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Effect of Tumor Necrosis Factor‐α on the Intracellular Ca 2+ Homeostasis in Human Sperm
Author(s) -
Carrasquel Gabriela,
Camejo Maria I.,
Michelangeli Fabian,
Ruiz Marie C.
Publication year - 2013
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12106
Subject(s) - sperm , tumor necrosis factor alpha , capacitation , sperm motility , calcium , extracellular , endocrinology , chemistry , ionomycin , acrosome reaction , andrology , medicine , calcium in biology , biology , intracellular , biochemistry
Problem Inflammation and genital infections promote the increase in leukocytes, pro‐inflammatory cytokines, and oxygen reactive species, impairing sperm functions such as motility, capacitation, and acrosome reaction. All these functions are primarily regulated by cytoplasmic concentration of Ca 2+ ([ Ca 2+ ] cyto ). This study evaluated the effect of tumor necrosis factor ( TNF )‐α on the [ Ca 2+ ] cyto and its regulation in human sperm. Method of study Sperm loaded with fura‐2 were incubated with or without TNF ‐ α (0–500 pg/mL) from 0 to 120 min. After incubation, the basal [ Ca 2+ ] cyto and membrane permeability to Ca 2+ were evaluated by spectrofluorometry, before and after Ca 2+ addition to the extracellular medium. Results Without TNF ‐α, the addition of Ca 2+ promotes an transitory increase in [ Ca 2+ ] cyto in the spermatozoa, that returns in a few minutes to a basal level, indicating calcium regulation activation. TNF ‐α decreases the Ca 2+ permeation and increases the basal level of [ Ca 2+ ] cyto after a Ca 2+ pulse ( P  < 0.04); affecting calcium regulation in a way that is time and concentration dependent. TNF ‐α effect was partially prevented by the addition of an antioxidant (butylated hydroxytoluene) ( P   <  0.03). Conclusion Tumor necrosis factor‐α decreases membrane permeability to Ca 2+ and affects Ca 2+ regulation in sperm cells in vitro , probably via lipid peroxidation, which may explain the decrease in sperm fertilizing capacity during inflammatory and infectious processes.

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