Impacts of Oxidative Stress and Antioxidants on Semen Functions
By A. Bansal, G. S. Bilaspuri. Veterinary Medicine International, 2010
759 citations recorded by the source corpus.
Oxidative stress (OS) has been considered a major contributory factor to the infertility. Oxidative stress is the result of imbalance between the reactive oxygen species (ROS) and antioxidants in the body which can lead to sperm damage, deformity, and eventually male infertility. Although high concentrations of the ROS cause sperm pathology (ATP depletion) leading to insufficient axonemal phosphorylation, lipid peroxidation, and loss of motility and viability but, many evidences demonstrate that low and controlled concentrations of these ROS play an important role in sperm physiological processes such as capacitation, acrosome reaction, and signaling processes to ensure fertilization. The supplementation of a cryopreservation extender with antioxidant has been shown to provide a cryoprotective effect on mammalian sperm quality. This paper reviews the impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS. In addition, we also highlight the emerging concept of utilizing OS as a tool of contraception.
Subfields: Physiology, Public Health, Environmental and Occupational Health, Reproductive Medicine
View Paper: https://www.semanticscholar.org/paper/2f997713dbafc157c88c7c05856e60c6b6010178
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Physiology
In Public Health, Environmental and Occupational Health
In Reproductive Medicine
Citations in the corpus
- Diabetes mellitus and oxidative stress—A concise review (2015, background): “The free radicals induce damage to cells by passing the unpaired electron resulting in oxidation of cell components and molecules (Bansal and Bilaspuri, 2011).”
- Effect of Oxidative Stress on Male Reproduction (2014, background): “Subsequently, a rapid loss of intracellular adenosine tri-phosphate (ATP) from LPO causes axonemal damage, decreased sperm viability, and increased mid-piece sperm morphological defects, all of which contribute to decreased sperm motility [9,10].”