. Mainly the CF3CHCl radical was identified by ESR analysis in heart tissues exposed to halothane and the concentration of this radical was reduced by vitamin E. Electron microscopy showed cytoplasmic vacuolisation and dilation in sarcoplasmic reticulum in the heart tissues exposed to halothane: both were prevented by vitamin E. CONCLUSION: Although halothane causes impairment in enzymatic antioxidant defence potential, due to lowered GSH-Px and CAT activity, and accelerates peroxidative reactions in the tissues affected, no subcellular damage occurred. Vitamin E may protect tissues against free radical attack by scavenging toxic free radicals formed in heart tissue during halothane anaesthesia.

Halothane hepatotoxicity and hepatic free radical metabolism in guinea pigs; the effects of vitamin E.

PURPOSE: The aim of this study was to investigate the relation between halothane hepatotoxicity and hepatic free radical metabolism and to establish a possible protective role of vitamin E against halothane hepatotoxicity. METHODS: Twenty-eight guinea pigs were used in the experiments. Halothane (1.5% v/v) in oxygen (100%) was given to the animals for 90 min over three days. Livers from animals were then taken and prepared for the assays. In the enzymatic study, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities were measured. As a peroxidation index, the malondialdehyde (MDA) concentration was determined. Also, electron spin resonance (ESR) analysis and electron microscopy (EM) were performed. RESULTS: Superoxide dismutase (1168.3 +/- 78.2 U.mg-1) and glutathione peroxidase (14.9 +/- 6.2 mIU.mg-1) activities were decreased, but catalase activity (1260.0 +/- 250.6 IU.mg-1) and malondialdehyde concentration (11.5 +/- 1.8 ppb) were increased in liver tissues exposed to halothane compared with control values (1382.2 +/- 91.8 U.mg-1 for SOD, 27.8 +/- 5.2 mIU.mg-1 for GSH-Px, 840.2 +/- 252.4 IU.mg-1 for CAT and 10.0 +/- 1.0 ppb for MDA). Electron spin resonance analysis revealed a peak of CF3CHCl. radical in the exposed tissue. Electron microscopy indicated ultrastructural changes in the hepatic cells of both halothane groups with and without vitamin E treatment. CONCLUSION: Halothane causes impairment in the hepatic antioxidant defense system and accelerates peroxidation reactions. As a result, some ultrastructural changes in hepatic tissues occur due to halothane treatment. Although vitamin E prevents peroxidative damage, it does not ameliorate ultrastructural changes caused by halothane treatment. This shows that halothane toxicity results not only from impaired hepatic antioxidant defense system but also from other, unknown causes.