Literature DB >> 17565233

The effects of chronic cadmium toxicity on the hemostatic system.

Mehtap Koçak1, Ethem Akçil.   

Abstract

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.

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Year:  2006        PMID: 17565233     DOI: 10.1159/000102047

Source DB:  PubMed          Journal:  Pathophysiol Haemost Thromb        ISSN: 1424-8832


  8 in total

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2.  Celastrol prevents cadmium-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network.

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4.  Cadmium chronotoxicity at pituitary level: effects on plasma ACTH, GH, and TSH daily pattern.

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5.  Rapamycin ameliorates cadmium-induced activation of MAPK pathway and neuronal apoptosis by preventing mitochondrial ROS inactivation of PP2A.

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6.  The ER stress regulator Bip mediates cadmium-induced autophagy and neuronal senescence.

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8.  The anticoagulant properties of cadmium telluride quantum dots.

Authors:  Ciarán M Maguire; Michelle Lavin; Mairead Doyle; Mary Byrne; Adriele Prina-Mello; James S O'Donnell; Yuri Volkov
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  8 in total

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