Δημοσίευση

Effects of primary testicular damage on sperm DNA oxidative status and embryonic and foetal development.

ΤίτλοςEffects of primary testicular damage on sperm DNA oxidative status and embryonic and foetal development.
Publication TypeJournal Article
Year of Publication2009
AuthorsDimitriadis, F., Giannakis D., Pardalidis N., Tsoukanelis K., Kanakas N., Saito M., Watanabe T., Miyagawa I., Tsounapi P., & Sofikitis N.
JournalAndrologia
Volume41
Issue5
Pagination282-96
Date Published2009 Oct
ISSN1439-0272
Λέξεις κλειδιά8-Hydroxy-2'-Deoxyguanosine, Animals, Body Temperature, Deoxyguanosine, DNA Damage, Embryonic Development, Epididymis, Fertilization in Vitro, Fetal Development, Male, Organ Size, Rats, Seminal Vesicles, Sperm Count, Sperm Motility, Spermatozoa, Testis, Testosterone, Veins
Abstract

We evaluated the development of embryos generated from the fertilisation of oocytes with spermatozoa isolated from animals with primary testicular damage (PTD). Embryos derived in vivo or in vitro from oocytes fertilised with spermatozoa produced by PTD rats that had undergone surgical treatment for the PTD (group A1), or PTD rats (group A2), or control rats (group B) were cultured and transferred to recipients. At the end of the experimental period, the fertilisation potential of each rat was assessed in vitro (IVF trials). Sperm 8-oxodG/dG ratio (a marker of DNA oxidative status) was significantly larger in group A2 than in groups A1 and B. Blastocysts of the group A2 transferred to recipients demonstrated a significantly larger loss before implantation than transferred blastocysts of groups A1 or B. In addition, the proportion of implanted blastocysts that could not complete the intrauterine development was significantly larger in group A2 than in groups A1 and B. This study reveals a post-fertilisation detrimental effect in animals with PTD on the capacity of oocytes (fertilised either in vitro or in vivo) to develop in vitro and implant after transferring them to recipients probably attributable to sperm DNA oxidative damage.

DOI10.1111/j.1439-0272.2009.00929.x
Alternate JournalAndrologia
PubMed ID19737276

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