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台灣視網膜色素病變協會
:::左側區塊

Light Induced Retinal Degeneration is Prevented by Zinc, a Component in the AREDS

發佈日期:2012/03/22 am10:26:59

內容:
Light Induced Retinal Degeneration is Prevented by Zinc, a Component in the AREDS
Formulation(†).

Organisciak D, Wong P, Rapp C, Darrow R, Ziesel A, Rangarajan R, Lang J.

Petticrew Research Laboratory, Department of Biochemistry and Molecular Biology,
Boonshoft Schoolof Medicine, Wright State University, Dayton, OH. Department of
Ophthalmology, Emory University, Atlanta, GA. Alcon Research Ltd. Fort Worth, TX.

Mineral supplements are often included in multivitamin preparations because of
their beneficial effects on metabolism. In this study we used an animal model of
light-induced retinal degeneration to test for photoreceptor cell protection by
the essential trace element zinc. Rats were treated with various doses of zinc
oxide and then exposed to intense visible light for as long as 8h. Zinc treatment
effectively prevented retinal light damage as determined by rhodopsin and retinal
DNA recovery, histology and electrophoretic analysis of DNA damage and oxidized
retinal proteins. Zinc oxide was particularly effective when given before light
exposure and at doses 2-4 fold higher than recommended by the age-related eye
disease study (AREDS) group. Treated rats exhibited higher serum and retinal
pigment epithelial zinc levels and an altered retinal gene expression profile.
Using an Ingenuity database, 512 genes with known functional annotations were
found to be responsive to zinc supplementation, with 45% of these falling into a
network related to cellular growth, proliferation, cell cycle and cell death.
While these data suggest an integrated and extensive regulatory response, zinc
induced changes in gene expression also appear to enhance antioxidative capacity
in retina and reduce oxidative damage arising from intense light exposure. © 2012
Wiley Periodicals, Inc. Photochemistry and Photobiology © 2012 The American
Society of Photobiology.
© 2012 Wiley Periodicals, Inc. Photochemistry and Photobiology © 2012 The
American Society of Photobiology.

PMID: 22385127 [PubMed - as supplied by publisher]

中文簡述:
礦物質相關的補充劑,對於人體代謝是有益的作用,包括在多種維生素裡面。在這項研究中,我們測試光致視網膜病變動物模型感光細胞保護測試所必需的微量元素:氧化鋅,然後暴露強烈的可見光只要8H。發現氧化鋅的治療有效地防止視網膜光損傷的視紫紅質和以及幫助視網膜的DNA恢復,組織學和DNA損傷和氧化的視網膜蛋白質電泳分析確定。氧化鋅是前燈照射劑量的2-4倍,高於年齡相關性眼病研究(AREDS)組建議時特別有效。測試用的大鼠表現出較高的血清和視網膜色素上皮鋅含量和改變視網膜基因表達譜。使用獨創性數據庫,512個基因與已知的功能註釋被發現的有45%,這些細胞的生長、繁殖與死亡會造成鋅的補充。這些數據表明,集成和廣泛的監管反應,氧化鋅誘導基因表達的變化也出現在視網膜上,以提高抗氧化能力和降低強烈的光線照射所產生的氧化損傷。