2007 Fiscal Year Final Research Report Summary
Study on the mechanisms of the reproductive damages caused by glycol ethers using transgenic mouse
| Project/Area Number |
17590529
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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 | National Institute of Occupational Safety and Health, Japan |
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Principal Investigator |
WANG Rui-Sheng National Institute of Occupational Safety and Health, Japan, Mechanism of Health Effects Research Group, Senior Researcher (10321895)
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| Co-Investigator(Kenkyū-buntansha) |
HONMA Takeshi National Institute of Occupational Safety and Health, Director of the Department of Research Planning and Coordination, 部長 (90332402)
SUDA Megumi National Institute of Occupational Safety and Health, Hazard Evaluation and Epidemiology Research Group, Senior Researcher (90415969)
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| Project Period (FY) |
2005 – 2007
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| Keywords | glycol ethers / ethylene glycol monoethyl ether / organic solvent / reproductive toxicity / Aldh2 / transgenic mouse |
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| Research Abstract |
Ethylene glycol monoethyl ether (EGEE) can cause damage to testes and sperm, and its metabolites are believed to play an important role in its toxicity. Aldehyde dehydrogenase 2 (ALDH2) is involved in the metabolism of this chemical. To investigate whether and how the enzyme affects the toxicity of EGEE, we conducted experiments comparing Aldh2 knockout mice with wild-type mice. Administration of EGEE at 100 and 600mg/kg/day for one week did not induce any significant change in the weight and body weight ratios of testes, prostate and epididymides in either Aldh2 knockout or wild-type mice. However, motion of sperm from the spermaduct, as analyzed with a Hamilton-Thorne Sperm analyzer, was slightly decreased in the low dose group, and significantly lower in the high dose group; and the percentage of progressive sperm was also reduced in the two EGEE groups. This effect of EGEE treatment was observed in the wild-type, but not in the Aldh2 knockout mice. Sperm motion from the cauda epididymides was not affected. On the other hand, the concentration of ethoxyacetic acid, a metabolite of EGEE, in 24h pooled urine of EGEE-treated Aldh2 knockout mice was not significantly lower than that of the wild-type mice on most days of urine sampling. These results suggest that inactivation of the ALDH2 enzyme due to gene mutation may be linked to differences in the susceptibility to EGEE-induced sperm toxicity.
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