无毛鼹鼠可能掌握着长寿的秘诀，它们的寿命可达到30年，超过了任何啮齿类动物的寿命
鼹鼠看上去并不是漂亮的动物，但是最新研究发现无毛鼹鼠可能掌握着长寿的秘密，它们的寿命可达到30年，比任何啮齿类动物的寿命都长。相关论文发表在美国《国家科学院院刊》（PNAS）上。
身体组织老化现象是由于体内产生氧化物所导致的，这些氧化物将逐渐磨损DNA分子和蛋白质，当氧化物磨损了分子之后，再去破坏身体细胞。虽然无毛鼹鼠与老鼠相比，它们体内的氧化物含量十分接近，但是无毛鼹鼠的寿命却是老鼠的3.5倍。
美国德克萨斯州保健科学中心的罗谢尔·巴芬斯滕(Rochelle Buffenstein)和同事们对无毛鼹鼠进行了深入研究，他们从无毛鼹鼠和老鼠身体上提取了肝脏组织，并施用化学药物，“拆散”肝脏组织中的蛋白质，从而揭示受损状况。他们发现无毛鼹鼠体内未受损的蛋白质数量是老鼠的两倍，这意味着无毛鼹鼠的蛋白质循环体系非常活跃。
研究小组猜测无毛鼹鼠能够制造出一些额外数量的分子，用于标注受损的蛋白质，从而加快了体内蛋白质循环体系，并将受损蛋白质对细胞的影响降至最低。研究人员希望进一步的研究能够鉴别和测试这些特殊分子，尽可能地用于人类抗衰老的药物研究中。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS February 17, 2009, doi: 10.1073/pnas.0809620106
Protein stability and resistance to oxidative stress are determinants of longevity in the longest-living rodent, the naked mole-rat
Viviana I. Péreza,b, Rochelle Buffensteina,b,c,d,1, Venkata Masamsettib, Shanique Leonardb, Adam B. Salmonb, James Meleb,c, Blazej Andziakd, Ting Yangd, Yael Edreyd, Bertrand Friguete, Walter Wardb,c, Arlan Richardsona,b,f and Asish Chaudhurib,f,g,1
aDepartments of aCellular and Structural Biology,
gBiochemistry, and
cPhysiology, and
bBarshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78229;
fGeriatric Research Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, TX 78284;
eLaboratoire de Biologie et Biochimie Cellulaire du Vieillissement, EA 3106, IFR 117, Université Paris 7, Denis Diderot, 2 Place Jussieu, 75251 Paris Cedex 05, France; and
dDepartment of Biology, Graduate School of the City University of New York, New York, NY 10016
Edited by Eviatar Nevo, University of Haifa, Haifa, Israel, and approved January 7, 2009 (received for review October 2, 2008)
Abstract
The widely accepted oxidative stress theory of aging postulates that aging results from accumulation of oxidative damage. Surprisingly, data from the longest-living rodent known, naked mole-rats [MRs; mass 35 g; maximum lifespan (MLSP) > 28.3 years], when compared with mice (MLSP 3.5 years) exhibit higher levels of lipid peroxidation, protein carbonylation, and DNA oxidative damage even at a young age. We hypothesize that age-related changes in protein structural stability, oxidation, and degradation are abrogated over the lifespan of the MR. We performed a comprehensive study of oxidation states of protein cysteines [both reversible (sulfenic, disulfide) and indirectly irreversible (sulfinic/sulfonic acids)] in liver from young and old C57BL/6 mice (6 and 28 months) and MRs (2 and >24 years). Furthermore, we compared interspecific differences in urea-induced protein unfolding and ubiquitination and proteasomal activity. Compared with data from young mice, young MRs have 1.6 times as much free protein thiol groups and similar amounts of reversible oxidative damage to cysteine. In addition, they show less urea-induced protein unfolding, less protein ubiquitination, and higher proteasome activity. Mice show a significant age-related increase in cysteine oxidation and higher levels of ubiquitination. In contrast, none of these parameters were significantly altered over 2 decades in MRs. Clearly MRs have markedly attenuated age-related accrual of oxidation damage to thiol groups and age-associated up-regulation of homeostatic proteolytic activity. These pivotal mechanistic interspecies differences may contribute to the divergent aging profiles and strongly implicate maintenance of protein stability and integrity in successful aging.
