In this study, histopathological and biochemical changes due to chronic usage of morphine or tramadol in liver and kidney were assessed in rats. Thirty male Wistar rats (180-220 g) were included and divided into three groups. Normal saline (1 ml) was given intraperitoneally as placebo in the control group (n = 10). Morphine group (n = 10) received morphine intraperitoneally at a dose of 4, 8, 10 mg/kg/day in the first, second and the third ten days of the study, respectively. Tramadol group (n = 10), received the drug intraperitoneally at doses of 20, 40 and 80 mg/kg/day in the first, second and the third ten days of the study, respectively. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatinin, blood urea nitrogen (BUN) and malondialdehyde (MDA) levels were measured in the serum. Liver and kidney specimens were evaluated by light microscopy. Serum ALT, AST, LDH, BUN and creatinin levels were significantly higher in morphine group compared to the control group. Serum LDH, BUN and creatinin levels were significantly increased in the morphine group compared to the tramadol group. The mean MDA level was significantly higher in morphine group compared to the tramadol and control groups (P < 0.05). Light microscopy revealed severe centrolobular congestion and focal necrosis in the liver of morphine and tramadol groups, but perivenular necrosis was present only in the morphine group. The main histopathologic finding was vacuolization in tubular cells in morphine and tramadol groups. Our findings pointed out the risk of increased lipid peroxidation, hepatic and renal damage due to long term use of opioids, especially morphine. Although opioids are reported to be effective in pain management, their toxic effects should be kept in mind during chronic usage.

Psoriasis is a common, chronic inflammatory skin disease with unknown etiology. Recently it has been suggested that increased ROS production and deficient function of antioxidant systems activities may be involved in the pathogenesis of the disease. Although there are several studies investigating oxidant/antioxidant systems in psoriatic patients, the data obtained from these studies is not concordant. In this study, superoxide dismutase (SOD) enzyme activity, and malondialdehyde (MDA) and antioxidant potential (AOP) levels in thirty-five patients with psoriasis were investigated and compared with those of twenty-four control subjects. Clinical severity of the disease was determined according to the Psoriasis Area and Severity Index (PASI) scores in the patients. Plasma SOD activity and MDA levels were significantly higher (p=0.012 and p=0.005 respectively), whereas AOP levels were lower, in patients than controls (p=0.001). There was no correlation between PASI scores and plasma SOD, MDA, and AOP levels. Our findings may provide some evidence for a potential role of increased ROS production and decreased antioxidant activity in psoriasis.

Recurrent aphthous stomatitis (RAS) is recognized as one of the most common oral mucosal diseases worldwide. The aim of this study was to determine the oxidant/antioxidant status in erythrocyte and plasma samples from patients with RAS in comparison with healthy controls. Twenty-two patients with RAS and 23 healthy controls were recruited. Superoxide dismutase, glutathione peroxidase (GSHPx) and catalase (CAT) activities, and malondialdehyde (MDA) and antioxidant potential (AOP) levels were measured in plasma and erythrocytes from patient with RAS and controls. We found decreased CAT and GSHPx activities and AOP levels in the erythrocytes, and decreased AOP and increased MDA plasma levels in patients with RAS in comparison with control subjects. In summary, this study demonstrated that enzymatic and nonenzymatic antioxidant defence systems are impaired in patients with RAS.

Glutathione S-transferases (GSTs) are a major group of phase II detoxification enzymes involved in the metabolism of both endogenous and xenobiotic compounds. In addition to their catalytic function in detoxification, GSTs participate in binding to nonsubstrate ligands such as bilirubin. Ligandin, which is one of the principal hepatic-binding proteins, is also a member of the GST family. The aim of the present study was to investigate the possible relationship between neonatal jaundice and the GST gene polymorphisms. The study cohort consisted of a patient group of 116 newborns (plasma bilirubin levels > or = 15 mg/dl) and a control group of 54 newborns (plasma bilirubin levels <13 mg/dl). In the patient group, the null genotype frequencies in GSTM1 and GSTT1 were 52.6 and 19%, respectively; in the control group, these were 63 and 27.8%, respectively. The frequencies of GSTM1 and GSTT1 were similar in the patient and control groups (p > 0.05). Total bilirubin levels were found to be significantly higher in patients with the GSTM1 null genotype than in patients with the GSTM1 wild genotype (p = 0.042). There was no statistically significant difference in total bilirubin levels between patients with the null GSTT1 genotype and those with the wild GSTT1 genotype. It is conceivable that there is a relation between GSTM1 gene polymorphism and total bilirubin levels in neonatal jaundice. We suggest that GSTM1 gene polymorphisms may affect ligandin functions in hepatocytes, which are important in bilirubin transportation. Consequently, patients with the GSTM1 null genotype may have higher total levels of bilirubin.

These data emphasize that poly (ADP-ribose) polymerase may have a role in testicular damage caused by ischemia-reperfusion and the inhibition of poly (ADP-ribose) polymerase may be a novel approach to therapy for ischemia-reperfusion injury of the testis.