1997 Fiscal Year Final Research Report Summary
Biological defense mechanisms against environmental stress.
| Project/Area Number |
08044268
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Nagoya University |
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Principal Investigator |
INOUYE Minoru Research Institute of Environmental Medicine Nagoya University, Associate Professor, 環境医学研究所, 助教授 (20090425)
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| Co-Investigator(Kenkyū-buntansha) |
WALSH David A. Department of Veterinary Clinical Sciences University of Sydney, Senior Research, 獣医学部, 研究室主任
KANOU Yasuhiko Research Institute of Environmental Medicine Nagoya University, Research Associa, 環境医学研究所, 助手 (50252292)
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| Project Period (FY) |
1996 – 1997
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| Keywords | stress response / radioadaptive response / stress protein / heat-shoch protein / chaperone / mouse / rat / embryo |
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| Research Abstract |
All living organisms appear to have developed protective mechanisms collectively known as the heat shock response. Heat shock triggers the abrupt suspension in the normal protein synthesis and the concurrent induction of heat shock genes (hsp) and the synthesis of a set of multi-gene protein families known as the hrat shock proteins (HSP). Each hsp has at least two copies, one which appears to function in normal embryonic development (cognate) and another that is stress-induced (inducible) and can result in acquired tolerance, offering some protection against further damage. The inducible HSP are usually activated at critical inductive stages of organ development, suggesting they have a major role in cell differentiation. The HSPs appear to protect cells through their chaperone functions by binding to adhesive sites on newly synthesized or heat damaged and partially unfolded structural and functional proteins. This prevents the formation of functionless aggregates. Exposure to ionizing
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radiation also triggered the heat shock response. Pregnant mice were exposed to 0.05 Gy X-radiation on day 8 of pregnancy, and their embryos were examined for HSPs and other stress-related proteins. HSP27, HSP47 and HSP71, as well as c-Fos, Ras protein and PCNA (proliferating cell nuclear antigen) were induced 4 hours after exposure and dramatically increased 8 hours after exposure. Then, pregnant mice were exposed to 0.05 Gy X-radiation followed by 0.5 or 1.0 Gy 4 hours later. To compare with the effect of single doses, four other groups were exposed to 0.5,0.55,1.0 or 1.05 Gy. All dams were put to death on day 18 and fetuses were examined for malformations. The frequency of neural tube defects induced by the fractionated irradiation into 0.05 Gy and 1.0 Gy was significantly higher than those by single doses of 1.0 and 1.05 Gy. Among groups exposed to a dose split into 0.05 and 0.5 Gy, and single doses of 0.5 and 0.55 Gy, there was no significant difference in incidence of the malformation. The present findings suggested that although HSPs and stress-related proteins were induced in mouse embryos by low-dose X-irradiation, they were not adapted to X-irradiation. Less
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Research Products
(4 results)
