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ROS & Sperm Physiology: Animal Reproduction Science, 278

ROS

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0% found this document useful (0 votes)
8 views2 pages

ROS & Sperm Physiology: Animal Reproduction Science, 278

ROS

Uploaded by

styloxsakib199
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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ROS & Sperm Physiology

Good quality sperm is crucial for successful animal reproduction but production of
ROS is major obstacle in this case. (H. Zhang et al., 2025). ROS has both regulatory
and detrimental effects on sperm physiology. Optimum ROS levels maintain a
functional redox state and play crucial physiological role in reproductive events -
sperm maturation, hyperactivation, acrosome reaction and sperm-oocyte fusion
with their short half-life and limited diffusion. These molecules induce
capacitation by increasing cholesterol efflux, bicarbonate inflow, calcium influx
and as well helps in increasing membrane fluidity and normal sperm functioning.
(V.R. Upadhyay et al., 2022). Mitochondrial activity of spermatozoa influences the
production of reactive oxygen species. ROS are the sub-products of respiration
derived mainly from mitochondria complexes I & III and from sperm activity.
Functionally sound spermatozoa produces more ROS but excessive amount ROS
or imbalance between produced ROS and buffering function of antioxidant
systems of seminal plasma can cause oxidative stress which can damage
spermatozoa irreversibly. (E. Giaretta et al, 2022). Oxidative stress due to
excessive ROS production is known to hinder normal sperm function and
influences infertility. ROS are also associated with affecting cellular lipids, proteins
and sperm DNA which can have profound implications for normal embryonic
development and long-term progeny health. As we know spermatozoa are rich in
mitochondria and integrity of it is established by the amount of cytochrome c in
the seminal plasma. Higher the cytochrome c ,more the mitochondrial damage
meaning more ROS which possibly causing DNA damage leading to infertility.
Damages to sperm DNA causes DNA to fragment which means programmed cell
death or apoptosis of spermatozoa. Motility is inversely related to apoptosis
which is again linked to the excessive ROS production. (Wang et al., 2003).

References
1. Zhang, H., Qin, X., Bojan, N., Cao, C., Chai, J., & Pang, W. (2025). Nicotinamide mononucleotide
enhances porcine sperm quality by activating the SIRT3-SOD2/ROS pathway and promoting
oxidative phosphorylation. Animal Reproduction Science, 278, 107607.
https://doi.org/10.1016/j.anireprosci.2025.107607
2. Upadhyay, V. R., Ramesh, V., Dewry, R. K., Yadav, D. K., & Ponraj, P. (2022). Bimodal interplay of
reactive oxygen and nitrogen species in physiology and pathophysiology of bovine sperm
function. Theriogenology, 187, 82–94. https://doi.org/10.1016/j.theriogenology.2022.04.024
3. Giaretta, E., Mislei, B., Martínez-Pastor, F., Nesci, S., Spinaci, M., Galeati, G., Nerozzi, C., Mari, G.,
Tamanini, C., & Bucci, D. (2022). Use of specific mitochondrial complex inhibitors to investigate
mitochondrial involvement on horse sperm motility and ROS production. Research in Veterinary
Science, 147, 12–19.
4. Wang, X., Sharma, R. K., Sikka, S. C., Thomas, A. J. Jr., Falcone, T., & Agarwal, A. (2003). Oxidative
stress is associated with increased apoptosis leading to spermatozoa DNA damage in patients
with male factor infertility. Fertility and Sterility, 80(3), 531–535. https://doi.org/10.1016/S0015-
0282(03)00756-8

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