Abstract
To evaluate the effects of oxidative stress in pregnant rats submitted to acute and chronic stress, relating to alterations in the uterus, placenta and fetus. Twenty-four female Wistar albino (Rattus norvegicus), were divided into four groups, for induction of oxidative stress the animals were submitted to cold and physical immobilization. Plasma fasting glucose and MDA were determined in all groups and the fetuses and placentas were measured. There were no statistical differences in the levels of malonic dialdehyde (MDA), however the averages of chronic stress group were higher compared to control groups, which could explain the observed adverse effects; there was no correlation between puppies' size, the weight of the placenta and MDA values. Chronic stress causes adverse effects, when compared to control groups; chronic stress group had fetuses, placentas and number of puppies, significantly lower compared to other groups. The rats exposed to chronic stress, also presented a higher frequency of fetal resorption.
Highlights
Reactive oxygen species (ROS) generating in oxidative stress promotes physiological and pathological changes in the female reproductive tract
ROS are detected in the ovaries, uterine tube and embryos which are involved in several physiological processes, such as oocyte maturation, steroidogenesis and corpus luteum[1]
High concentrations of estrogen contribute to a greater enzymatic antioxidant activity; oxidative stress has an impact on the production of steroid hormones produced by granulosa cells and that the oocyte within the follicle is naturally exposed to oxidative stress leading to lipid peroxidation and influencing the production glycoproteins produced by the granulosa cells[2]
Summary
Reactive oxygen species (ROS) generating in oxidative stress promotes physiological and pathological changes in the female reproductive tract. ROS are detected in the ovaries, uterine tube and embryos which are involved in several physiological processes, such as oocyte maturation, steroidogenesis and corpus luteum[1]. Oxidative stress causes embryos injury may due to peroxidation of membrane phospholipids and chemical modifications of different types of biomolecules. The consequences of these damages include mitochondrial activity, embryonic development and apoptosis. Oocytes and embryos are protected from oxidative stress by the presence of antioxidants from follicular and oviduct fluids[3]
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