earticle

영어

Peroxiredoxins (PRDXs), which are essential antioxidant enzymes for physiological activity, have reported that influence sperm function and consequently male fertility. Although PRDXs are well known as important factor to affect male fertility, there has been a lack of attempt to discover the accurate role and mechanism of PRDXs in male fertility. Therefore, the principal objective of this study is to elucidate the role of PRDXs in sperm function and fertilization. We treated mouse spermatozoa with different dose of specific inhibitor of PRDXs, conoidin A (1, 10, or 100 μM). Our results revealed that conoidin A significantly decreased oxidized form of PRDXs (PRDXs-SO3) in mouse spermatozoa. Inhibited PRDXs activity are then resulted in a significant decrease in sperm motility/motion kinematics, viability, mitochondrial membrane potential, and intracellular ATP levels. On the other hand, intracellular levels of ROS and DNA fragmentation index were significantly increased following exposure to conodin A. Next, we evaluated capacitation and acrosome reaction status, and subsequently tyrosine phosphorylation and protein kinase-A activity to investigated underlying mechanism of PRDXs on sperm capacitation status. Capacitation and acrosome reaction were significantly decreased perhaps due to reduction of tyrosine phosphorylation and protein kinase- A activity. Finally, we investigated the effect of PRDXs on fertilization and early embryonic development. Our results described that decreased PRDXs activity significantly decreased fertilization and early embryonic development. Consequently, we demonstrated that inhibition of PRDXs activity has a direct impact on male fertility via decreased important physiological sperm function, eventually resulted in poor fertilisation and embryonic development.