It has been suggested that reactive oxygen metabolites and trace elements play some role in the etiology and pathogenesis of rheumatoid arthritis (RA). Superoxide dismutase (SOD) is believed to exert an important protective role against oxygen toxicity. The aim of the study was to investigate the probable changes in the levels of trace elements and SOD activity in RA. Plasma and erythrocyte copper, zinc, and magnesium levels and erythrocyte SOD activity were measured in groups of controls and RA cases. Significantly increased erythrocyte SOD activity was found in RA patients in comparison with controls (p < 0.0001). A rise in erythrocyte Zn level (p < 0.0001) and plasma Cu level (p < 0.0001) and a decrease in erythrocyte Cu level (p < 0.05) and plasma Zn level (p < 0.05) were obtained in RA patients when compared to controls. Plasma and erythrocyte Mg levels of the RA patients showed slight and statistically insignificant reductions when compared to controls (p > 0.05). In RA patients, there were positive correlations between erythrocyte SOD activity and Mg level (r = 0.4345, p < 0.01) and between erythrocyte Zn level and plasma Cu level (r = 0.4132, p < 0.01). There were negative correlations between erythrocyte SOD activity and plasma Zn level (r = -0.3605, p < 0.05) and between plasma Zn level and erythrocyte Cu level (r = -0.4578, p < 0.01) in RA patients.

Cadmium, a highly toxic heavy metal, is distributed widely in the general environment. The characteristic clinical manifestations of chronic cadmium intoxication include renal proximal tubular dysfunction, osteomalacia and anemia. Accumulating evidence suggests that cadmium toxicity may also affect various organs such as the liver, lung, testis and hematopoietic system. The aim of this study was to determine the effect of chronic cadmium exposure on the anticoagulant system in rats. Fourty-five adult Wistar albino rats were randomly allocated into 2 groups. While the control group was given tap water, the animals in the cadmium group were treated with 15 ppm CdCl₂ for 4 weeks. Blood cadmium concentration, prothrombin time, activated partial thromboplastin time, plasma protein C and antithrombin activity, and platelet count were determined in the rats. Blood cadmium concentrations increased in the experiment group compared to the control group (p < 0.001). Results also show that cadmium exposure shortened prothrombin time (p < 0.05) and activated partial thromboplastin time (p < 0.01) in rats. Protein C (p < 0.001) and antithrombin (p < 0.001) decreased to statistically significantly lower levels in rat plasma after cadmium exposure when compared to the control group. When the number of thrombocytes was compared between 2 groups, a decrease was observed in the group treated with CdCl₂, which was, however, not statistically significant (p > 0.05). In conclusion, when the parameters of the hemolytic system are considered, the decrease in protein C and antithrombin activities and the shortening of prothrombin time and activated partial thromboplastin time suggests the presence of a hypercoagulable state during chronic cadmium intoxication. Therefore, it may be stated that chronic cadmium toxicity sets the stage for hypercoagulation and hence increases the risk of thrombosis.

We studied the effects of L-carnitine on left ventricular systolic function and the erythrocyte superoxide dismutase activity in 51 patients with ischemic cardiomyopathy. They all previously were under the treatment of angiotensin-converting enzyme Ž . inhibitor, digitalis and diuretics. Patients were randomized into two groups. In group I n s 31 , 2 grday L-carnitine was added Ž . Ž . to therapy. L-Carnitine was not given to the other 20 patients Group II . In group I mean age 64.3" 7.8 years , 27 of the Ž . patients were men, and four were women. In group II mean age 66.2" 8.7 years , 17 of the patients were men, and three were Ž . women. Twenty age-matched healthy subjects mean age: 60.1" 5.3 years constituted the control group. In each group, left Ž . ventricular ejection fraction LVEF by echocardiography and red cell superoxide dismutase activity by spectrophotometric Ž . method were measured initially and after 1 month of randomisation. Compared with normal healthy subjects n s 20 , patients Ž . Ž . ns51 had significantly higher red cell SOD activity 5633" 1225 vs. 3202 " 373 Urg Hb, P -0.001 . At the end of 1 month Ž . of L-carnitine therapy, red cell SOD activity showed an increase in group I 5918 " 1448 to 7218 " 1917 Urg Hb, P-0.05 . In Ž group II, red cell SOD activity showed no significant change after 1 month of randomisation 5190" 545 to 5234 " 487 Urg . Ž Hb, P s 0.256 . One month after randomisation there was a significant increase in LVEF in both groups I and II 37.8᎐42.3%, . P-0.001 in group I; 41.5᎐43.8%, P -0.001 in group II . The improvement in LVEF was more significant in the L-carnitine Ž . group 4.5% vs. 2.3%, P-0.01 . We conclude that, as a sign of increased free radical production, superoxide dismutase activity was further increased in patients with L-carnitine treatment. L-Carnitine treatment in combination with other traditional pharmacological therapy might have an additive effect for the improvement of left ventricular function in ischemic cardiomyopathy. ᮊ

The aim of this study was to investigate the effect of oral cadmium (Cd) intoxication on the antioxidant response and its relationship with essential bioelements like copper (Cu) and zinc (Zn). The experimental group was chronically exposed to Cd daily for 8 weeks via consumption of water containing 15 ppm cadmium chloride. Cu, Zn, and Cd concentrations and oxidative stress parameters were analyzed in liver, kidney, and heart tissues. Exposure to Cd led to a significant decrease in the activities of superoxide dismutase in all considered samples while a significant increase in the activity of glutathione peroxidase except for the kidney. We found a significant increase in malondialdehyde concentration in the tissues except for heart. Also oral administration of Cd caused a significant reduction of Zn and Cu in the tissues. Our results allow us to hypothesize that higher Cd concentration in the tissues causes oxidative stress by increasing malondialdehyde as a means of altering antioxidant defense system and deterioration of bioelements in rat liver, kidney, and heart. In addition, further studies are needed to explain the effect of long-term, low-dose exposure to Cd on distribution of bioelements and its relationship with oxidative stress.

Accumulation of the widespread environmental toxin cadmium (Cd) in tissues results in toxicity. Cd, which can induce a broad spectrum of biological effects, is a toxic substance and is associated with inflammation and apoptosis. Midkine (MK) has fibrinolytic, antiapoptotic, transforming, angiogenetic and chemotactic activities. After Cd toxicity, we found increased MK expression in liver cells in an in vitro cell culture model. The aim of this study was to determine the possibility of relationship between tissue MK expression levels, tumor necrosis factor α(TNF-α) levels and apoptosis in a chronic Cd toxicity model in rats. Male Wistar rats were exposed to Cd at the dose of 15 parts per million (ppm) for 8 weeks. MK levels were measured in kidney, heart and liver tissue by enzyme-linked-immunosorbent assay (ELISA). MK messenger RNA (mRNA) expression was evaluated by RT-PCR. Tissue apoptosis level was evaluated with tissue caspase-3 activity levels. Accumulation of Cd in liver is higher than the kidney and heart. Cd-treated rats had significantly higher tissue TNF-α and caspase-3 levels when compared with the control rats (p < 0.001). MK mRNA and protein levels were also significantly upregulated in the Cd-treated group (p < 0.05, p < 0.001, respectively). When compared with apoptosis in tissues, it was more prominent in the liver than kidney and heart. MK level is found increased 3, 1.7 and 1.3× folds in liver, kidney and heart, respectively. Our results showed that chronic Cd administration induces inflammation and apoptosis in rat liver, kidney and heart. MK involved in damage mechanisms of Cd-induced tissues. Further studies will show the underlying mechanism of increased MK expression in Cd toxicity.

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In this study, we investigated the impact of ischemia-reperfusion on antioxidant enzyme activities and trace element concentrations. For this purpose, ischemia was initiated by clamping superior mesenteric artery of Wistar (albino) rats for 30 min, followed by reperfusion for 20 min. Immediately after reperfusion, blood samples were taken and examined for red cell copper-zinc superoxide dismutase (Cu-Zn-SOD), catalase (CAT), and glutathione peroxidase (GPx) activities spectrophotometrically and plasma zinc, copper, and magnesium concentrations by atomic absorption spectrophotometer. In the ischemia-reperfusion group, red cell Cu-Zn-SOD activity and plasma zinc and copper concentrations were increased significantly (p < 0.001) when compared to the control group; however, the increases in GPx activity and plasma magnesium concentration were not significant (p > 0.05). We also found a significant (p < 0.01) decrease in catalase activity. Free radicals released as a consequence of ischemia-reperfusion caused significant alterations in antioxidant enzymes and in the concentrations of trace elements.

This study was planned to determine the probable changes in trace element levels and superoxide dismutase (SOD) activity in women with neoplastic breast diseases. Measurements were performed in three different groups. The first group consisted of 20 healthy women, control group, the second group contained 16 patients with benign breast disease and the third group contained 39 patients with malignant breast disease. The trace element concentrations were determined by using atomic absorption spectrophotometry and SOD activity by using spectrophotometry. When compared with the control values, the plasma copper levels were slightly increased in the second group and significantly in the third group (p < 0.001). The difference between the benign and malignant groups was also significant (p < 0.001). The red cell copper values showed a marked decrease in both groups (p < 0 001). Although there were increases in the plasma zinc levels of both patient groups, the differences were not significant statistically. But, the red cell zinc values showed an significant increase in benign and malignant patients compared to the control group (p < 0.001) (p < 0.001). The plasma magnesium and red cell magnesium values did not show significant differences. The red cell SOD activity showed an significant increase in the benign and malignant patient groups (p < 0.001). The results of this study suggested that reactive oxygen metabolites may play a pathogenetic role in the both benign and malignant tumor development, which is reflected by the change in SOD activity, and in trace element concentrations.