Effects of cadmium treatment in vitro on the antioxidant protection mechanism and activation of human blood platelets
| Autor: | Sila Mukhopadhyay, Sunil Mukhopadhyay, Sankar Addya, Dilip K. Bhattacharya, Gora Chand Chatterjee |
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| Rok vydání: | 1988 |
| Předmět: |
Adult
Blood Platelets Male medicine.medical_specialty Antioxidant medicine.medical_treatment Glutathione reductase chemistry.chemical_element Arachidonic Acids Cyclooxygenase pathway chemistry.chemical_compound Calcium Chloride Internal medicine Malondialdehyde medicine Humans Platelet Platelet activation chemistry.chemical_classification Cadmium Arachidonic Acid Aspirin Glutathione peroxidase Thrombin Hematology Glutathione Middle Aged Oxygen Endocrinology chemistry Biochemistry Prostaglandin-Endoperoxide Synthases Oxidation-Reduction |
| Zdroj: | Thrombosis research. 50(3) |
| ISSN: | 0049-3848 |
| Popis: | Interactions of human platelets with cadmium in vitro were studied with respect to the platelet activation process as indicated by malondialdehyde (MDA) formation and also to the components of the cellular antioxidant defence system such as catalase, glutathione peroxidase (GP), glutathione reductase (GR), glutathione-S-transferase (GST), glucose-6-phosphate dehydrogenase (G6PDH), and reduced glutathione (GSH). Cadmium treatment stimulated platelet MDA formation after a lag phase of at least 15 min and this effect was completely blocked by either 1 mM aspirin or 1 mM CaC12. Cadmium pretreated platelets also displayed a much higher (5 fold) MDA formation when stimulated by thrombin. Platelet catalase activity was decreased by almost 50% after incubation with cadmium. There was also a moderate decline in platelet GSH and GR activity along with a stimulation of GST and G6PDH activity. These results suggest : (1) the cadmium effect on platelets as observed by enhanced formation of MDA via the cyclooxygenase pathway involves intraplatelet accumulation of cadmium which is inhibited by calcium, (2) a modest decline in GSH, presumably due to the inadequacy of H202 detoxification mechanism, does not adversely affect platelet function because of the adaptive response of G6PDH, and (3) intracellular accumulation of cadmium may result in platelet hyperactivity through higher intraplatelet free calcium levels resulting directly through cadmium action or indirectly through higher H202 levels due to catalase inhibition. |
| Databáze: | OpenAIRE |
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