The effects of heat stress on intrauterine development, reproductive function, and ovarian gene expression of F1 female mice as well as gene expression of F2 embryos

Author:

Silva José R1,Souza-Fabjan Joanna M G12,Bento Tays F M1,Silva Robson Campos3,Moura Cristiane R F3,Bartlewski Pawel M4,Batista Ribrio I T P12

Affiliation:

1. Programa de Pós-Graduação em Ciência e Biotecnologia, Universidade Federal Fluminense , Niterói, RJ , Brazil

2. Faculdade de Veterinária, Universidade Federal Fluminense , Niterói, RJ , Brazil

3. Departamento de Ciências Básicas, Universidade Federal dos Vales do Jequitinhonha e Mucuri , Diamantina, MG , Brazil

4. Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph , Guelph, ON , Canada

Abstract

Abstract Exposure to heat stress (HS) in utero was postulated to trigger an adaptive molecular response that can be transmitted to the next generation. Hence, this study assessed the impact of HS exposure at different stages of the gestational period of mice on the female F1 population and their offspring. Heat stress exposure (41°C and 65% relative humidity—RH) occurred during the first half (FP), the second half (SP), or the entire pregnancy (TP). A control group (C) was maintained in normothermic conditions (25°C, 45% RH) throughout the experiment. Heat stress had a significant negative effect on intrauterine development, mainly when HS exposure occurred in the first half of pregnancy (FP and TP groups). Postnatal growth of FP and TP mice was hindered until 4 weeks of age. The total number of follicles per ovary did not vary (P > 0.05) between the control and HS-exposed groups. Mean numbers of primordial follicles were lower (P < 0.05) in the sexually mature FP than those in SP and TP F1 females. However, the mean number of viable embryos after superovulation was lower (P < 0.05) in TP compared with C group. The expression of genes associated with physiological and cellular response to HS, autophagy, and apoptosis was significantly affected in the ovarian tissue of F1 females and F2 in vivo-derived blastocysts in all HS-exposed groups. In conclusion, exposure to HS during pregnancy compromised somatic development and reproductive parameters as well as altered gene expression profile that was then transmitted to the next generation of mice.

Funder

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,General Medicine,Reproductive Medicine

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