1995 Fiscal Year Final Research Report Summary
Defense mechanism for retinal light damage.
| Project/Area Number |
06671769
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | Nagasaki University |
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Principal Investigator |
OHIRA Akihiro Nagasaki University, School of Medicine, Assistent Professor, 医学部, 助教授 (00169054)
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| Co-Investigator(Kenkyū-buntansha) |
KITAOKA Takashi Nagasaki University, School of Medicine Hospital, Lecturer, 医学部・附属病院, 講師 (80234235)
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| Project Period (FY) |
1994 – 1995
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| Keywords | LIGHT DAMAGE / REACTIVE OXYGEN INTERMEDIATES / RETINA / DEFENSE MECHANISM / SUPEROXIDE DISMUTASE / ANTIOXIDANTS / ADULTT CELL LEUKEMIA DERIVED FACTOR / GLUTATHIONE PEROXIDASE |
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| Research Abstract |
Manganese superoxide dismutase (Mn-SOD) is a naturally occurring scavenger of reactive oxygen intermediates. We hypothesized that Mn-SOD expression may be enhanced as a defensive mechanism against oxidative challenges, the intense light exposure. We examined the possibility that Mn-SOD expression is increased following light-induced damage of the retina. Rats were exposed to cyclic light (80 lux) for 2 weeks, and an intense light challenge (1800 lux) for 24 hours, and then returned to cyclic light. Eyes from these and control rats were obtained to 14 days after the light challenge, and protein expression was examined immunohistochemically using rabbit antisera against rat Mn-SOD.There was no significant difference between a light-exposed and a control groups with atrophy of the outer nuclear layrs. Mn-SOD were found in the photoreceptor inner segments on days 1,7 and 14 after light challenge in experimental animals.
Total retinal RNA was prepared from rat at different times during the induction of light exposure. Northern blot analysis was performed using a GSH-PX cDNA probe. Protein expression of GSH-PO was examined by immunohistochemical method using anti-GSH-PO antibody. The mRNA levels for GSH-PO in the neural retina were observed to be increased (100-145% of controls) as early as 3 hours after light exposure. however, resulted in a decrease in the levels of mRNA coding with other time points. GSH-PX immunoreactivity was found in photoreceptor inner segments on day 1, but not detected other time points. GSH-PX immunoreactivity appeared in ganglion cells at all time points. Histologically, there was no significant difference between a light-exposed and a control groups with atrophy of the outer nuclear layrs. These results suggest that in tissue, Mn-SOD and GSH-PX may be responsible for the pathophysiology of light exposure injury.
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