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IntrOductIOnSperm motility is essential factor of fertile men. During fertilization, sperm cells require large amount of energy for their movement of flagella and active functioning. Nearly, 100 mitochondria are present in the midpiece of every mature human spermatozoon to provide energy quickly and effectively for sperm motility [1]. The oxidative phosphorylation of mitochondria generates energy in the form of ATP for flagellar movement of spermatozoa. In mitochondria, Reactive Oxygen Species (ROS) is generated during oxidative phosphorylation and increase the risk of Mitochondrial (mtDNA) damage [2]. The oxidative phosphorylation comprises a series of protein complexes that are encoded by both nuclear genes and mitochondrial genes [3]. Mitochondria contain their own genomic DNA and express independently in matrix of mitochondria. It contains 16569 base pairs that are categorised in 13 genes of respiratory chain complex subunits, along with the 22 tRNAs and 2 rRNAs (12S and 16S) involved in protein synthesis [4]. The mtDNA replicates rapidly by D-loop mechanism without proof-reading and DNA repair mechanisms. So, it enhances mutation rate 10-100 times higher than that of nuclear DNA [5]. Furthermore, sperm cells are susceptible to damage from oxidants because they lack endogenous antioxidants activity and mtDNA is attached to the mitochondrial inner membrane where ROS are continuously generated as byproducts of electron ABStrActIntroduction: Mitochondria and mitochondrial DNA are essential to sperm motility and fertility. It controls growth, development and differentiation through oxidation energy supply. Mitochondrial (mtDNA) deletions or mutation are frequently attributed to defects of sperm motility and finally these deletions lead to sperm dysfunction and causes infertility in male.

Objective : To study the relationship between lipid peroxidation of spermatozoa and changes in functional intergrity of human spermatozoa membrane in male subjects. Materials and Methods : Sixty eight male partners of infertile couples were included in the study. Status of oxidative stress was assessed by determining malondialdehyde (MDA) in seminal plasma. Functinal intergrity of sperm membrance was tested subjecting the sperm to hypo-osmotic test (HOS). The seminal plasma MDA levels were compared with seminogram parameters as well as with the results of HOS test using Pearson's coefficient of correlation (r) and significance of coefficient of correlation calculated from the table. Result : A significant but weak negative correlation was observed between seminal plasma MDA level and sperm concentration (r=-0.33,p<0.05), sperm motility (r=-0.37,p<0.05), sperm morphology (r=-0.37,p<0.05), and percentage of HOS positive spermatozoa (r=-0.33,p<0.05). Percentages of HOS positive spermatozoa also exhibited a significant but weak negative relationship with sperm concentration (r=-0.47,p<0.01), sperm motility (r=-0.48,p<0.01), sperm morphology (r=-0.49,p<0.01). Conclusion : Lipid peroxidation of spermatozoa is likely to affect the functional intergrity of the spermatozoa membrane.

Spermatogenesis is regulated by complex tissue specific gene expression in the testis to achieve normal male fertility. X‐chromosome specific TATA binding protein (TBP)‐associated factor 7L (hTAF7L) is one of the transcriptional regulator genes considered essential for spermatogenesis. The aim of this study was to evaluate the role of variants/mutations in the testis‐specific hTAF7L gene in non‐obstructive azoospermia and severe oligozoospermia male infertility. We studied 156 idiopathic non‐obstructive azoospermic, severe oligozoospermic infertile males and 50 fertile proven controls. Infertile males and control subjects were genotyped for variants of the hTAF7L gene using polymerase chain reaction and a direct Sanger sequencing approach. The odds ratio evaluated the association of hTAF7L gene variants with idiopathic male infertility. The variants found in the hTAF7L gene were subjected to an in‐silico analysis study. In infertile study subjects, we observed 11 single base pair nucleotide changes at various exons and three frameshift variants at exon 10 in the hTAF7L gene. We also found more than one variant in some non‐obstructive azoospermia and severe oligozoospermia infertile males along with control subjects. All these variants changed the amino acid sequences in the hTAF7L gene. However, similar changes were also seen in fertile subjects, and the differences were not statistically significant. In‐silico tools also predicted that the variants were likely to be benign. The variants in cDNA of the hTAF7L gene were typical SNPs. It is found that the hTAF7L gene is highly polymorphic and these missense variants are not directly associated with male infertility. However, we feel that more studies are needed to elucidate the role of multiple variants of the hTAF7L gene in the process of normal spermatogenesis.