Acrosome Reaction

ROS also modulate the acrosome reaction [14, 31, 66, 131, 169-171]. Exogenous ROS, O2'- (xanthine+xanthine oxidase) or H2O2, at the same level as those used to stimulate capacitation, promote the acrosome reaction in previously capacitated spermatozoa [14,169]. Furthermore, SOD and catalase block the acrosome reaction whether the triggering agent is the calcium ionophore (A23187) or lysophosphati-dylcholine (LPC), and independently of the inducer previously used for capacitation [14]. Interestingly, the level of O2'- formation reached by acrosome reacting spermatozoa is twice that seen during capacitation indicating a stepwise increase in ROS production [14].

The acrosome reaction induced by LPC or A23187 is associated with an increase in protein Tyr phosphorylation that adds over that seen during capacitation, some of the proteins affected during the two events having similar molecular masses [14,103,172]. This increase in Tyr phosphorylation related to the acrosome reaction is partly reversed with SOD or catalase but completely abolished in the presence of both antioxidants [14].

The current indications for a role of NO' in the acrosome reaction are based mostly on data showing that NO' donors or l-Arg promote, and NOS inhibitors prevent, this process [31, 66, 103, 170, 173]. However, there is very little evidence for actual NO' synthesis, except for that noted in spermatozoa in which the acrosome reaction is induced with follicular fluid (by formation of l-citrulline from l-Arg and by a 24-h accumulation of nitrite) [66].

The targets for ROS and signal transduction events modulated by ROS during the acrosome reaction may be different from those reported for capacitation. This is expected since these two events proceed according to specific pathways [1, 174] and ROS, as in other cellular systems, enter the normal flow of events (e.g., activation/ inhibition of enzymes).

Therefore, even though experimental evidences point out for an important role for ROS in sperm hyperactivation and acrosome reaction, the relative scarcity of data as compared to those reporting on capacitation leaves open an interesting area for studies on the mechanisms of ROS action in these events associated to capacitation.

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