1999 Fiscal Year Final Research Report Summary
Mechanism of cellular damages caused by cholorophenol compounds and their prevention
| Project/Area Number |
10670330
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hygiene
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
IGISU Hideki Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health Professor, 産業生態科学研究所, 教授 (60108686)
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| Project Period (FY) |
1998 – 1999
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| Keywords | pentachlorophenol / hexachlorophene / cytotoxicity / c-Fos / c-Jun / mitogen-activated protein kinase / L-carnitine / N-acetylcysteine |
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| Research Abstract |
Pentachloropheno1 (PCP) increased oxygen consumption and decreased repiratory control ratio in mitochondria from rat liver (J UOEH 20:315, 1998). These effects of PCP were suppressed by L-carnitine but those of pentylenetetrazol (PTZ) were not. Other findings of ours include ; N-acetylcysteine suppressed cytotoxicity of cadmium in LLC-PK1 cells (J Pharmacol Exp Therap 287:344, 1998) ; cadmium activated c-Jun N-terminal kinase (JNX) in the same cells (Biochem Biphys Res Commun 251:527, 1998) ; carnitine suppressed PTZ-induced c-fos expression in the mouse brain (J Occup Health, in press) ; toxicity of cadmium was greater in fibroblasts lacking c-fos (Biochem Pharmacol, in press). Nevertheless, cells lacking c-fos showed no definite difference from the controls in response to PCP and hexachlorophene (HCP). Neither PCP nor HCP caused clear activation of JNK, ERK and p-38, suggesting that signal transduction system to c-Fos and c-Jun may not be involved in inducing cellar toxicity of above chlorophenol compounds. However, it is likely that toxicity of PCP on mitochondria may be lessened by L-carnitine.
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