Factors Affecting the Survival of Ram Spermatozoa during Liquid Storage and Options for Improvement.

Semen preservation is an essential component of reproductive technologies, as it promotes genetic gain and long-distance semen transport and multiplies the number of ewes able to be inseminated per single ejaculate. However, the reduced temperature during cold storage at 5 or 15 °C inflicts sub-lethal damage to spermatozoa, compromising sperm quality and the success of artificial breeding. New and emerging research in various species has reported the advantages of storing spermatozoa at higher temperatures, such as 23 °C; however, this topic has not been thoroughly investigated for ram spermatozoa. Despite the success of storing spermatozoa at 23 °C, sperm quality can be compromised by the damaging effects of lipid peroxidation, more commonly when metabolism is left unaltered during 23 °C storage. Additionally, given the biosafety concern surrounding the international transport of egg-yolk-containing extenders, further investigation is critical to assess the preservation ability of synthetic extenders and whether pro-survival factors could be supplemented to maximise sperm survival during storage at 23 °C.

Chronic Acrylamide Exposure in Male Mice Results in Elevated DNA Damage in the Germline and Heritable Induction of CYP2E1 in the Testes.

Acute acrylamide exposure in male rodents results in reduced reproductive performance and dominant lethality. However, the reproductive effects of low dose chronic exposure, which better reflects the nature of human exposure, remain far less certain. Human dietary consumption of acrylamide has been estimated at an average of 1-4 µg/kg bw/day. In order to simulate this exposure, male mice were provided with acrylamide (1 µg/ml) via their drinking water continuously for six months, which was equivalent to a human dose of 10.5 µg/ kg bw/day. This exposure regime increased DNA damage in the spermatozoa, without affecting a concomitant reduction in overall fertility. The offspring of acrylamide treated mice did not have an increased incidence of skin papilloma formation following the two-stage tumor induction protocol. However, the male offspring of acrylamide treated fathers had significantly increased levels of DNA damage in their spermatozoa, despite having had no direct toxicant exposure. It was also found that the F0, and most crucially, F1 mice had increased levels of CYP2E1 protein in their germ cells. This is significant as CYP2E1 is the sole enzyme responsible for conversion of acrylamide to its harmful metabolite glycidamide. This altered expression may be due to epigenetic alterations. Additionally, the F0 and F1 mice had increased oxidative adducts in the DNA of their germ cells, which was hypothesized to arise as a byproduct of increased CYP2E1 activity. Therefore, chronic paternal acrylamide exposure in mice has consequences for their offspring, and raises concerns for the effects of acrylamide exposure in the human population and the accumulated effects with multiple generations of exposure.