Increased oxidative stress inhibit the electron transport
chain leading to free radical build up in spermatocytes (Aitken et al., 2014). The
sperm cell’s unique compartmentalization prevents apoptosis from occurring, but
cannot offer complete protection from mutations (Aitken et al., 2014). Reactive
oxygen species lead to DNA damage in spermatocytes, particularly in repair
proteins (Aitken et al., 2014). The spermatocyte is uncappable of self-repair
and is in need of the oocyte’s reparative abilities (Aitken
et al., 2014). The mutated spermatocyte still remains capable of
fertilization and if fertilization does occur the mechanisms of the oocyte are responsible
for fixing this mutation prior to the first round of cell division (Aitken et
al., 2014). If this mutation is not corrected the mutation will be past to the
offspring (Aitken et al., 2014).
Aitken RJ, Smith TB, Jobling MS,
Baker MA, De Iuliis GN. Oxidative stress and male reproductive health. Asian J
Androl. 2014 Jan-Feb;16(1):31-8. doi: 10.4103/1008-682X.122203. PMID: 24369131;
PMCID: PMC3901879.5.
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