Introduction
Infertility is defined as the inability of couples to have children
despite one year of unprotected sexual intercourse (Sharlip et al. ,
2002).The worldwide incidence of infertility is approximately 15%, and
male infertility accounts for 50% of all cases (WHO, 2000). Male
infertility can be linked to a variety of conditions including
congenital factors, varicocele, undescended testicle, testicular cancer,
hypogonadism, infection, autoimmune diseases, systemic diseases, and
genetic abnormalities. In about 30 to 40% of cases, there is no
identified cause, which is referred to as idiopathic
oligoasthenoteratozoospermia (OAT) (Nieschlag, Behre, & Nieschlag,
2010). In men without any disease that may affect fertility, idiopathic
OAT is diagnosed based on the combination of a low sperm concentration
(<15×106/mL), reduced motility (progressive motility
<32% and total motility <40%) and abnormally
shaped spermatozoa (<30% normal morphology according to the
2010 World Health Organization criteria and<4% normal
morphology according to the Kruger strict criteria) (Cooper et al.,
2010). Levels of reactive oxygen species (ROS) have also been associated
with male infertility, and studies have reported higher levels of ROS
and suppressed antioxidant capacity in the semen of infertile men
compared to their fertile counterparts (Dorostghoal et al.2017, Agarwal
et al., 2014). ROS are normally found in seminal plasma to some extent
since they are necessary for capacitation, acrosome reaction, and
fertilization, but spermatozoa are also vulnerable to oxygen radicals
because plasma membranes and cytoplasm are rich in polyunsaturated fatty
acids (Agarwal et al., 2014). In particular, high ROS exposure leads to
functional changes that result in membrane damage, membrane instability,
and cell death (6-Agarwal et al., 2014). Oxidative stress (OS) occurs
when in the presence of an imbalance between oxidants and antioxidants
(Agarwal, Hamada and Esteves, 2012).In general, an oxidative environment
can lead to cellular degeneration with apoptosis or necrosis, and a
reduced environment can support cell survival (Durackova et al., 2014).
Therefore, a therapeutic strategy is to use supplements in order to
enhance sperm energy metabolism, minimize sperm-free radical damage, and
improve cellular processes associated with sperm formation and
maturation. Many studies have confirmed the beneficial effect of
antioxidants on at least one of the semen parameters, but the greatest
effect has been determined in relation to sperm motility. In most of
these studies, multiple combinations of antioxidants were used, but the
optimal dose of one or more antioxidants was not defined. ( Imamovic
Kumalic S, Pinter B.,2014 ).Several clinical studies have shown that the
oral intake of L-carnitine and acetyl-l-carnitine in asthenozoospermic
patients increases the percentage of motile spermatozoa, fast forward
motility, mean velocity, sperm motility, and linearity (Balercia et al.,
2005; Lenzi et al., 2004). It has been reported that the use of
selenium, coenzyme Q10 (CoQ10), citric acid, vitamin C, vitamin B12, and
zinc has positive effects on spermatozoa (Busetto et al., 2018).
Although many studies have noted the positive effects of the use of
antioxidants, it has not been determined exactly which combination
should be used and at which ratio. In this study, we investigated the
effects of two different antioxidant combinations on sperm parameters in
patients with idiopathic OAT and whether the use of each combination
resulted in different effects.