Melatonin as a potential tool against oxidative damage and apoptosis in ejaculated human spermatozoa.

It is assumed somatic cells can die in the apoptotic, the autophagic, or the necrotic way; however, the mechanisms of sperm death are not clear.

Here, ejaculated human spermatozoa were evaluated for apoptosis and reactive oxygen species production in the absence or presence of melatonin, and we concluded that melatonin reverses sperm apoptosis due to its free radical scavenging actions.

Effects of melatonin on the caspase activity, phosphatidylserine (PS) exposure, mitochondrial reactive oxygen species and sperm viability. A portion of the sperms was pre-incubated with 1 mM melatonin (Mel) for 30 minutes. Subsequently, apoptosis in both groups, control group and that treated with melatonin, was induced for 60 minutes using 10 μgM H₂O₂ and 20 μM P (PROG).
• A caspase-3 activity
• B caspase-9 activity
• C PS exposure
• D mitochondrial reactive oxygen species concentration
• E sperm viability.
The values are represented as mean values ± SD of four to six independent experiments, referring to the respective starting values at point of time 0 (before start of exposure).

▪▪ p <0,01 und ▪▪▪ p<0,001 vs. control values * p <0,05; ** p <0,01; p < 0,001 vs. H₂O₂ or P alone. (Source: modified according to Espino J et al., 2010)