Associated Events 451 Hyper activation

Sperm hyperactivation that occurs during capacitation is blocked by SOD and cata-lase and, as counterpart, O2'- (xanthine+xanthine oxidase) and H2O2 (as such is or from glucose+glucose oxidase) trigger this specific type of motility [2, 37, 38, 41]. Furthermore, hyperactivation induced by FCSu is blocked by Zn2+ and Sg [2, 89] that are seminal plasma inhibitors of ROS production.

The role of NO' in sperm hyperactivation is still not clear. Some NO' donors, such as sodium nitroprusside, trigger hyperactivation [31] but others (DA-NONOate and spermine-NONOate) do not [45]. This may be due to differences in experimental design or in kinetics for the release of NO' from the chemicals tested. However, proper controls, such as the effects of nitrite and nitrate (decomposition products of NO') and of preincubated NO' donor (to test what is left after NO' release) are sometimes missing. For example, spermine-NONOate, whether fresh or after a 24-h pre-incubation, promotes hyperactivation to a same extent, indicating that the effect observed is not related to NO' [45],

The sharp peak in O2 tension in the fluids from the female genital tract (golden hamster) at the time of ovulation [51] is proposed to induce ROS formation and as a result hyperactivation, thus providing enough force to spermatozoa to detach from the oviduct and to progress further toward the eggs [6]. The scarcity of data on the mechanisms of ROS action during sperm hyperactivation allows only hypothesizing that ROS may act via the stimulation of cAMP synthesis (activation of adenylyl cyclase) and PKA activity both of these being key players in sperm motility [1, 6, 35, 168].

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