| Popis: |
The sea urchin has been described recently as “the most facile experimental system for studying molecular mechanisms of fertilization” (1). A major contributor to successful fertilization is the induction of hydrogen peroxide (H202), which is produced, with the participation of protein kinase C, by the oxidative burst caused by the sperm’s entry into the ovum. During the oxidative burst, NADPH reduces oxygen to superoxide anion radical (. O,J in a NADPH-oxidase catalyzed reaction, and Hz02 is formed by dismutation of . 02-. H202 could prevent entry of other sperms in two ways: conversion by myeloperoxidase to hypochlorite, which would kill excess sperms (2) that are ready to enter and fertilize the ova; and by hardening the cell envelope by a cross-linking reaction catalyzed by a peroxidase that couples the tyrosyl residues between proteins (1). The oxidative burst induced by the sperm’s entry has a mechanism similar to that induced by a tumor promoter, such as 12-O-tetradecanoyl-phorbol-13-acetate (TPA) in human neutrophils; i.e., both involve the production of H202. In contrast, many chemopreventive agents, including protease inhibitors (that are capable of inhibiting chymotrypsin) and tamoxifen (an anti-cancer agent), suppress the formation of H202 in TPA-treated human neutrophils |
