During spermatogenesis, fatty acids play an important role both as structural components and messengers that trigger male germ cell line differentiation. The spontaneous oxidation of fatty acids causes a decrease in mammalian fertility. Here, we examine the effects of nonenzymatically oxidized arachidonic acid (AAox ) on mouse spermatogenic T-type Ca2+ currents (ICaT ) due to their physiological relevance during spermatogenesis. AAox is 25-fold more potent than AA at inhibiting ICaT and it left shifts the I-V curve peak and both activation and steady-state inactivation curves. In addition, ICaT deactivation kinetics and their recovery from inactivation are slower in the presence of AAox . Therefore, the fraction of inactivated Ca2+ channels is increased. AAox -induced ICaT inhibition could contribute to male infertility affecting Ca2+ regulation in spermatogenic cells.
Keywords: T-type Ca2+ channels; arachidonic acid; developmental biology; oxidized fatty acids; spermatogenic cells.
© 2019 Federation of European Biochemical Societies.