Lipid peroxidation and antioxidant status in lichen planus.

BACKGROUND: Lichen planus (LP) is an inflammatory skin disease of unknown aetiology. Recently, increased oxidative stress has been implicated in the pathogenesis of various skin diseases such as atopic dermatitis, psoriasis vulgaris and vitiligo. AIM: To evaluate the status of the oxidative stress and antioxidant defence system in patients with LP. METHODS: In total, 40 patients with LP (23 men, 17 women; mean +/- SD age 43.27 +/- 1.96 years) and 40 control subjects, matched for age and gender, were enrolled in this prospective study. The exclusion criteria included medication with immunosuppressive agents, history of trauma and surgery, and history of alcohol ingestion for at least 1 month prior to the study. The serum nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels and the erythrocyte catalase (CAT) levels were investigated in both groups. RESULTS: Mean +/- SD levels of serum NO (74.60 +/- 17.96 micromol/L) and MDA (18.24 +/- 5.21 micromol/L) in patients with LP were higher than those of the control group (P = 0.007 and P = 0.031, respectively). Serum SOD levels (18.19 +/- 3.71 U/mL) in patients with LP were also higher than in healthy controls (P = 0.002). In contrast, erythrocyte CAT levels (13 557.80 +/- 4134.42 U/kg haemoglobin) were significantly lower in the patient group than in the control group (P = 0.009). CONCLUSIONS: The findings of this study suggest that increased oxidative stress, increased lipid peroxidation and an imbalance in the antioxidant defence system may be involved in the pathogenesis of LP.

The effect of Nigella sativa oil against experimental allergic encephalomyelitis via nitric oxide and other oxidative stress parameters.

Reactive oxygen species (ROS) including nitric oxide (NO) are thought to be involved in inflammatory processes, exacerbating inflammation and tissue damage in multiple sclerosis (MS). The oil extracts of Nigella sativa (N. sativa) has been known as an antioxidant and antiinflammatory agent. The aim of the present study was to investigate the hypothesis that N. sativa components provide protection against oxidative stress induced by experimental autoimmune encephalomyelitis (EAE) in rats. For this purpose, EAE was induced in rats by using guinea pig myelin basic protein (MBP) in Freud's adjuvant with addition of heat-killed M. Tuberculosis H37Ra to test this hypothesis. In study groups, N. sativa was given by oral gavage to the rats. Treatment of the rats with N. sativa inhibited ROS production induced by EAE showing diminished levels of MDA of both brain and medulla spinalis tissues. Although there was a significant decrease in brain NO level, there was an increase in medulla spinalis NO level after EAE induction in rats. N. sativa regulated tissue NO levels in some extend when applied together with EAE. When N. sativa was given alone to the rats, no changes were shown in brain, medulla spinalis, and serum oxidant/antioxidant parameters. In conclusion, N sativa may protect brain and medulla spinalis tissues against oxidative stress induced by EAE. In addition, N. sativa display its antioxidant and regulatory effects via inflammatory cells rather than the host tissue (brain and medulla spinalis) for EAE in rats.

Melatonin administration prevents the nephrotoxicity induced by gentamicin.

OBJECTIVE: To investigate the effect of melatonin on the antioxidant enzyme activity and renal tubular necrosis induced by gentamicin. MATERIALS AND METHODS: Twenty-four adult male Sprague-Dawley rats were divided into three equal groups. In group 1, the rats were injected with vehicle (controls), in group 2 they were injected with gentamicin for 5 days and in group 3 injected with gentamicin plus melatonin for 5 days. At 24 h after the last injection, rats were killed and the renal cortex separated from the medulla. Most of the cortex was homogenized but a small sample was fixed in formaldehyde solution for histological examination by light microscopy. Blood samples were also taken to assess the serum levels of urea, creatinine, Na+, K+ and gamma-glutamyl transpeptidase (gamma-GT); before death, urine samples were analysed for protein content. Crude extracts of the cortex were used to determine lipoperoxides, reduced glutathione (GSH-Px), catalase and superoxide dismutase (SOD). The results were compared using the Mann-Whitney U-test. RESULTS: Compared with the controls rats, gentamicin caused hyperproteinuria, an increase in the level of gamma-GT in serum, a marked increase in lipoperoxides and a significant decrease of GSH-Px, catalase and SOD activity in the kidney. In the rats in group 3 there was a marked restoration in lipid peroxidation, GSH-Px, catalase, SOD activity and proteinuria, and in gamma-GT in serum. In rats in group 2 there was widespread tubular necrosis (grade 2-4) but in rats in group 3 there was a marked reduction in the extent of tubular damage. There was no significant difference in serum levels of Na+, K+, blood urea nitrogen and creatinine. CONCLUSION: These results indicate that melatonin prevents the tubular necrosis induced by gentamicin in rats, presumably because it is a potent antioxidant and restores antioxidant enzyme activity in the rat kidney.

Increased nitric oxide production in the spermatic vein of patients with varicocele.

OBJECTIVE: To define the level of nitric oxide (NO) in the spermatic vein of patients with varicocele and its relation with male infertility. MATERIALS AND METHODS: Following physical and color Doppler ultrasonographic examination, whole blood samples were drawn from a peripheral vein and a dilated varicocele vein from fourteen patients with clinically palpable varicocele (G2-3) before ligation. NO levels in the serum were determined as total nitrite by Greiss reaction and results were compared with Mann-Whitney U test. RESULTS: NO levels in the internal spermatic vein were 36.05 +/- 8. 92 micromol/l, compared to 19.41 +/- 4.12 micromol/l in the peripheral vein and the difference was statistically significant (p < 0.01). CONCLUSION: In view of our results, increased NO levels in the dilated varicocele vein might be responsible for spermatozoa dysfunction.