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| INTRODUC TI ONIn recent years, many researchers have focused on possible factors leading to male infertility and revealed the existence of many cellular and molecular defects during sperm production and maturation. These defects finally affect the count and structure of spermatozoa and reduce the ability of spermatozoa to reach and fertilise the egg. A decrease in sperm motility, called "asthenozoospermia," is one of these important deficiencies, which is influenced by various cellular and molecular factors. After a brief explanation of the main cellular and molecular factors involved in reducing sperm motility, this review article presents some important treatment strategies to overcome sperm motility reduction. | DEFINITI ON AND PRE VALEN CEAccording to the reports released by the World Health Organization (WHO), about 20% of couples are infertile and infertility can be, at least partly, attributed to the male partner (Petok, 2015). Low sperm count, abnormal morphology and poor sperm motility are the common causes related to male factors. Based on the WHO guideline (2010), asthenozoospermia was defined as total motility <40% and progressive motility <32% in a semen sample (WHO, 2010).Severe asthenozoospermia was also characterised by total sperm immobility or very low motile spermatozoa in the semen sample. It seems that total sperm immobility is related to genetic disorders (Blouin et al., 2000). This will be explained in more detail below.Understating the cellular and molecular processes leading to sperm motility is required to help the researchers to address the subject of reduced sperm motility and produce an accurate diagnosis (Turner, 2003).To diagnose asthenozoospermia in individuals in an andrology laboratory, some important points must be taken into consideration to prevent false asthenozoospermia diagnosis. For instance, semen should not be collected in long abstinence days since the number of immotile spermatozoa is high in abstinence days. Also, semen AbstractSemen sample with poor sperm motility, which called asthenozoospermia, is considered as one of the main factors contributing to male infertility. Recognition of the cellular and molecular pathways contributing to sperm motility reduction may lead to applying novel treatment strategies for overcoming low sperm motility in asthenozoospermia individuals. In this review, we intend to discuss the main causes of sperm motility reduction in asthenozoospermia and some treatment strategies used to overcome low sperm motility. K E Y W O R D Sapoptosis, reactive oxygen species, spermiogenesis

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Background: The effect of antioxidant therapy on sperm DNA fragmentation index (DFI)and achieving natural pregnancy were under debate. Very few studies have showedthe rate of pregnancy rate after the antioxidant therapy due to ethical and technicallimitations.Objective: The aim of this cohort study was to determine the improvement rate ofsperm DFI and natural pregnancy rate after the antioxidant therapy in infertile men.Materials and Methods: 1645 infertile men were subjected for this study from May2015 to December 2017. The Spermogram and sperm DFI were assessed using WorldHealth Organization (WHO) 2010-based protocols and sperm chromatin structure assay(SCSA), respectively, in sperm samples before and after antioxidant therapy.Results: The total sperm DFI improvement rate was 38.9% in the total population.Sperm DFI improvement had close correlation with total motility (r= 0.731, p= 0.001)and progressive motility improvement (r= 0.885, p= 0.001); 16.8% of individuals whocompleted antioxidant therapy for nine months achieved natural pregnancy.Conclusion: The results of the current study suggested that SCSA along withspermogram might be a suitable option for the evaluation of fertility potential. Inaddition, antioxidant therapy may be useful for men with high levels of sperm DFI.However, the rate of pregnancy was still low and other treatment protocols such asassisted reproductive technology may be necessary.

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