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.