Etiologies of sperm oxidative stress.
TLDR
Spermatozoa need small amounts of ROS to acquire the ability of nuclear maturation regulation and condensation to fertilize the oocyte, indicating that oxidative stress is one of the main cause of DNA damage in the germ cells, then there should be good reason for antioxidant therapy in these conditions.Abstract:
Sperm is particularly susceptible to reactive oxygen species (ROS) during critical phases of spermiogenesis. However, the level of seminal ROS is restricted by seminal antioxidants which have beneficial effects on sperm parameters and developmental potentials. Mitochondria and sperm plasma membrane are two major sites of ROS generation in sperm cells. Besides, leukocytes including polymer phonuclear (PMN) leukocytes and macrophages produce broad category of molecules including oxygen free radicals, non-radical species and reactive nitrogen species. Physiological role of ROS increase the intracellular cAMP which then activate protein kinase in male reproductive system. This indicates that spermatozoa need small amounts of ROS to acquire the ability of nuclear maturation regulation and condensation to fertilize the oocyte. There is a long list of intrinsic and extrinsic factors which can induce oxidative stress to interact with lipids, proteins and DNA molecules. As a result, we have lipid peroxidation, DNA fragmentation, axonemal damage, denaturation of the enzymes, over generation of superoxide in the mitochondria, lower antioxidant activity and finally abnormal spermatogenesis. If oxidative stress is considered as one of the main cause of DNA damage in the germ cells, then there should be good reason for antioxidant therapy in these conditions.read more
Citations
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Journal ArticleDOI
Oxidative stress and sperm function: A systematic review on evaluation and management
TL;DR: OS is an important cause of male factor infertility and its assessment provides essential information that can guide treatment strategies aimed at improving the male’s reproductive potential.
Journal ArticleDOI
Oxidative stress and male infertility: current knowledge of pathophysiology and role of antioxidant therapy in disease management
TL;DR: Physiological ROS production, roles of genetic and epigenetic factors on the OS and male infertility with various mechanisms such as lipid peroxidation, DNA damage, and disorder of male hormone profile, inflammation, and varicocele are described.
Journal ArticleDOI
Differential Production of Reactive Oxygen Species by Subsets of Human Spermatozoa
TL;DR: The results of this study indicate that there is significant cell-to-cell variation in ROS production in subsets of spermatozoa at different stages of maturation and that oxidative damage of mature spermatoza by ROS-producing immature spermatozosa during sperm migration from the seminiferous tubules to the epididymis may be an important cause of male infertility.
Journal ArticleDOI
Role of oxidative stress, infection and inflammation in male infertility.
Ashok Agarwal,Mohit Rana,Emily Qiu,Hashem AlBunni,Albert D. Bui,Albert D. Bui,Ralf Henkel,Ralf Henkel +7 more
TL;DR: This review is focusing on infection and inflammation‐mediated OS, the inflammatory markers underlying pathology, clinical significance in male infertility, and a brief description of the recommended treatment modalities.
Journal ArticleDOI
POHaD: why we should study future fathers.
TL;DR: A better understanding of pre-conceptional origins of disease through the paternal exposome will be informative to the field of transgenerational epigenetics and will ultimately help instruct and guide public health policies in the future.
References
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Journal Article
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TL;DR: It is concluded that sperm maturation is a dynamic, redox regulated process, any imbalance in which could lead to the production of spermatozoa that are compromised in terms of their potential for fertilization and the integrity of their DNA.
Journal ArticleDOI
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Journal ArticleDOI
Effect of di(n‐butyl) phthalate on testicular oxidative damage and antioxidant enzymes in hyperthyroid rats
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TL;DR: It is suggested that hyperthyroidism can cause a change in the expression level of PPAR‐r in testes, and may increase the levels of oxidative damage induced by the metabolic activation of DBP.