Several factors are present in infertile males with sperm
function defects caused by asthenozoospermia [1]. Gene
defects, including DNMT3B and MTHFR, have been
well documented to correlate with this phenotype [2].
Mitochondria DNA haplogroups may affect sperm motility
[3]. Systemic disorders such as polycystic kidney
disease [4] also affect fertility and cause asthenozoospermia.
Sperms are highly vulnerable to oxidative stress because
they contain high concentrations of free unsaturated
fatty acids, lack intracellular antioxidant enzymes, and
have a limited capacity for DNA repair [5]. The precise
mechanisms of motility loss in the sperm, the ability of
this cell to fuse with the oocyte under oxidative stress,
and the subsequent initiation of lipid peroxidation are
not known