title: Ovarian responses to undernutrition in pregnant ewes, USA.
abstract: In most mammals oogonia proliferate by mitosis and begin meiotic development during fetal life. Previous studies indicated that there is a delay in the progression to the first stage of meiotic arrest in germ cells of female fetuses of undernourished ewes. We report that underfeeding (50% NRC requirement beginning on Day 28 of pregnancy) provokes an increase in oxidative base lesions within DNA of mid-gestational (Day 78) fetal oogonia; this condition was associated with up-regulation of the tumor suppressor/cell-cycle arrest modulator p53, antiapoptotic factor Bcl-2, and base-excision repair polymerase beta. Fetal ovarian weights and germ cell concentrations were not altered by nutrient deprivation. Ovaries of ewes on control diets (100% NRC) contained more tertiary follicles than their restricted counterparts; however, peripheral venous estradiol-17beta was not different between groups. There was no effect of treatment on p53 accumulation in maternal oocytes. Luteal structure-function was not perturbed by undernutrition. No fetal losses were attributed to the dietary restriction. It is proposed that DNA of interphase fetal oogonia is vulnerable to oxidative insults perpetrated by a nutritional stress to the dam, and that multiple/integrated adaptive molecular response mechanisms of cell-cycle inhibition (providing the time required for base repairs) and survival hence sustain the genomic integrity and population stability of the germline.
authors.affiliation: Department of Animal Science, University of Wyoming, Laramie 82071. wmurdoch@uwyo.edu
authors.forename: William J
authors.initials: WJ
authors.lastname: Murdoch
authors.forename: Edward A
authors.initials: EA
authors.lastname: Van Kirk
authors.forename: Kimberly A
authors.initials: KA
authors.lastname: Vonnahme
authors.forename: Stephen P
authors.initials: SP
authors.lastname: Ford
mesh_terms: D000222:Adaptation, Physiological; D000821:Animal Feed; D000818:Animals; D017209:Apoptosis; D002453:Cell Cycle; D003338:Corpus Luteum / Q000098:blood supply / Q000503:physiopathology; D019951:DNA Polymerase beta / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D005333:Fetus / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D019254:Genes, bcl-2; D016158:Genes, p53; D005865:Gestational Age; D012739:Gonadal Steroid Hormones / Q000096:biosynthesis; D006147:Guanine / Q000031:analogs & derivatives* / Q000378:metabolism; D007399:Interphase; D044342:Malnutrition / Q000503:physiopathology*; D008540:Meiosis; D009866:Oogenesis; D009929:Organ Size; D006080:Ovarian Follicle / Q000473:pathology; D010053:Ovary / Q000196:embryology / Q000378:metabolism / Q000503:physiopathology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*; D011297:Prenatal Exposure Delayed Effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D012756:Sheep / Q000502:physiology*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
chemical_list: D012739:Gonadal Steroid Hormones; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; C024829:8-hydroxyguanine; D006147:Guanine; D019951:DNA Polymerase beta