Advancing maternal age predisposes to mitochondrial damage and loss during maturation of equine oocytes invitro

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Publication date

2014-04-15

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Rambags, B. P BISNI 0000000393519276
van Boxtel, D. C J
Tharasanit, T.
Lenstra, HansISNI 0000000394040750
Colenbrander, B.ISNI 0000000393560420
Stout, Tom A.E.ORCID 0000-0001-5321-8095ISNI 0000000387838262

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Abstract

In many mammalian species, reproductive success decreases with maternal age. One proposed contributor to this age-related decrease in fertility is a reduction in the quantity or functionality of mitochondria in oocytes. This study examined whether maternal age or (in vitro maturation). IVM affect the quantity of mitochondria in equine oocytes. Oocytes were collected from the ovaries of slaughtered mares categorized as young (<12years) or aged (≥12years) and either denuded and prepared for analysis immediately (not-IVM) or matured invitro for 30hours before preparation (IVM). The mean oocyte mitochondrial DNA copy number was estimated by quantitative polymerase chain reaction and found to be significantly lower in oocytes from aged mares and that had been subjected to IVM than in any other group. Transmission electron microscopy demonstrated that mitochondria in aged mare oocytes subjected to IVM experienced significantly more swelling and loss of cristae than in other groups. We conclude that maternal aging is associated with a heightened susceptibility to mitochondrial damage and loss in equine oocytes, which manifests during IVM. This predisposition to mitochondrial degeneration probably contributes to reduced fertility in aged mares.

Keywords

Horse, Invitro maturation, Maternal age, Mitochondrion, Oocyte, Animal Science and Zoology, Equine, Food Animals, Small Animals

Citation

Rambags, B P B, van Boxtel, D C J, Tharasanit, T, Lenstra, J A, Colenbrander, B & Stout, T A E 2014, 'Advancing maternal age predisposes to mitochondrial damage and loss during maturation of equine oocytes invitro', Theriogenology, vol. 81, no. 7, pp. 959-965. https://doi.org/10.1016/j.theriogenology.2014.01.020