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Reactive oxygen species in spermatozoa: methods for monitoring and significance for the origins of genetic disease and infertility
Open accessAbstract
Human spermatozoa generate low levels of reactive oxygen species in order to stimulate key events, such as tyrosine phosphorylation, associated with sperm capacitation. However, if the generation of these potentially pernicious oxygen metabolites becomes elevated for any reason, spermatozoa possess a limited capacity to protect themselves from oxidative stress. As a consequence, exposure of human spermatozoa to intrinsically- or extrinsically- generated reactive oxygen intermediates can result in a state of oxidative stress characterized by peroxidative damage to the sperm plasma membrane and DNA damage to the mitochondrial and nuclear genomes. Oxidative stress in the male germ line is associated with poor fertilization rates, impaired embryonic development, high levels of abortion and increased morbidity in the offspring, including childhood cancer. In this review, we consider the possible origins of oxidative damage to human spermatozoa and reflect on the important contribution such stress might make to the origins of genetic disease in our species.
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ROS have been associated with impaired metabolism, morphology, motility and male infertility.
“ROS have been associated with impaired metabolism, morphology, motility and male infertility (Baker and Aitken, 2005;Hsieh et al., 2006), retention of excess residual amorphous cytoplasm that human spermatozoa are not capable of remodeling or discharging.”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Baker and Aitken, 2005
In “ROS generation in spermatozoa” (page unavailable), the paper links oxidative stress to male infertility and reduced sperm motility, and says excess ROS disrupts sperm function. It does not establish that ROS impairs metabolism or morphology; its discussion of abnormal residual cytoplasm instead describes a possible source of ROS. (LLM, conf=0.86)
Experimental — accuracy not yet measuredHuman spermatozoa produce ROS which enhance tyrosine phosphorylation through suppression of tyrosine phosphorylase activity by H2O2 and stimulation of cAMP production, regulating signal transduction pathways that control sperm capacitation.
“Human spermatozoa produce ROS which enhance tyrosine phosphorylation through the suppression of tyrosine phosphorylase activity by H 2 O 2 and stimulation of cAMP production, that play a role in regulating signal transduction pathways that control sperm capacitation.”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Baker and Aitken, 2005
The ‘ROS generation in spermatozoa’ passage says human spermatozoa generate ROS that promote tyrosine phosphorylation during capacitation through H2O2 suppression of tyrosine phosphatase activity and stimulation of cAMP generation. The Conclusion links this redox activity to pathways controlling capacitation. The claim says ‘tyrosine phosphorylase’ rather than the phosphatase named in the source, so its stated mechanism is not fully supported. (LLM, conf=0.88)
Experimental — accuracy not yet measuredA low, steady state of ROS production appears important for gamete cell stability and capacitation.
“A low, steady state of ROS production appears to be important for gamete cell stability (Hsieh et al., 2006) and capacitation (Baker and Aitken, 2005).”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Baker and Aitken, 2005
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A Ca2+-activated NADPH Oxidase in Testis, Spleen, and Lymph Nodes
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Mechanism of Ca2+ Activation of the NADPH Oxidase 5 (NOX5)
Bánfi, B., Tirone, F., Durussel, I., Knisz, J., Moskwa, P., Molnár, G. Z., Krause, K.-H., & Cox, J. A. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m310268200 · Cited by 389
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Metadata
- Authors
- Baker, M. A., & Aitken, R. J.
- Affiliations
- University of Newcastle Australia (AU)
- Corresponding author
- Aitken, R John
- Venue
- Reproductive Biology and Endocrinology
- Published
- 2005-11-29
- Volume
- 3
- Issue
- 1
- Pages
- 67-67
- ISSN
- 1477-7827 (ISSN-L)
- PMC
- PMC1315356
- OpenAlex
- W2155948635
- Cited by
- 194
- References
- 2
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 5 · 2023: 2 · 2022: 8 · 2021: 7 · 2020: 7 · 2019: 3 · 2018: 12 · 2017: 7 · 2016: 9 · 2015: 9 · 2014: 7 · 2013: 15 · 2012: 19
- FWCI
- 2.32
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Reproductive Biology and Endocrinology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Health Sciences › Medicine › Reproductive Medicine › Reproductive Biology and Fertility
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- reactive oxygen species, spermatozoa, oxidative stress, sperm capacitation, sperm DNA damage, mitochondrial DNA damage, male infertility, tyrosine phosphorylation, fertilisation (biology), embryonic development, childhood cancer
- MeSH terms
- Acridines, Child, Cytoplasm, Electron Transport, Humans, Infertility, Male, Male, NAD, NADP, Neoplasms, Nitric Oxide, Paternal Age, Spermatozoa, Reactive Oxygen Species, Germ-Line Mutation, Oxidative Stress, NADPH Oxidases, Genetic Diseases, Inborn, Luminescence
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