지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2011.9
- 수록면
- 161 - 166 (6page)
이용수
초록· 키워드
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Carbon black, a particulate form of pure elemental carbon, is an industrial chemical with the high potential of occupational exposure. Although the relationship between exposure to particulate matters (PM) and cardiovascular diseases is well established, the cardiovascular risk of carbon black has not been characterized clearly. In this study, the cytotoxicity of carbon black to vascular smooth muscle and endothelial cells were examined to investigate the potential vascular toxicity of carbon black. Carbon black with distinct particle size, N330 (primary size, 28~36 ㎚) and N990 (250~350 ㎚) were treated to A-10, rat aortic smooth muscle cells and human umbilical vein endothelial cell line, ECV304, and cell viability was assessed by lactate dehydrogenase (LDH) leakage assay. Treatment of carbon black N990 resulted in the significant reduction of viability in A-10 cells at 100 ㎍/㎖, the highest concentration tested, while N330 failed to cause cell death. Cytotoxicity to ECV304 cells was induced only by N330 at higher concentration, 200 ㎍/㎖, suggesting that ECV304 cells were relatively resistant to carbon black. Treatment of 100 ㎍/㎖ N990 led to the elevation of reactive oxygen species (ROS) detected by dichlorodihydrofluorescein (DCF) in A-10 cells. Pretreatment of antioxidants, N-acetylcysteine (NAC) and sulforaphane restored decreased viability of N990-treated A-10 cells, and N-acetylcysteine, but not sulforaphane, attenuated N990-induced ROS generation in A-10 cells. Taken together, present study shows that carbon black is cytotoxic to vascular cells, and the generation of reactive oxygen contributes to the development of cytotoxicity. ROS scavenging antioxidant could be a potential strategy to attenuate the toxicity induced by carbon black exposure.
목차
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLWDGMENTS
REFERENCES
참고문헌 (22)
참고문헌 신청
Ahmed, T. / 2010 / Assessment of phosphamidon-induced apoptosis inhuman peripheral blood mononuclear cells: protective effects ofN-acetylcysteine and curcumin / J. Biochem. Mol. Toxicol 24:286~292
Baan,R.A / 2007 / Carcinogenic hazards from inhaled carbonblack, titanium dioxide, and talc not containing asbestos orasbestiform fibers: recent evaluations by an IARC MonographsWorking Group / Inhal. Toxicol 19(1):213~228
Brook, R.D. / 2010 / Particulate matter airpollution and cardiovascular disease: An update to the scientificstatement from the American Heart Association / Circulation 121:2331~2378
Chang, C.C. / 2007 / Interaction effects of ultrafine carbon black with iron and nickelon heart rate variability in spontaneously hypertensive rats / Environ. Health Perspect 115:1012~1017
Dinkova-Kostova, A.T. / 2002 / Direct evidence that sulfhydryl groups of Keap1 are thesensors regulating induction of phase 2 enzymes that protectagainst carcinogens and oxidants / Proc. Natl. Acad. Sci 99:11908~11913
Baan,R.A / 2007 / Carcinogenic hazards from inhaled carbonblack, titanium dioxide, and talc not containing asbestos orasbestiform fibers: recent evaluations by an IARC MonographsWorking Group / Inhal. Toxicol 19(1):213~228
Brook, R.D. / 2010 / Particulate matter airpollution and cardiovascular disease: An update to the scientificstatement from the American Heart Association / Circulation 121:2331~2378
Chang, C.C. / 2007 / Interaction effects of ultrafine carbon black with iron and nickelon heart rate variability in spontaneously hypertensive rats / Environ. Health Perspect 115:1012~1017
Dinkova-Kostova, A.T. / 2002 / Direct evidence that sulfhydryl groups of Keap1 are thesensors regulating induction of phase 2 enzymes that protectagainst carcinogens and oxidants / Proc. Natl. Acad. Sci 99:11908~11913
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UCI(KEPA) : I410-ECN-0101-2013-513-000310522