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논문 기본 정보

자료유형
학술저널
저자정보
Ha Ryong Kim (Sungkyunkwan University) Bo Hee Son (Sungkyunkwan University) Soo Yeun Lee (Keimyung University) Kyu Hyuck Chung (Sungkyunkwan University) Seung Min Oh (Hoseo University)
저널정보
환경독성보건학회 Environmental Analysis Health and Toxicology Environmental Health and Toxicology 제27권
발행연도
2012.1
수록면
104 - 111 (8page)

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초록· 키워드

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Objectives: Marijuana is one of the most frequently abused drug in Korea and its adverse health effects are controversial. p53 is known to be crucial in regulating the DNA damage responses, and adverse effects can occur when it is regulated by marijuana smoke. We evaluated a role of p53 on genotoxic effect and apoptosis in lung cancer cells exposed to marijuana smoke condensates (MSCs).
Methods: The p53-related genotoxicity and apoptosis of MSCs were evaluated using in vitro bioassay, viz., comet assay, cytokinesis-block micronucleus assay and apoptosis assay. We used two cell lines with differential p53 expression (p53-wildtype (WT) H460 and p53-null H1299).
Results: MSCs significantly increased DNA breakages and chromosomal changes in p53-WT H460 and p53-null H1299 cells. The genotoxicity induced by MSCs in p53-null H1299 cells showed greater sensitivity than p53-WT H460 cells. Moreover, MSCs showed a significant increase in reactive oxygen species production and apoptosis. The apoptotic responses induced by MSCs were higher in p53-WT H460 cells than in p53-null H1299 cells. Significantly increased mRNA expression or apoptosis related genes, including p53, caspase-3, and Bax/Bcl-2 ratio were observed in the p53-WT H460 cells exposed to MSCs.
Conclusions: These results suggest that MSCs induce DNA/chromosomal damages and apoptosis in human lung cancer cells and p53 plays an important role in the cellular response to MSCs. The present study may have border implications for our understanding of pulmonary diseases.

목차

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
CONFLICT OF INTEREST
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2014-539-000804734