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抗氧化饮食补充剂可减轻暴露于质子辐射的小鼠中与细胞程序性死亡相关的基因表达。

Antioxidant dietary supplementation in mice exposed to proton radiation attenuates expression of programmed cell death-associated genes.

机构信息

Department of Radiation Oncology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.

出版信息

Radiat Res. 2011 May;175(5):650-6. doi: 10.1667/RR2330.1. Epub 2011 Mar 28.

DOI:10.1667/RR2330.1
PMID:21443425
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3382992/
Abstract

Dietary antioxidants have radioprotective effects after ionizing radiation exposure that limit hematopoietic cell depletion. We sought to determine the mechanism of proton-induced hematopoietic cell death in animals receiving a moderate dose of whole-body proton radiation. In addition, animals were maintained on diets supplemented with or without dietary antioxidants. In the presence of the dietary antioxidants, total bone marrow mRNA and protein expression of apoptosis-related genes were decreased compared to the expression profiles in the irradiated mice not receiving the antioxidant formulation. These data confirm high-energy proton-induced gene expression of classical apoptosis markers including BAX, caspase-3 and PARP-1. Antioxidant supplementation resulted in decreased expression of these genes in addition to increased protein expression of the anti-apoptosis markers Bcl2 and Bcl-xL. In conclusion, oral supplementation with antioxidants appears to be an effective approach for radioprotection against hematopoietic cell death.

摘要

膳食抗氧化剂在电离辐射暴露后具有放射防护作用,可以限制造血细胞的耗竭。我们试图确定动物接受中等剂量全身质子辐射后,质子诱导造血细胞死亡的机制。此外,动物的饮食中补充或不补充膳食抗氧化剂。与未接受抗氧化剂配方的辐照小鼠相比,在存在膳食抗氧化剂的情况下,骨髓总 mRNA 和与凋亡相关的基因的蛋白表达降低。这些数据证实了高能质子诱导包括 BAX、caspase-3 和 PARP-1 在内的经典凋亡标志物的基因表达。抗氧化剂补充不仅增加了抗凋亡标志物 Bcl2 和 Bcl-xL 的蛋白表达,还导致这些基因的表达降低。总之,口服补充抗氧化剂似乎是一种针对造血细胞死亡的放射防护的有效方法。

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Coenzyme Q10 prevents human lens epithelial cells from light-induced apoptotic cell death by reducing oxidative stress and stabilizing BAX / Bcl-2 ratio.辅酶 Q10 通过降低氧化应激和稳定 BAX/BCL-2 比值来防止人晶状体上皮细胞发生光诱导的细胞凋亡。
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