Human sperm hyperactivation and capacitation as parts of an oxidative process

Abstract

Capacitation of spermatozoa is essential for fertilization ans is visually characterized by hyperactivated motility. Previous reports have shown that foetal cord serum (FCS) and superoxide anion, O 2 ⋅ , can trigger human sperm hyperactivation (HA) and capacitation and that superoxide dismutase (SOD) could prevent these processes. We investigated further the role of O 2 ⋅ and FCS components in human spern HA and capacitation. Percoll-washed spermatozoa were incubated, at 37°C, in Ham's F-10 medium with 75% of FCS, dialyzed FCS (> 12kdD), ultrafiltrate from FCS (FCSu;<3kD), or xanthine + xanthine oxidase + catalase (X + XO + cat). Spermatozoa incubated with FCSu were also supplemented with catalse to prevent the loss of motility often after 2–3 h of incubation. FCS and dialyzed FCS induced significant levels of HA (10 ±1% and 7.7 ±0.7%, respectively) that were, however, lower than those observed with FCSu (19 ± 1%) or X + XO + cat (16 ± 2%). Similar results were obtained when the lysophorphatidylcholine-induced acrosome raction (LPC-AR, a measure of sperm capacitation) was evaluated. The presence of SOD in the incubation medium blocked the induction of HA and capaciatation by FCS. FCSu, X + XO + cat, as well as the spontaenous HA and capacitation. The enzymatic activity of SOD was needed for the prevention of these processes. Desferioxamine, up to 100 μM, had no effect on HA and LPC-AR iniduced by FCSu and X + XO + cat. Addition of SOD to already hyperactivated spermatozoa reversed the HA. These data suggest that spermatozoa need a sustaned O 2 ⋅ generation to maintain HA and proceed to capacitation. We hypothesize that FDSu or the O 2 ⋅ generated by X + XO + cat activate enzymeds, possible a reduced nicotinamide adeninie dinucleotide dinucleotide phosphate [NAD(P)H] oxidase at the level of sperm membrane.