The Effects of Chronic Cadmium Toxicity on the Hemostatic SystemKoçak M. · Akçıl E.
Department of Pathophysiology, Faculty of Medicine, Ankara University, Ankara, Turkey
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.
Mehtap Koçak, MD, PhD
Ziyabey C. No:19
TR–06520 Balgat-Ankara (Turkey)
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This article is part of the doctoral thesis of Mehtap Koçak.
This work was presented at the 30th World Congress of the International Society of Hematology, 28 September to 2 October 2005, Istanbul, Turkey, and the 5th International Congress of Pathophysiology, June 28 to July 1 2006, Beijing, China.
Received: September 20, 2006
Accepted after revision: December 14, 2006
Number of Print Pages : 6
Number of Figures : 0, Number of Tables : 1, Number of References : 64
Pathophysiology of Haemostasis and Thrombosis
Vol. 35, No. 6, Year 2006 (Cover Date: June 2007)
Journal Editor: Rosing, J. (Maastricht)
ISSN: 1424–8832 (print), 1424–8840 (Online)
For additional information: http://www.karger.com/PHT