Nitrosative stress in human spermatozoa causes cell death characterized by induction of mitochondrial permeability transition-driven necrosis

Peroxynitrite is a highly reactive nitrogen species and a potent inducer of apoptosis and necrosis in somatic cells. Peroxynitrite-induced nitrosative stress has emerged as a major cause of impaired sperm function; however, its ability to trigger cell death has not been described in human spermatozo...

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Bibliographic Details
Published in:Asian journal of andrology 2018-11, Vol.20 (6), p.600-607
Main Authors: Uribe, Pamela, Cabrillana, María, Fornés, Miguel, Treulen, Favián, Boguen, Rodrigo, Isachenko, Vladimir, Isachenko, Evgenia, Sánchez, Raúl, Villegas, Juana
Format: Article
Language:English
Subjects:
Apoptosis
Causes of
Cell death
Cytotoxicity
Data analysis
Gangrene
Infertility
Lipid peroxidation
Morphology
Motility
Necrosis
necrosis
nitrosative stress
oxidative stress
peroxynitrite
sperm cell death
Nitrogen compounds
Original
Oxidation
Oxidative stress
Permeability
Phosphorylation
Physiological aspects
Sperm
Spermatozoa
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Summary:Peroxynitrite is a highly reactive nitrogen species and a potent inducer of apoptosis and necrosis in somatic cells. Peroxynitrite-induced nitrosative stress has emerged as a major cause of impaired sperm function; however, its ability to trigger cell death has not been described in human spermatozoa. The objective here was to characterize biochemical and morphological features of cell death induced by peroxynitrite-mediated nitrosative stress in human spermatozoa. For this, spermatozoa were incubated with and without (untreated control) 3-morpholinosydnonimine (SIN-1), in order to generate peroxynitrite. Sperm viability, mitochondrial permeability transition (MPT), externalization of phosphatidylserine, DNA oxidation and fragmentation, caspase activation, tyrosine nitration, and sperm ultrastructure were analyzed. The results showed that at 24 h of incubation with SIN-1, the sperm viability was significantly reduced compared to untreated control (P < 0.001). Furthermore, the MPT was induced (P < 0.01) and increment in DNA oxidation (P < 0.01), DNA fragmentation (P < 0.01), tyrosine nitration (P < 0.0001) and ultrastructural damage were observed when compared to untreated control. Caspase activation was not evidenced, and although phosphatidylserine externalization increased compared to untreated control (P < 0.001), this process was observed in
ISSN:1008-682X
1745-7262
DOI:10.4103/aja.aja_29_18