The new biological estimation for air pollution, indoor pollution and working environment
空气污染、室内污染和工作环境的新生物学估计
基本信息
- 批准号:01570304
- 负责人:
- 金额:$ 1.41万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1989
- 资助国家:日本
- 起止时间:1989 至 1991
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
In this research project, we studied new biological indicators which were useful to assess the risk of chronic obstructive lung diseases and cancer promoting action by air pollution, indoor pollution and working environment. The biological effects of main pollutans, i. e. cigarette smoke, nitorgen dioxide (NO_2), benzo[a]pyrene (BaP), etc, were investigated in vivo and in vitro. Rats were exposed to side stream of cigarette smoke and NO_2 in an experimental chamber, 8 hours/day for 5 days. The activities of aryl hydrocarbon hydroxylase of lung, kidney and liver were increased by the exposure to cigarette smoke, but not by NO_2. Though total contents of cytochrome P-450 were not induced by either cigarette smoke or NO@_2, the dose-dependent inductions of cytochrome P-450b, c, d isozymes by the cigarette smoke wererecognized using Western Immunoblot analysis. The protein concentration, alkaline phosphatase and lactate dehydrogenase acticities in the bronchoalveolar lavage fluid (BALF) were also increased in the rats exposed to cigarette smoke or NO_2. The change of BALF was the most sensitive indicator that we examined in this study. The binding assay of epidermal growth factor (EGF) was also performed using HeLa cell and C3H/1OT1/2 cell. The binding of EGF to EGF receptor reached at a plateau 60-80 min after starting the incubation. This binding was varied by the density of cells on the plate. The plate with low density of the cells shows high binding capacity per cell number. We examined the effect of BaP on the EGF binding in the condition of the same density of the cells, however, it was not recognized that BaP inhibits EGF binding. In this experiment, some biological indicators did not show the result that we had expected. Further investigations were required to clarify the reason.
在该研究项目中,我们研究了新的生物学指标,这些指标对于评估慢性阻塞性肺部疾病的风险和通过空气污染,室内污染和工作环境促进癌症的风险。主要污染的生物学作用,即。 e。在体内和体外研究了香烟烟雾,二氧化碳(NO_2),苯并[A] pyrene(Bap)等。将大鼠暴露于香烟烟雾的侧面流,在实验室中,每天8小时,持续5天。暴露于香烟烟雾的情况下,增加了肺,肾脏和肝脏的芳基羟化酶的活性,而不是NO_2。尽管没有香烟烟雾或没有@_2诱导细胞色素P-450的总含量,但使用西方免疫印象分析对细胞色素p-450b,c,d同工酶的剂量依赖性诱导。在暴露于香烟烟雾或NO_2的大鼠中,还增加了支气管肺泡灌洗液(BALF)中蛋白质浓度,碱性磷酸酶和乳酸脱氢酶的作用。 BALF的变化是我们在这项研究中检查的最敏感的指标。还使用HeLa细胞和C3H/1OT1/2细胞进行表皮生长因子(EGF)的结合测定。 EGF与EGF受体的结合在开始孵育后60-80分钟时达到了高原。这种结合因板上细胞的密度而变化。细胞密度低的板显示每个细胞数的结合能力很高。我们检查了BAP在相同密度的条件下BAP对EGF结合的影响,但是,尚未认识到BAP抑制EGF的结合。在此实验中,一些生物学指标并未显示我们预期的结果。需要进一步调查以澄清原因。
项目成果
期刊论文数量(16)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Masahiro Yoshikawa, Keiichi Arashidani, Toshihiro Kawamoto, Yasushi Kodama: "Organ specifificity of aryl hydrocabonhydroxylase induction by cigarette smoke" Bulletin of Environmental Contamination and Toxicology. 44. 940-947 (1990)
Masahiro Yoshikawa、Keiichi Arashidani、Toshihiro Kawamoto、Yasushi Kodama:“香烟烟雾诱导芳基氢化碳羟化酶的器官特异性”环境污染与毒理学通报。
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- 影响因子:0
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Manabu Hirai, Toshihiro Kawamoto, Yasushi Kodama et al.: "The inhibition of EGF binding by air pollutants" Japanese Journal of Industrial Health. 3i. 715 (1990)
Manabu Hirai、Toshihiro Kawamoto、Yasushi Kodama 等人:“空气污染物对 EGF 结合的抑制”日本工业健康杂志。
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Masahiro Yoshikawa;Keiichi Arashidani;Toshihiro Kawamoto;Yasushi Kodama: "Organ specificity of aryl hydrocarbon hydroxylase induction by cigarette smoke" Bulletin of Environmental Contamination and Toxicology. 44. 940-947 (1990)
Masahiro Yoshikawa;Keiichi Arashidani;Toshihiro Kawamoto;Yasushi Kodama:“香烟烟雾诱导芳烃羟化酶的器官特异性”环境污染和毒理学通报。
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- 影响因子:0
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小山 倫浩,川本 俊弘,児玉 泰他: "二酸化窒素およびタバコ煙曝露による肺胞洗浄液の変化" 日本衛生学雑誌. 45. 363 (1990)
Michihiro Koyama、Toshihiro Kawamoto、Yasushi Kodama 等人:“由于暴露于二氧化氮和香烟烟雾导致的肺泡灌洗液的变化”日本卫生杂志 45. 363 (1990)。
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- 影响因子:0
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土屋 健三郎,児玉 泰他: "地球環境問題から室内汚染までーリスクアセスメントー" 産業医科大学雑誌. 12. 457-461 (1990)
Kenzaburo Tsuchiya、Yasushi Kodama 等:“从全球环境问题到室内污染 - 风险评估”职业医学大学杂志 12. 457-461 (1990)。
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KODAMA Yasushi其他文献
KODAMA Yasushi的其他文献
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