Koçak Mehtap, Akçil Ethem
Department of Pathophysiology, Faculty of Medicine, Ankara University, Ankara, Turkey.
Pathophysiol Haemost Thromb. 2006;35(6):411-6. doi: 10.1159/000102047.
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 CdCl(2) 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 CdCl(2), 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.
镉是一种剧毒重金属，在一般环境中广泛分布。慢性镉中毒的典型临床表现包括肾近端小管功能障碍、骨软化症和贫血。越来越多的证据表明，镉毒性可能还会影响肝脏、肺、睾丸和造血系统等多个器官。本研究的目的是确定慢性镉暴露对大鼠抗凝系统的影响。45只成年Wistar白化大鼠被随机分为2组。对照组给予自来水，镉组动物用15 ppm氯化镉处理4周。测定大鼠的血镉浓度、凝血酶原时间、活化部分凝血活酶时间、血浆蛋白C和抗凝血酶活性以及血小板计数。与对照组相比，实验组的血镉浓度升高（p < 0.001）。结果还显示，镉暴露使大鼠的凝血酶原时间缩短（p < 0.05）和活化部分凝血活酶时间缩短（p < 0.01）。与对照组相比，镉暴露后大鼠血浆中的蛋白C（p < 0.001）和抗凝血酶（p < 0.001）降至统计学上显著更低的水平。当比较两组之间的血小板数量时，在氯化镉处理组中观察到数量减少，然而，差异无统计学意义（p > 0.05）。总之，从溶血系统参数来看，蛋白C和抗凝血酶活性降低以及凝血酶原时间和活化部分凝血活酶时间缩短表明慢性镉中毒期间存在高凝状态。因此，可以说慢性镉毒性为高凝状态奠定了基础，从而增加了血栓形成的风险。
