An update on Telomeres Dynamics in Reproduction; Specifically in Females & Ageing: A Narrative Review

Abstract

The oocyte portrays a postmitotic cell having a longer life working as locus of reproductive ageing in women. Female germ cells replication occurs in fetal life which age right through reproductive period. Modes behind oocyte ageing are oxidative injury, mitochondrial impairment and disturbed protein inclusive of cohesion. BobEdwards invented the “generation line” at the time of oogonial proliferation in mouse oogenesis, where the initial oocytes to leave the oogonial proliferation while fetal life are the ones which undergo ovulation first at puberty and the last oocytes to leave the oogonial proliferation are the last to undergo ovulation in adult. Hence Kalmbach K group posited ‘’second hit’’ hypothesis of reproductive ageing for incorporating to plethora of characteristics of the oocyte ageing. The 1st hit being oocyte continuing in the older women pass via more cell cycles while fetal oogenesis. The 2nd hit was oocytes which continued had>accrual of environmental & endogenous oxidative injury right through woman’s life. Telomeres (T’s) might modulate both parts of oocyte ageing. T’s offer a mitotic clock, with T debilitation becoming a granted inimical sequelae of cell division due to end replication cell botheration. The guanine enrichment of the telomeres makes them more vulnerable to oxidative injury, in post mitotic cell also. Since telomerase,/ the reverse transcriptase is more adept in sustenance rather than T lengthening. Furthermore telomerase continues to be inactive in maximum oogenesis & early generation. Thus oocytes possess small T’s on the border of viability. To corroborate this posit mice having induced T debilitation and women having natural telomeropathies have diminished ovarian reserve (DOR), aberrant embryonic generation & infertility. Conversely sperms form all through life of male by ALT, have telomerase active progenitor, spermatogonia, longest body T’s. Numerous queries arise i) does normal T debilitation of human oocytes aid in meiotic nondisjunction (MN)? ii) does recombination dependent T lengthening make embryos more prone to MN / mosaicism? iii) can certain features of T’s work as oocyte quality markers.