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Seminal plasma leptin and spermatozoon apoptosis in patients with varicocele and leucocytospermia
Author(s) -
Wang H.,
Lv Y.,
Hu K.,
Feng T.,
Jin Y.,
Wang Y.,
Huang Y.,
Chen B.
Publication year - 2015
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.12313
Subject(s) - spermatozoon , leptin , apoptosis , endocrinology , medicine , reactive oxygen species , semen , andrology , male infertility , biology , sperm , infertility , obesity , microbiology and biotechnology , biochemistry , pregnancy , genetics
Summary Excessive apoptotic spermatozoon death is associated with male infertility. Leptin regulates apoptosis in several cell types. We prospectively investigated if seminal plasma leptin mediates spermatozoon apoptosis in 74 varicocele (VC) patients and 70 leucocytospermia patients. Spermatozoa from 40 normospermic men were used as controls. Routine semen analysis, spermatozoon apoptosis rate, seminal plasma leptin, reactive oxygen species (ROS) and tumour necrosis factor‐alpha ( TNF ‐α) levels were measured. In VC and leucocytospermia patients, seminal plasma leptin levels and spermatozoon apoptosis rates were significantly higher compared with controls. In the VC group, seminal plasma ROS levels were significantly higher compared with controls; there were no significant differences in TNF ‐α levels. In the leucocytospermia group, both ROS and TNF ‐α levels were significantly higher compared with controls. In both the VC and leucocytospermia groups, there was a significant positive correlation between the spermatozoon apoptosis rate and leptin levels and ROS and leptin levels. There was a significant correlation between leptin and TNF ‐α levels in the leucocytospermia group. Seminal plasma leptin levels correlate significantly with spermatozoon apoptosis rate, and leptin may be a spermatozoon pro‐apoptotic factors. The generation of ROS is a possible mechanism. Leptin may induce apoptosis via TNF ‐α in leucocytospermia patients.