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Overexpression of human thioredoxin in transgenic mice controls oxidative stress and life span.

机译:人硫氧还蛋白在转基因小鼠中的过表达控制氧化应激和寿命。

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摘要

Transgenic (Tg) mice overexpressing human thioredoxin (TRX), a small redox-active protein, were produced to investigate the role of the protein in a variety of stresses. Bone marrow cells from TRX-Tg mice were more resistant to ultraviolet C-induced cytocide compared with those from wild type (WT) C57BL/6 mice. TRX-Tg mice exhibited extended median and maximum life spans compared with WT mice. Telomerase activity in spleen tissues in TRX-Tg mice was higher than that in WT mice. These results suggest that overexpression of TRX results in resistance against oxidative stress and a possible extension of life span without apparent abnormality in mammals.
机译:产生了过表达人硫氧还蛋白(TRX)(一种小的氧化还原活性蛋白)的转基因(Tg)小鼠,以研究该蛋白在多种应激中的作用。与来自野生型(WT)C57BL / 6小鼠的骨髓细胞相比,来自TRX-Tg小鼠的骨髓细胞对紫外线C诱导的杀细胞剂更具抵抗力。与WT小鼠相比,TRX-Tg小鼠的中位寿命和最大寿命延长。 TRX-Tg小鼠的脾脏组织端粒酶活性高于WT小鼠。这些结果表明TRX的过表达导致对氧化应激的抗性和寿命的可能延长,而在哺乳动物中没有明显的异常。

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