Effect of heat-stress on bovine embryo development in vitro

Ryan, David P.; Blakewood, E.G.; Lynn, John W.; Munyakazi, L.; Godke, R.A.

doi:10.2527/1992.70113490x

Cited by 48 publications

(28 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Until recently, it has been believed that maternal high body temperature per se is the main cause of heat stress-induced early embryonic death [8,9], and that this phenomenon has been ascribed, mainly based on in vitro study, to the inability of early embryos (up to the 8-cell stage) to produce molecules, such as heat shock protein 70 and GSH, that protect the cells against heat shock [30]. However, it is unclear why exposure of embryos to moderately high temperatures similar to those experienced by heat-stressed animals does not compromise the normal development [5,10].…”

Section: Discussionmentioning

confidence: 99%

“…Although this is a common phenomenon in many mammalian species, e.g., in cattle [1], pigs [2], sheep [3], rats [4] and mice [5], the syndrome is more pronounced in high performance lactating cows because of their elevated metabolic heat production [6,7]. Hyperthermia-induced early embryonic death is generally ascribed to the high susceptibility of early embryos to elevated maternal body temperature [8,9]. However, recent studies have indicated that the disruption of embryonic development in heatstressed animals is connected with heat-stressassociated changes in the maternal body.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Effects of Heat Stress on the Redox Status in the Oviduct and Early Embryonic Development in Mice

et al. 2005

View full text Add to dashboard Cite

Abstract. This study examined the association between redox status in the oviduct and early embryonic death in heat-stressed mice. In Experiment 1, non-pregnant mice were heat-stressed at 35 C with 60% relative humidity for 12, 24, or 36 h, and the maternal redox status was verified by measuring the levels of reactive oxygen species (ROS) and free radical scavenging activity (FRSA) in the oviduct, and thiobarbituric acid reactive substances (TBARS) and glutathione peroxidase (GSHPx) activity in the liver. In Experiment 2, zygotes were collected from mice heat-stressed for 12 h on the day of pregnancy, and their developmental abilities were assessed in vitro, along with the intensity of DNA damage at the 2-cell stage. The TBARS value and GSH-Px activity in the liver, and ROS level in the oviduct were significantly higher in heat-stressed mice, and this increase appeared to depend on the duration of the heat stress. Maternal heat stress significantly reduced the percentage of zygotes that developed to the morula and blastocyst and the total cell number in the blastocyst. In addition, DNA damage at the 2-cell stage was significantly higher in maternally heat-stressed embryos. These results suggest that heat stress induces systemic changes in redox status in the maternal body, and the resultant increase in oxidative stress in the oviduct is possibly involved in heat stress-induced early embryonic death . Key words: Early embryo death, Heat stress, Oxidative stress, Reactive oxygen species (J. Reprod. Dev. 51: [281][282][283][284][285][286][287] 2005) aternal hyperthermia during early pregnancy in heat-stressed animals often leads to preimplantation embryonic death. Although this is a common phenomenon in many mammalian species, e.g., in cattle [1], pigs [2], sheep [3], rats [4] and mice [5], the syndrome is more pronounced in high performance lactating cows because of their elevated metabolic heat production [6,7]. Hyperthermia-induced early embryonic death is generally ascribed to the high susceptibility of early embryos to elevated maternal body temperature [8,9]. However, recent studies have indicated that the disruption of embryonic development in heatstressed animals is connected with heat-stressassociated changes in the maternal body. Rivera and Hansen [10] have shown that in vitro exposure of bovine zygotes to a fluctuating high temperature (39.5-40.5 C), that carefully mimicked the rectal temperature of heat-stressed hyperthermic cows f or 2 4 h , d i d n ot c om p rom i s e s u bs e q ue nt development to the blastocyst stage. Similarly, we observed that the deleterious effects of maternal heat stress on mouse zygotes were not related to high body temperature alone, but were mediated

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Effects of Heat Stress on the Redox Status in the Oviduct and Early Embryonic Development in Mice

et al. 2005

View full text Add to dashboard Cite

show abstract

“…In fact, recent reports have demonstrated that culturing zygotes at high temperatures, within the physiological range, in hyperthermic cows (40.5 8C) for 12 h did not alter subsequent development to the blastocyst stage (Ryan et al 1992. Our previous study has also indicated that in vitro exposure of zygotes to high temperature, mimicking the average rectal temperature of hyperthermic mice (39.5 8C), does not alter the blastocyst development rate, whereas maternal heat exposure for 12 h soon after mating drastically arrests subsequent embryonic development and is accompanied by increased H 2 O 2 levels, decreased GSH levels (Ozawa et al 2002) and damaged genomic DNA in the embryos, as assessed by elongation of the ladder tail in a comet assay, which is typical of ROS-mediated injury (Matsuzuka et al 2005a).…”

Section: Discussionmentioning

confidence: 98%

DL- -Tocopherol acetate mitigates maternal hyperthermia-induced pre-implantation embryonic death accompanied by a reduction of physiological oxidative stress in mice

Sakamoto

Ozawa²,

Yokotani-Tomita³

et al. 2008

Reproduction

View full text Add to dashboard Cite

Maternal hyperthermia induces pre-implantation embryo death, which is accompanied by enhanced physiological oxidative stress. We evaluated whether the administration of DL-a-tocopherol acetate (TA) to hyperthermic mothers mitigated pre-implantation embryo death. Mice were exposed to heat stress (35 8C, 60% relative humidity) for 12 h or not heated (25 8C) on the day of mating. Twelve hours before the beginning of temperature treatment, TA was injected intraperitoneally at a dose of 1 g/kg body weight. After the treatment, zygotes were recovered and the developmental abilities and intracellular glutathione (GSH) levels were evaluated. Another set of mice, with or without TA treatment, was exposed to heat stress for 12, 24 and 36 h, and the urinary levels of the oxidative stress marker 8-hydroxy-2 0 -deoxyguanosine (8-OHdG) were measured. Heat stress significantly decreased the blastocyst development rate and the GSH content in zygotes, as compared with the non-heat-stressed embryos, while TA administration significantly mitigated the deleterious effects of heat stress with regard to both parameters. Moreover, although the urinary levels of 8-OHdG gradually increased according to the duration of heat exposure, with or without TA administration, the levels were lower in the TA-administered group than in the placeboinjected mice. These results suggest that heat stress enhances physiological oxidative stress, and that TA administration alleviates the hyperthermia-induced death of pre-implantation embryos by reducing physiological oxidative stress.

show abstract

“…In summer, 80% of estrus may be undetectable [15]. Also indicated, Ryan et al, [22] that when the rectal temperature of the animals increased from 38.5°C to 40°C in 72 hours after insemination service, pregnancy rates can decrease up to 50%.…”

Section: On Fertilitymentioning

confidence: 98%