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Role of oxidative stress in female reproduction

DOI: 10.1186/1477-7827-3-28

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Abstract:

Free radical species are unstable and highly reactive. They become stable by acquiring electrons from nucleic acids, lipids, proteins, carbohydrates or any nearby molecule causing a cascade of chain reactions resulting in cellular damage and disease [1-4], figure 1) . There are two major types of free radical species: reactive oxygen species (ROS) and reactive nitrogen species (NOS).The three major types of ROS are: superoxide (O2?-), hydrogen peroxide (H2O2), hydroxyl (OH?). The superoxide radical is formed when electrons leak from the electron transport chain [5]. The dismutation of superoxide results in the formation of hydrogen peroxide. The hydroxyl ion is highly reactive and can modify purines and pyrimidines and cause strand breaks resulting in DNA damage [6]. Some oxidase enzymes can directly generate the hydrogen peroxide radical.ROS have been implicated in more than 100 diseases [7-10]. They have a physiological and pathological role in the female reproductive tract. Numerous animal and human studies have demonstrated the presence of ROS in the female reproductive tract: ovaries, [11-15], fallopian tubes [16] and embryos [17]. ROS is involved in the modulation of an entire spectrum of physiological reproductive functions such as oocyte maturation, ovarian steroidogenesis, corpus luteal function and luteolysis [11,12,18]. ROS-related female fertility disorders may have common etiopathogenic mechanisms. ROS may also originate from embryo metabolism and from its surroundings.Nitric oxide (NO) is synthesized during the enzymatic conversion of L-arginine to L-citrulline by nitric oxide synthase (NOS) [19-21]. With an unpaired electron, NO, which is a highly reactive free radical, damages proteins, carbohydrates, nucleotides and lipids and, together with other inflammatory mediators, results in cell and tissue damage, low-grade, sterile inflammation and adhesions [20]. NO potently relaxes arterial and venous smooth muscles and, less strongly, inhibits platelet a

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