Study of the mechanisms of cigarette smoke gas phase cytotoxicity

被引：0

作者：

Piperi, C ^{[1
]}

Pouli, AE ^{[1
]}

Katerelos, NA ^{[1
]}

Hatzinikolaou, DG ^{[1
]}

Stavridou, A ^{[1
]}

Psallidopoulos, MC ^{[1
]}

机构：

[1] Inst Biomed Res & Biotechnol, Athens 10432, Greece

来源：

ANTICANCER RESEARCH | 2003年 / 23卷 / 3A期

关键词：

cigarette smoke; gas phase; cytotoxicity; apoptosis; flow cytometry; protein tyrosine nitration; MAPK phosphorylation;

D O I：

暂无

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Background: The cytotoxicity of cigarette smoke (CS) in humans is well-documented, but the mechanism behind CS toxicity and carcinogenicity remains unknown. We are interested in the toxicological effects of CS gas phase and the biological mechanisms of its action. Materials and Methods: Gas phase CS cytotoxicity was measured by Wst-1 and LDH assays, in cultured cells. The mechanism of cell death was investigated by flow cytometric analysis using Annexin V and P] staining. Gas phase CS-induced oxidative damage was evaluated by estimating cellular glutathione (GSH) levels. Protein modifications (nitration of tyrosines) induced by gas phase CS and activation of key signalling proteins (Mitogen-activated protein kinase, MAPK) were detected by immunoblotting. Results: The cytotoxicity of gas phase CS was found to be dose-dependent. The mechanism of cell death was found to be both apoptotic and necrotic depending on the concentrations used. Exposure to gas phase CS resulted in depletion of cellular GSH levels, increased nitrotyrosine immunoreactivity and phosphorylation of p44/42 MAPK proteins. Conclusion: These results suggest that the CS gas phase alone contributes significantly to the deleterious effects of CS in cellular systems.

引用

页码：2185 / 2190

页数：6

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[22] Acrolein-induced cytotoxicity in cultured human bronchial epithelial cells. Modulation by alpha-tocopherol and ascorbic acid [J].