title: DNA damage and its cellular response in mother and fetus exposed to hyperglycemic environment.
abstract: The increased production of reactive oxygen species (ROS) plays a key role in pathogenesis of diabetic complications. ROS are generated by exogenous and endogenous factors such as during hyperglycemia. When ROS production exceeds the detoxification and scavenging capacity of the cell, oxidative stress ensues. Oxidative stress induces DNA damage and when DNA damage exceeds the cellular capacity to repair it, the accumulation of errors can overwhelm the cell resulting in cell death or fixation of genome mutations that can be transmitted to future cell generations. These mutations can lead to and/or play a role in cancer development. This review aims at (i) understanding the types and consequences of DNA damage during hyperglycemic pregnancy; (ii) identifying the biological role of DNA repair during pregnancy, and (iii) proposing clinical interventions to maintain genome integrity. While hyperglycemia can damage the maternal genetic material, the impact of hyperglycemia on fetal cells is still unclear. DNA repair mechanisms may be important to prevent the deleterious effects of hyperglycemia both in mother and in fetus DNA and, as such, prevent the development of diseases in adulthood. Hence, in clinical practice, maternal glycemic control may represent an important point of intervention to prevent the deleterious effects of maternal hyperglycemia to DNA.
authors.affiliation: Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil.
authors.forename: Jusciele Brogin
authors.initials: JB
authors.lastname: Moreli
authors.affiliation: Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences (NIEHS), NC, USA.
authors.forename: Janine Hertzog
authors.initials: JH
authors.lastname: Santos
authors.affiliation: Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo (USP), SP, Brazil.
authors.forename: Clarissa Ribeiro
authors.initials: CR
authors.lastname: Rocha
authors.affiliation: Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil.
authors.forename: Débora Cristina
authors.identifier: 0000-0002-7003-9643
authors.initials: DC
authors.lastname: Damasceno
authors.affiliation: Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil.
authors.forename: Glilciane
authors.identifier: 0000-0001-8216-9931
authors.initials: G
authors.lastname: Morceli
authors.affiliation: Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil.
authors.forename: Marilza Vieira
authors.initials: MV
authors.lastname: Rudge
authors.affiliation: Department of Cell and Developmental Biology, Institute of Biomedical Sciences, USP, University of São Paulo, São Paulo, Brazil.
authors.forename: Estela
authors.initials: E
authors.lastname: Bevilacqua
authors.affiliation: Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil ; Department of Obstetrics and Gynecology, Botucatu Medical School, São Paulo State University (UNESP), Distrito de Rubião Jr. s/n, 18618-000 Botucatu, SP, Brazil.
authors.forename: Iracema Mattos Paranhos
authors.initials: IM
authors.lastname: Calderon
mesh_terms: D004249:DNA Damage; D004260:DNA Repair; D005260:Female; D005333:Fetus / Q000473:pathology*; D042822:Genomic Instability; D006801:Humans; D006943:Hyperglycemia / Q000473:pathology*; D018384:Oxidative Stress; D011247:Pregnancy