Nonenzymatically oxidized arachidonic acid regulates T-type Ca2+ currents in mouse spermatogenic cells

被引：3

作者：

Bondarenko, Olga ^{[1
]}

Corzo, Gerardo ^{[2
]}

Santana, Felix L. ^{[2
]}

Rio-Portilla, Federicodel ^{[3
]}

Darszon, Alberto ^{[1
]}

Lopez-Gonzalez, Ignacio ^{[1
]}

机构：

[1] Univ Nacl Autonoma Mexico, Inst Biotecnol, Dept Genet Desarrollo & Fisiol Mol, Av Univ 2001 Col Chamilpa, Mexico City 62210, DF, Mexico

[2] Univ Nacl Autonoma Mexico, Inst Biotecnol, Dept Med Mol & Bioproc, Mexico City, DF, Mexico

[3] Univ Nacl Autonoma Mexico, Inst Quim, Dept Biomacromol, Mexico City, DF, Mexico

来源：

FEBS LETTERS | 2019年 / 593卷 / 14期

关键词：

arachidonic acid; developmental biology; oxidized fatty acids; spermatogenic cells; T-type Ca2+ channels; LIPID-PEROXIDATION; MAMMALIAN SPERMATOZOA; SUPEROXIDE-DISMUTASE; CALCIUM-CHANNELS; OXIDATIVE STRESS; RAT SERTOLI; FATTY-ACIDS; MODULATION; 20-HETE; PHOSPHOLIPIDS;

D O I：

10.1002/1873-3468.13448

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 (AA(ox)) on mouse spermatogenic T-type Ca2+ currents (I-CaT) due to their physiological relevance during spermatogenesis. AA(ox) is 25-fold more potent than AA at inhibiting I-CaT and it left shifts the I-V curve peak and both activation and steady-state inactivation curves. In addition, I-CaT deactivation kinetics and their recovery from inactivation are slower in the presence of AA(ox). Therefore, the fraction of inactivated Ca2+ channels is increased. AA(ox)-induced I-CaT inhibition could contribute to male infertility affecting Ca2+ regulation in spermatogenic cells.

引用

页码：1735 / 1750

页数：16

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