Abstract 554: Mitochondrial Biomarkers for Assessing Early Tobacco Product Induced Cardiovascular Injury in Human Participants
| العنوان: | Abstract 554: Mitochondrial Biomarkers for Assessing Early Tobacco Product Induced Cardiovascular Injury in Human Participants |
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| المؤلفون: | Aruni Bhatnagar, Jessica L. Fetterman, Robert M. Weisbrod, Rachel J. Keith, Monica Holbrook, Elica Inagaki, Erika A Linder, Rosa Bretón-Romero, Naomi M. Hamburg, Brittany D Berk |
| المصدر: | Arteriosclerosis, Thrombosis, and Vascular Biology. 36 |
| بيانات النشر: | Ovid Technologies (Wolters Kluwer Health), 2016. |
| سنة النشر: | 2016 |
| مصطلحات موضوعية: | business.industry, Stressor, Mitochondrion, medicine.disease_cause, Bioinformatics, Cigarette smoking, Mitochondrial abnormalities, Toxicity, medicine, Cardiovascular Injury, Cardiology and Cardiovascular Medicine, business, Oxidative stress, Tobacco product |
| الوصف: | Smoking is a major cause of preventable cardiovascular deaths worldwide. A number of new and emerging tobacco-related products including electronic(e)-cigarettes have become readily available as tobacco cigarette alternatives and are often marketed as being less harmful despite growing evidence that toxic aldehydes are absorbed into the circulation following use. However, there is insufficient scientific data to develop policy to regulate and evaluate the claims and toxicity of new tobacco-related products. Prior studies suggest that tobacco cigarette smoking induces cardiovascular oxidative stress which may be linked to mitochondrial abnormalities. Mitochondria are key cellular organelles that are sensitive to environmental toxins and are essential for maintaining cardiovascular health. Upon exposure to environmental stressors, mitochondria become damaged characterized by elevated oxidant production which drives further damage and oxidative stress. Hence, measures of mitochondrial function and damage may serve as novel biomarkers of tobacco product induced injury. We measured mitochondrial biomarkers as a detector of early toxicity of tobacco product-induced injury in peripheral blood mononuclear cells (PBMCs) from non-smoking controls, tobacco cigarette smokers, and e-cigarette users. Following antimycin A stimulation, mitochondrial oxidant production was elevated in PBMCs from both tobacco cigarette smokers and e-cigarette users compared to cells from non-smokers (8.5±0.6, 9.8±0.9 vs 7.0±0.4, p=0.03). Additionally, we assessed the mitochondrial oxidant production in vascular tissue from people utilizing novel techniques developed within our laboratory that allow us to study freshly isolated endothelial cells. Early preliminary data in freshly isolated venous endothelial cells from tobacco cigarette smokers suggests that mitochondrial oxidant production is elevated compared to cells from non-smokers (1.47±0.38 vs 0.96±0.1). This further suggests that mitochondrial biomarkers may have enhanced early sensitivity to tobacco product toxicity prior to overt clinical disease. Whether mitochondrial biomarkers relate to measures of vascular function will be the subject of future studies. |
| تدمد: | 1524-4636 1079-5642 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_________::5ad6eb9fc95b07c0a7baeb5f8f413309 https://doi.org/10.1161/atvb.36.suppl_1.554 |
| رقم الأكسشن: | edsair.doi...........5ad6eb9fc95b07c0a7baeb5f8f413309 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15244636 10795642 |
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