Abstract

The action of HgCl 2 on intracellular pH (pH i) and H + excretion has been investigated in unfertilized and fertilized sea urchin eggs. The results show that HgCl 2 in the micromolar range stimulated acid release by increasing the Na +/H + antiporter activity in both unfertilized and fertilized eggs, altering pH i regulation and cell metabolism. However, the mechanism of HgCl 2-induced acid excretion appeared to be different before and after fertilization. Furthermore, HgCl 2 induced cell alkalinisation in unfertilized eggs and cell acidification in fertilized eggs. The mechanism of HgCl 2 alteration of pH i and origin of excreted H + were studied. In unfertilized eggs, it is postulated that HgCl 2 stimulates the diacylglycerol pathway of the phosphatidyl-inositol cycle probably by acting on protein kinase C in a similar manner to the phorbol ester TPA, leading to activation of the Na +/H + exchange. In fertilized eggs, HgCl 2 induced H + excretion appeared to be dependent on an increase in Ca 2+ influx, which in turn may have been responsible for activating the Ca 2+-dependent Na +/H + exchange. Furthermore, internal H + production was stimulated: the cyanide-sensitive H + source involved uncoupling of mitochondria, the cyanide-insensitive part of H + production likely resulted from action on acidic intracellular compartments, both events mediated by an HgCl 2-induced Ca 2+ release.

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