Abstract

Background: Nicotine is the foremost chemical constituent responsible for addiction in tobacco products, in the non-ionized condition can be easily absorbed via epithelial tissue of the lung, the mouth, the nose and across the skin
 Objective:The study examines the harmful effect of the nicotine which is an important component of cigarette in vitro.
 Type of the study: Cross-sectional study.
 Methods: Examines the harmful effect of the nicotine which is an important component of cigarette in vitro by using two types of lung cancer cell lines (H460 TP53+/+, H441 TP53-/-).
 Results: The results showed the total count of H460( TP53+/+) cancer lung cell lines was (5.2 ×106 cells /ml) , the number (4.9 ×106 cells /ml) of them were alive and (3.6×105 cells /ml) of them were dead, with percentage of viability (93.15%), while the total count of H441( TP53-/-) lung cancer cells was (5.1 ×106 cells /ml), the number (4.1 ×106 cells /ml) of them were alive, and the number (9.9×105 cells /ml) of them were dead with percentage of viability (80.55%). And it revealed that the nicotine inhibited viability of H460 lung cancer cell lines in all concentrations (1, 10, 500 and 1000 μ M) and the cells were completely abolished by treatment with (1000 μ M) when the viability reached to minimum percentage (3.43%), while nicotine induced proliferation in H441 lung cancer cell lines even in lowest concentration (1 μ M), whereas the viability reached to maximum percentage (41.04%) at concentration (1000 μ M). Also it noticed that the treatment with nicotine at concentrations (1,10, 500 and 1000 μ M ) for 24 and 48 hr induced the apoptosis but not necrosis in H460 lung cancer cell lines, especially at the highest concentrations (1000 μ M) for 48hr when the percentage of apoptosis reached to the maximum value (55.5%), however it was induced proliferation in H441 lung cancer cell lines with highest proliferation at concentration (1000 μ M), when the percentage apoptosis value reached to the minimum percentage (1.5%) when compared to un treated cells (control).
 Conclusions: the cells lack to TP53(H441 TP53-/-) will proliferate when exposed to nicotine and some of these cells will suffer from necrosis as a replacement of apoptosis.

Highlights

  • Nicotine is the foremost chemical constituent responsible for addiction in tobacco products, in the nonionized condition can be absorbed via epithelial tissue of the lung, the mouth, the nose and across the skin Objective:The study examines the harmful effect of the nicotine which is an important component of cigarette in vitro

  • Evaluation apoptotic and necrotic cells: Apoptotic and necrotic cells were measured by apoptosis assay using Annexin V- apoptosis kit (Abnova, Taiwan) and flow cytometery (Thermo fisher, USA) as mentioned by (10) after treated H460 and H441cells with nicotine at (1 μ M,10 μ M, 5 00 μ M and 1000 μ M ) concentrations, untreated cells were established as control

  • The result of H460 cancer lung cell lines showed that the total count was (5.2 ×106 cells /ml), a number (4.9 ×106 cells /ml) of them were alive and (3.6×105 cells /ml) of them were dead, with percentage of viability (93.15%), while the result of H441 lung cancer cells appeared a total count (5.1 ×106 cells /ml), the number (4.1 ×106 cells /ml) of them were alive, and the number (9.9×105 cells /ml) of them were dead with percentage of viability (80.55%)

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Summary

Introduction

Nicotine is the foremost chemical constituent responsible for addiction in tobacco products, in the nonionized condition can be absorbed via epithelial tissue of the lung, the mouth, the nose and across the skin Objective:The study examines the harmful effect of the nicotine which is an important component of cigarette in vitro. In the present study we have tried to indicate the effect of four concentrations of nicotine (1,10, 500 and 1000 μ M.) on lung cells viability, apoptosis and necrosis when the cells have wild type of p53 (H460 TP53+/+) and prove that TP53 plays an essential role in regulating apoptosis depending of nicotine stimulation .

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Conclusion
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