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.
Highlights
Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia resulting from a defect in insulin action and/or production [1]
It is clear that hyperglycemia can damage the maternal genetic material, the results obtained for cord blood are not yet clear
The data seem to support the hypothesis that umbilical cord blood cells have more efficient mechanisms to protect the genome than the mother’s cells
Summary
Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia resulting from a defect in insulin action and/or production [1]. Hyperglycemia poses a risk to maternal, fetal, and perinatal health [2,3,4]. The current literature acknowledges this adverse environment as associated with increased long-term risk for the development of diabetes, obesity, cardiovascular, and malignant diseases (Figure 1) [9,10,11,12,13,14]. Previous findings by our group have shown that maternal hyperglycemia is adversely involved in fetal development by changing the placental production of proinflammatory cytokines, that is, TNF-α (tumor necrosis factor alpha) [15, 16]. The cellular redox status may be an important connection between inflammation and adverse perinatal outcomes in hyperglycemic pregnancies [17]. There is considerable evidence that hyperglycemia and inflammation results in the generation of reactive oxygen species (ROS), leading to increased oxidative stress. In the absence of an appropriate antioxidant response, the system becomes overwhelmed leading to production of reactive molecules that can cause cellular damage and are responsible for the BioMed Research International
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