期刊
ANDROLOGY
卷 1, 期 3, 页码 456-463出版社
WILEY
DOI: 10.1111/j.2047-2927.2013.00077.x
关键词
asthenozoospermia; human spermatozoa; sperm metabolism; sperm mitochondrion; spinal cord injury
类别
资金
- Ministero dell'Universita e Ricerca
The aetiology of severe asthenozoospermia in men with spinal cord injury includes an adverse impact of seminal plasma (SP) on sperm motility. In this study we investigated the effect exerted by SP from men with SCI on donor sperm mitochondrial activity and its reflection on motility. Donor spermatozoa were exposed (1h) to SP from 22 ejaculates of men with SCI. Only SP from samples exhibiting both a low fructose level and an inhibitory effect on mitochondrial membrane potential (m), assessed at flow cytometry with JC-1, affected donor sperm motility when evaluated 1h after co-incubation. This effect was reverted by washing from SP and sperm re-suspension in medium containing glucose, in spite of persistently depressed m. In the same samples, sperm motility and vitality dramatically decreased when evaluated 6h after washing and re-suspension in the glucose-containing medium. Seminal plasmas which induced a disruption of m, also enhanced a mitochondrial ROS generation, as assessed by MitoSOX red. The enhanced mitochondrial ROS generation was associated with a late induction of sperm membrane lipid peroxidation, as assessed by BODIPY C11, when evaluated at 6h, but not at 1h, after washing from SP. Furthermore, activation of caspase-9 and caspase-3 accompanied the loss of m. In conclusion, a double energetic blockage (glycolysis and mitochondrial respiration) can represent a metabolic determinant of the early adverse effect exerted by SP from men with SCI on sperm motility. Mitochondrial dysfunction-related oxidative/apoptotic mechanisms can account for later consequences on sperm motility/vitality.
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