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.

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.

Anadolu Kardiyoloji Dergisi, Anadolu Kardiyol Derg, The Anatolian Journal of Cardiology, Anatol J Cardiol, Cardiology, Cardiovascular Medicine, Surgery, Pediatric Cardiology, Angiology

Cadmium (Cd) is a heavy metal which affects many systems in humans and animals as a consequence of environmental and industrial pollution. The aim of this study was to investigate the effect of chronic Cd toxicity on blood pressure and plasma viscosity. Experimental group rats were given doses that contained 15 ppm CdCl2 in drinking water for 8 weeks. The systolic blood pressure and heart rate were measured from rats’ tails and recorded by plethysmography every two weeks. Blood samples were drawn, Cd levels were determined by atomic absorption spectrophotometer and plasma viscosity values by viscometer. Blood Cd levels were found to be significantly higher in the experimental group compared to the control group (p < 0.001). The whole blood analysis was made by an analyzer. Polymorphonuclear leukocytes and monocytes increased (p < 0.01) and lymphocyte number (p < 0.05) decreased in the experimental group. Viscosity values were 2.21 ± 0.54 and 1.62 ± 0.31 centipoises in the experimental and control groups, respectively (p < 0.001). In the experimental group, changes in systolic blood pressure between weeks were significant (p < 0.001) and were found to be correlated with plasma viscosity (p < 0.001). In the experimental group, changes in heart rate between weeks were significant (p < 0.001). According to our findings, Cd toxicity may lead to an increase in blood pressure by increasing plasma viscosity.