期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 280, 期 3, 页码 H1293-H1300出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2001.280.3.H1293
关键词
cell death; mitochondrial membrane depolarization; stress proteins; reactive oxygen species; atherosclerosis
资金
- NHLBI NIH HHS [R01 HL-55627] Funding Source: Medline
Smoking is an important risk factor for atherosclerosis. We compared tobacco smoke filtrate with benzo[a] pyrene (a prominent xenobiotic component of tobacco smoke) for the capacity to induce stress proteins and cause cell death in human monocytes and vascular endothelial cells, two cell types that are involved in the formation of atherosclerotic lesions. Exposure to freshly prepared filtrates of tobacco smoke induced in both monocytes and endothelial cells expression of the inducible heat shock protein (HSP) 70 and heme oxygenase-1 (HO-1) and produced loss of mitochondrial membrane potential. Later, cell death by apoptosis or necrosis occurred depending on the concentration of tobacco smoke. These toxic effects could be prevented by the antioxidant N-acetylcysteine. In contrast, exposure of these cells to benzo[a] pyrene alone evoked neither stress proteins nor mitochondrial damage but did induce cell death by necrosis. Thus our results indicate that tobacco smoke rapidly induces complex oxidant-mediated stress responses in both vascular endothelial cells and circulating monocytes that are independent of the benzo[a] pyrene content of the smoke.
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