一項刊登在PNAS上的研究提出，男性進(jìn)行生育的年齡可能決定了他的孫輩的端粒——在染色體末端的被認(rèn)為用于防止衰老和疾病的分子帽——的長度,。與鞋帶的塑料末端類似，端粒保護(hù)染色體末端免于分解,。
在大多數(shù)細(xì)胞中,，端粒隨著衰老而縮短。但是在精子中,，端粒隨著衰老而加長,。相應(yīng)地，在較大年齡進(jìn)行生育的男性得到的孩子的端粒比在較小年齡進(jìn)行生育的男性的孩子的端粒更長,。Dan Eisenberg及其同事使用來自對菲律賓人的多代人研究的信息調(diào)查了男性進(jìn)行生育的年齡是否影響幾代人的端粒長度,。這組作者用1799位年輕的成年人及其母親的血樣測量了端粒長度，然后確定了這些人的父親和祖父的年齡,。
這組作者發(fā)現(xiàn),，個體的端粒長度不僅隨著他們出生時父親的年齡而增加，而且隨著他們的父親出生時祖父的年齡而進(jìn)一步增加,。父親推遲生育1年帶來的端粒長度的增加大致相當(dāng)于在中年成年人身上觀察到的每年的端?？s短量。這組作者說,，這些發(fā)現(xiàn)提示,，推遲父親的生育可以導(dǎo)致后代端粒長度的累積的,、多代人的增加，這可能促進(jìn)長壽,。（生物谷Bioon.com）
doi:10.1073/pnas.1202092109
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Delayed paternal age of reproduction in humans is associated with longer telomeres across two generations of descendants
Dan T. A. Eisenberga,b,c,1, M. Geoffrey Hayesa,d,e,2, and Christopher W. Kuzawaa,b,2
Telomeres are repeating DNA sequences at the ends of chromosomes that protect and buffer genes from nucleotide loss as cells divide. Telomere length (TL) shortens with age in most proliferating tissues, limiting cell division and thereby contributing to senescence. However, TL increases with age in sperm, and, correspondingly, offspring of older fathers inherit longer telomeres. Using data and samples from a longitudinal study from the Philippines, we first replicate the finding that paternal age at birth is associated with longer TL in offspring (n = 2,023, P = 1.84 × 10−6). We then show that this association of paternal age with offspring TL is cumulative across multiple generations: in this sample, grandchildren of older paternal grandfathers at the birth of fathers have longer telomeres (n = 234, P = 0.038), independent of, and additive to, the association of their father’s age at birth with TL. The lengthening of telomeres predicted by each year that the father’s or grandfather’s reproduction are delayed is equal to the yearly shortening of TL seen in middle-age to elderly women in this sample, pointing to potentially important impacts on health and the pace of senescent decline in tissues and systems that are cell-replication dependent. This finding suggests a mechanism by which humans could extend late-life function as average age at reproduction is delayed within a lineage.
