Enzymatic antioxidant defense system and antioxidant defense potential (AOP) were studied in kidney tissue from rabbits treated with cyclosporine (CsA, 25 mg/kg/day), antioxidant vitamins (E, 100 mg/kg/day plus C, 200 mg/kg/day), and CsA plus antioxidant vitamins, and in kidney tissue from control animals. Although no change was observed in superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) and catalase (CAT) activities were found decreased in kidney tissue exposed to CsA for 10 days compared with control tissue. The level of thiobarbituric acid-reagent substances (TBARS) was higher and antioxidant defense potential (AOP) lower in the CsA-treated group compared with the other groups. Histopathological examination reveals important subcellular damage in the renal tissue from the animals treated with CsA. Antioxidant vitamin therapy caused full improvement in the enzyme activities, TBARS levels and AOP, but the subcellular damage was partly ameliorated in the CsA plus vitamin group. Results suggest that CsA impairs the antioxidant defense system and reduces the antioxidant defense potential in the renal tissue. Antioxidant vitamin treatment protects the tissue in part against toxic effects of the drug.

It has been suggested that enzymatic and/or non-enzymatic antioxidant systems are impaired in rheumatoid arthritis (RA) and hence patients are exposed to oxidant stress. This study aimed to establish whether this is really the case. Fasting blood samples were obtained from 24 patients with rheumatoid arthritis and 20 controls. The activities of erythrocyte superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and xanthine oxidase (XO) enzymes and malondialdehyde (MDA), oxidant resistant (OR) and non-enzymatic superoxide radical scavenger activity (NSSA) values were measured in both groups. Patients with RA had higher SOD and XO activities and MDA levels than did the controls. However, NSSA and OR levels were found to be decreased, and CAT and GSH-Px activities unchanged in the study group. Results suggest that excessive free radical production through the xanthine-xanthine oxidase system is the primary factor in rheumatoid arthritis, rather than an impaired antioxidant system. The therapeutic use of XO enzyme inhibitors and some antioxidants can be beneficial in this regard.

Migraine patients have an increased risk to develop deep white matter hyperintensities (WMH) than the general population. Oxidative stress is believed to play a role in the pathogenesis of migraine. The present study was undertaken to assess oxidant/antioxidant balance of migraineurs with and without WMH. We hypothesized that increased oxidative stress and decreased antioxidant response may play a role in the pathophysiology of WMH in migraineurs. The study included 32 patients in the migraine group and 17 age- and sex-matched healthy subjects without headache in the control group. The migraine group comprised 18 with WMH and 14 without WMH. We evaluated oxidative status with malondialdehyde (MDA) and to determine the activities of antioxidant enzymes: superoxide dismutase, glutathione peroxidase and catalase (CAT) in serum of migraineurs and controls. Comparison of the patient and control groups for oxidative parameters revealed significantly lower level of CAT and higher level of MDA in the patient group. Two-way comparison for CAT and MDA of the migraine with and without WMH and the controls revealed that CAT serum level significantly decreased in migraine patients with WMH than migraine patients without WMH and controls. In this preliminary study, we demonstrated that the levels of CAT were decreased in migraine patients with WMH compared to patients without WMH and controls. These findings suggest that decreased antioxidant response may play a role in the pathophysiology of WMH in migraineurs. Besides, our results encourage the new treatment and follow-up options based on antioxidant systems.

Parkinson's disease (PD) is one of the common neurodegenerative disorders. Oxidative stress is considered as a contributing factor to the development of PD. The present study aims to investigate serum oxidative stress status in patients with PD. Oxidative stress was assessed by measuring serum nitric oxide levels, lipid hydroperoxide concentrations, and nitric oxide synthase activity. In addition, total serum antioxidant capacity (TAC) was evaluated using the serum 2,2-Diphenyl-1-picryl-hydrazyl (DPPH) free-radical scavenging method in 32 patient with Parkinson's disease and 32 control subjects. Our results indicated that serum nitric oxide and lipid hydroperoxide levels were significantly lower in patients with PD than controls. Moreover, nitric oxide levels were found to be negatively correlated with Unified Parkinson's Disease Rating Scale (UPDRS). However, no statistical difference was observed in total serum antioxidant capacities and nitric oxide synthase activities between patients and controls. The present study indicates that although antioxidant capacity was not changed, lipid hydroperoxide (LPO) level was found decreased. This might show pre-oxidative process in these patients. In addition, decreased nitric oxide (NO) level and negative correlation observed between NO level and disease rating scale implicated a role for NO in the disease process.

Our results reflect oxidative stress in placenta tissues of early pregnancy failure, as the oxidative processes seem to be counteracted by the physiologic activation of antioxidant enzymes such as CAT and GSH-Px. Moreover, a compensatory mechanism might be developed against possible oxidative damage in patients with miscarriage.