Abstract
Human ejaculated spermatozoa take up zinc in a time- and concentration-dependent manner. The kinetics of 65Zn2+ uptake is suggestive of an at least partly carrier-mediated transport. The lack of effect of the respiratory chain inhibitor antimycin A could mean that mitochondrial ATP is not required as an energy source for the uptake. The failure of nonpermeant SH reagent mersalyl to modify zinc uptake indicates that functional membrane sulfhydryl groups are not involved in the process. A dose-dependent inhibition of 65Zn2+ uptake was induced by the "anticalmodulin" drug trifluoperazine, suggesting that the calcium-binding protein calmodulin could have a role in zinc transport. In in vitro experiments this cation brought about a powerful effect in protecting the spermatozoa from being damaged by hypo-osmosis.
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