Analysis of post-implantation mouse embryos after maternal heat stress during meiotic maturation

Baumgartner, Adi; Chrisman, C. L.

doi:10.1530/jrf.0.0840469

Cited by 19 publications

(4 citation statements)

References 11 publications

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“…Exposure of oocytes to the room temperature, as well as to a low temperature, for as short as 1 min caused depolymerization of the spindle as reported by Aman and Parks (1994). Similarly, Baumgartner and Chrisman (1987, 1988) found that maternal heat stress caused disruption of the meiosis I spindle in maturing mouse oocytes which in turn might result in interruption of meiosis II and polar body extrusion. The mitotic spindle was found disrupted in cultured cells after HS, which resulted in chromosomal dispersion and polyploidy and ultimately the death of the cell line (Streffer 1985).…”

Section: The Effect Of Hyperthermic Conditions On the Chromatin And Tsupporting

confidence: 52%

Influences of Follicular Size on Parthenogenetic Activation and in Vitro Heat Shock on the Cytoskeleton in Cattle Oocytes

Tseng¹,

Chen²,

Chou³

et al. 2004

Reprod Domestic Animals

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The availability of cow ovaries from the slaughterhouse has been very limited in Taiwan. To maximize the use of cow ovaries for research purposes, whole ovary dissection was performed and the developmental competence of the oocytes derived from different sizes of follicles was assessed by the rates of in vitro maturation (IVM) and parthenogenetic activation of the oocytes in Experiment 1 (Exp 1). Cumulus-oocyte complexes (COCs) derived from small (1-2 mm) and large (3-8 mm) follicles were subjected to standard IVM culture for 24 h. Mature oocytes were selected and then parthenogenetically activated using A23187 (5 microm, 5 min) or thimerosal (200 microm, 10 min) alone or combined with 6-dimethylaminopurine (2.5 mm and 3.5 h, respectively). Activation rates of the oocytes, neither from the large nor small follicles, were affected by different activation treatments (single or combined stimuli). Whereas maturation rates for the oocytes from large follicles were superior to those from small follicles in both the single (59% vs 45%) and combined treatments (76% vs 40%; p < 0.05). To understand how prolonged heat shock (HS) influences cytoskeletal configurations of mature bovine oocytes, in Experiment 2 (Exp 2), matured oocytes derived from large follicles were randomly allocated to different durations of HS treatments at 41.5 degrees C for 0 (C0h, control, n = 12), 1 (HS1h, n = 28), 2 (HS2h, n = 31), and 4 h (HS4h, n = 30). An additional control group was cultured for 4 h without HS (38.5 degrees C, 4 h, n = 35). Alterations in nuclear structures, microtubules (MTs), and microfilaments (MFs) of the oocytes were examined. Abnormalities in the chromosomes, spindle MTs and the percentages of oocytes with cytoplasmic MTs increased with time of HS treatment. The intensity of the MF distribution in the HS oocytes was also altered. Significant changes in the cytoskeleton after HS may be associated with the reduced development under hyperthermia and, perhaps, with the low pregnancy rates of the animals during hot seasons.

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Section: The Effect Of Hyperthermic Conditions On the Chromatin And Tsupporting

confidence: 52%

Influences of Follicular Size on Parthenogenetic Activation and in Vitro Heat Shock on the Cytoskeleton in Cattle Oocytes

Tseng¹,

Chen²,

Chou³

et al. 2004

Reprod Domestic Animals

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“…Many in vitro and in vivo studies have examined the effects of heat stress on maturation and developmental competence of oocytes. Exposing females to heat stress after fertilization caused decreases in the quality and quantity of embryos in cows after superovulation [69,70] and mice [71][72][73][74][75], and caused decreases in fetal growth in pigs [67], mice [74] and beef cows [76]. In vitro studies also revealed the effect of heat stress on oocyte maturation.…”

Section: Effects Of Heat Stress On Oocyte Growth Fertilization and Ementioning

confidence: 99%

Heat stress on reproductive function and fertility in mammals

Takahashi

2011

Reprod Medicine & Biology

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In most mammalian species including cattle, heat stress has deleterious effects on nutritional, physiological and reproductive functions. Exposure of animals to a hot environment causes an increase in body temperature in mammals, including domestic animals. High ambient temperature also causes a decrease in the length and intensity of estrus by disturbing ovarian function as well as decreasing pregnancy rate after artificial insemination. Therefore, it is important to understand the effects of heat stress on reproductive function in order to improve the production of domestic animals. Heat stress decreases appetite, weight gain, and milk yield in dairy cattle. It also adversely affects the reproductive performance of both sexes. In males, it reduces spermatogenic activity, while in females it adversely impacts oogenesis, oocyte maturation, fertilization development and implantation rate. Detection and evaluation of the deteriorating effects of heat stress on reproductive organs and cells can help to design measures to prevent them and improve reproductive functions. In this review, we discuss the impacts of heat stress on reproductive functions.

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“…The oocyte remains susceptible to heat stress through the preovulatory period. As shown in cows (Putney et al 1989) and mice (Baumgartner & Chrisman 1988;Aroyo et al 2007;Roth et al 2008), experimental heat stress coincident with ovulation and oocyte maturation may or may not have an effect on the capacity of oocytes to be fertilized but the resultant embryos are more likely to develop slowly or abnormally. Damage to the oocyte during the preovulatory period could reflect hormonal perturbations.…”

Section: The Female (A)mentioning

confidence: 99%

Effects of heat stress on mammalian reproduction

Hansen

2009

Phil. Trans. R. Soc. B

559

417

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Heat stress can have large effects on most aspects of reproductive function in mammals. These include disruptions in spermatogenesis and oocyte development, oocyte maturation, early embryonic development, foetal and placental growth and lactation. These deleterious effects of heat stress are the result of either the hyperthermia associated with heat stress or the physiological adjustments made by the heat-stressed animal to regulate body temperature. Many effects of elevated temperature on gametes and the early embryo involve increased production of reactive oxygen species. Genetic adaptation to heat stress is possible both with respect to regulation of body temperature and cellular resistance to elevated temperature.

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Analysis of post-implantation mouse embryos after maternal heat stress during meiotic maturation

Cited by 19 publications

References 11 publications

Influences of Follicular Size on Parthenogenetic Activation and in Vitro Heat Shock on the Cytoskeleton in Cattle Oocytes

Influences of Follicular Size on Parthenogenetic Activation and in Vitro Heat Shock on the Cytoskeleton in Cattle Oocytes

Heat stress on reproductive function and fertility in mammals

Effects of heat stress on mammalian reproduction

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