抗氧化剂谷胱甘肽水平低导致端粒延长:与长寿的性别特异性联系?

IF 2.2 4区 生物学 Q2 BIOLOGY
Integrative Organismal Biology Pub Date : 2023-09-23 eCollection Date: 2023-01-01 DOI:10.1093/iob/obad034
A A Romero-Haro, J Figuerola, C Alonso-Alvarez
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引用次数: 0

摘要

端粒是染色体末端的重复DNA序列,可以保护它们免受降解。它们一直是紧张研究的焦点,因为短端粒可以预测脊椎动物的衰老加速和寿命缩短。氧化应激被认为是端粒缩短和寿命缩短的生理驱动因素。在对抗氧化应激的分子中,谷胱甘肽参与了许多抗氧化途径。文献支持氧化应激可能会引发一种补偿性的“激素”反应,增加谷胱甘肽水平和端粒长度。在这里,我们测试了圈养鸟类(斑胸雀;喉带绦虫)的总谷胱甘肽浓度和端粒长度之间的联系。在鸟类生长过程中,使用谷胱甘肽合成的特异性抑制剂(丁硫氨酸磺酰亚胺;BSO),通过实验降低了总谷胱甘肽水平。我们监测了这些鸟在出生第一个月在户外鸟舍的繁殖表现,以及它们近9年的寿命。在对照个体中,发育过程中红细胞谷胱甘肽水平正预测成年后红细胞端粒长度。然而,BSO治疗的女性,而不是男性,在成年后表现出比对照女性更长的端粒。这一违反直觉的发现表明,雌性会产生补偿性反应。这种补偿与在同一人群中的先例研究结果一致,BSO治疗增加了女性的生长和成年体重,但没有增加男性。BSO不影响任何性别的寿命或生殖产量。然而,早期谷胱甘肽水平和成年端粒长度仅在对照女性中相互预测寿命。那些在筑巢时谷胱甘肽水平“自然”较低(未经控制),但在成年后能够产生更长端粒的雌性似乎活得更长。研究结果表明,由早期谷胱甘肽水平低引发的激素反应能力可以通过端粒长度改善健康状况。总的来说,研究结果可能表明谷胱甘肽和端粒值之间存在性别特异性联系。端粒酶活性和性类固醇(雌激素)是解释氧化应激对成人端粒长度的早期影响的性别偏见机制的好候选者。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Low Antioxidant Glutathione Levels Lead to Longer Telomeres: A Sex-Specific Link to Longevity?

Low Antioxidant Glutathione Levels Lead to Longer Telomeres: A Sex-Specific Link to Longevity?

Low Antioxidant Glutathione Levels Lead to Longer Telomeres: A Sex-Specific Link to Longevity?

Low Antioxidant Glutathione Levels Lead to Longer Telomeres: A Sex-Specific Link to Longevity?

Telomeres are repetitive DNA sequences at the end of chromosomes that protect them from degradation. They have been the focus of intense research because short telomeres would predict accelerated ageing and reduced longevity in vertebrates. Oxidative stress is considered a physiological driver of the telomere shortening and, consequently, short lifespan. Among molecules fighting against oxidative stress, glutathione is involved in many antioxidant pathways. Literature supports that oxidative stress may trigger a compensatory "hormetic" response increasing glutathione levels and telomere length. Here, we tested the link between total glutathione concentration and telomere length in captive birds (zebra finches; Taeniopygia guttata). Total glutathione levels were experimentally decreased during birds' growth using a specific inhibitor of glutathione synthesis (buthionine sulfoximine; BSO). We monitored the birds' reproductive performance in an outdoor aviary during the first month of life, and their longevity for almost 9 years. Among control individuals, erythrocyte glutathione levels during development positively predicted erythrocyte telomere length in adulthood. However, BSO-treated females, but not males, showed longer telomeres than control females in adulthood. This counterintuitive finding suggests that females mounted a compensatory response. Such compensation agrees with precedent findings in the same population where the BSO treatment increased growth and adult body mass in females but not males. BSO did not influence longevity or reproductive output in any sex. However, early glutathione levels and adult telomere length interactively predicted longevity only among control females. Those females with "naturally" low (non-manipulated) glutathione levels at the nestling age but capable of producing longer telomeres in adulthood seem to live longer. The results suggest that the capability to mount a hormetic response triggered by low early glutathione levels can improve fitness via telomere length. Overall, the results may indicate a sex-specific link between glutathione and telomere values. Telomerase activity and sexual steroids (estrogens) are good candidates to explain the sex-biased mechanism underlying the early-life impact of oxidative stress on adult telomere length.

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CiteScore
3.70
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6.70%
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