Consequential exposure to hypothermia in gestational diabetic rats induces oxidative changes in the brain of offspring

Abstract

Background: Prenatal stress is unique due to range of problems and can affect the embryo/fetus beginning with conception. Gestational diabetes mellitus is the concern for expectant-mothers wherein glucose intolerance with consistent hyperglycemia is a threatening factor during pregnancy. Objectives: In the event of multiple stressors posing their effects on intrauterine life and placenta being the target of increased sympathetic tone during gestation, there is a possibility of functional vulnerabilities that may contribute to the pathogenesis in post-natal life. Studying brain regional discrepancies in offspring might help to know the prenatal stress-induced variation in the antioxidant barrier and promoted oxidative stress. Materials and Methods: The changes occurring in oxidative stress indices in discrete brain regions of rat offspring born as a consequential exposure to gestational diabetes (streptozotocin induction) and cold stress (15 and 20°C) are assessed in this study. Results: The findings specify the involvement of cold-stress provoked induction of higher degree oxidative stress within brain compartments as evidenced by a decrease in antioxidant enzymes, namely, superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase, and GSH as well as increase in the concentration of malondialdehyde. Results highlight the synergistic actions of stressors due to the increased generation of free radicals. Cold stress at 15°C found to cause exacerbatory actions by depleting antioxidant enzymes in diabetic subjects than the exposures made at 20°C. Conclusion: The findings prove that cold stress is a crucial stimulus to a fetus during gestation and acts as a trigger of oxidative stress especially in diabetic subjects and can pose an adverse impact. These changes could partly explain the increased vulnerability of prenatally stressed subjects to functional disorders including deficits in memory and cognitive processes in later life.