Environmental high temperature affects pre-implantation embryo development by impairing the DNA repair ability.

Environmental high temperature poses a significant threat to human health, however, limited information is available for understanding the relationship between the hot weather and infertility. This study aims to assess the adverse effect of the hot weather to early embryonic cells. Our results indicated that environmental high temperature exposure could cause the decline of early embryo quality and implantation ability. In detail, it led to early embryonic development retardation, embryo degeneration rate increased, the rate of blastocyst and hatching decreased, and reduced the number of implants. And the finding also the impairment of environmental high temperature on early embryonic cells may be due to oxidative damage of DNA caused by ROS, while BER repair ability is decreased, failing to repair oxidative damage of DNA in time, resulting in a large number of early embryonic apoptosis. The work underscored that pregnant women should stay away from high-temperature environments.

Saikosaponin-D attenuates heat stress-induced oxidative damage in LLC-PK1 cells by increasing the expression of anti-oxidant enzymes and HSP72.

Heat stress stimulates the production of reactive oxygen species (ROS), which cause oxidative damage in the kidney. This study clarifies the mechanism by which saikosaponin-d (SSd), which is extracted from the roots of Bupleurum falcatum L, protects heat-stressed pig kidney proximal tubular (LLC-PK1) cells against oxidative damage. SSd alone is not cytotoxic at concentrations of 1 or 3 µg/mL as demonstrated by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. To assess the effects of SSd on heat stress-induced cellular damage, LLC-PK1 cells were pretreated with various concentrations of SSd, heat stressed at 42°C for 1 h, and then returned to 37°C for 9 h. DNA ladder and MTT assays demonstrated that SSd helped to prevent heat stress-induced cellular damage when compared to untreated cells. Additionally, pretreatment with SSd increased the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) but decreased the concentration of malondialdehyde (MDA) in a dose-dependent manner when compared to controls. Furthermore, real-time PCR and Western blot analysis demonstrated that SSd significantly increased the expression of copper and zinc superoxide dismutase (SOD-1), CAT, GPx-1 and heat shock protein 72 (HSP72) at both the mRNA and protein levels. In conclusion, these results are the first to demonstrate that SSd ameliorates heat stress-induced oxidative damage by modulating the activity of anti-oxidant enzymes and HSP72 in LLC-PK1 cells.