Meijer L, Guerrier P, Maclouf J
Dev Biol. 1984 Dec;106(2):368-78. doi: 10.1016/0012-1606(84)90235-5.
In starfish oocyte maturation (meiosis reinitiation) is induced by the natural hormone 1-methyladenine (1-Me-Ade). This paper shows that arachidonic acid (AA) induces oocyte maturation at concentrations above 0.5 microM. This maturation shares many characteristics with 1-MeAde-induced maturation: same kinetics, same required contact time, same stimulations of protein phosphorylation and sodium influx. Although calcium facilitates the AA-induced but not the 1-MeAde-induced maturation, AA, like 1-MeAde, does not stimulate the uptake of calcium. Calcium does not facilitate the uptake of AA by oocytes. Out of 36 different fatty acids (saturated and unsaturated), only eicosatetraenoic (AA) and eicosapentaenoic acids were found to mimic 1-MeAde. Calcium-dependent phospholipases A2 from bee venom and Naja venom also induce maturation (0.1-1 unit/ml) when added externally to the oocytes. Phospholipase A2 inhibitors (quinacrine, bromophenacylbromide) block maturation; inhibition is reversed by increasing the 1-MeAde concentration and only occurs during the hormone-dependent period. AA is usually metabolized through oxidation by cyclooxygenase or lipoxygenase. Cyclooxygenase inhibitors (acetylsalicylic acid, indomethacin, tolazoline) do not block maturation; prostaglandins E2, D2, F2 alpha, I2, and thromboxane B2 do not induce meiosis reinitiation. On the other hand, lipoxygenase inhibitors (quercetin, butylated hydroxytoluene, and eicosatetraynoic acid) block 1-MeAde-induced maturation; although leukotrienes (A4, B4, C4, D4, E4) have no effects on oocytes, two other lipoxygenase products, 12- and 15-hydroxyeicosatetraenoic acids (and their corresponding hydroperoxy-) induce oocyte maturation (around 1 microM). The possible mode of action of the fatty acids inducing oocyte maturation is discussed.
在海星中,卵母细胞成熟(减数分裂重新启动)是由天然激素1-甲基腺嘌呤(1-Me-Ade)诱导的。本文表明,花生四烯酸(AA)在浓度高于0.5微摩尔时可诱导卵母细胞成熟。这种成熟与1-MeAde诱导的成熟具有许多共同特征:相同的动力学、相同的所需接触时间、相同的蛋白质磷酸化刺激和钠内流。虽然钙促进AA诱导的但不促进1-MeAde诱导的成熟,但AA与1-MeAde一样,不会刺激钙的摄取。钙不会促进卵母细胞对AA的摄取。在36种不同的脂肪酸(饱和脂肪酸和不饱和脂肪酸)中,仅发现二十碳四烯酸(AA)和二十碳五烯酸可模拟1-MeAde。当从外部添加到卵母细胞中时,来自蜂毒和眼镜蛇毒的钙依赖性磷脂酶A2也可诱导成熟(0.1-1单位/毫升)。磷脂酶A2抑制剂(喹吖因、溴苯那敏溴化物)可阻断成熟;通过增加1-MeAde浓度可逆转抑制作用,且仅在激素依赖期发生。AA通常通过环氧化酶或脂氧合酶的氧化作用进行代谢。环氧化酶抑制剂(乙酰水杨酸、吲哚美辛、妥拉唑啉)不会阻断成熟;前列腺素E2、D2、F2α、I2和血栓素B2不会诱导减数分裂重新启动。另一方面,脂氧合酶抑制剂(槲皮素、丁基化羟基甲苯和二十碳四炔酸)可阻断1-MeAde诱导的成熟;虽然白三烯(A4、B4、C4、D4、E4)对卵母细胞无影响,但另外两种脂氧合酶产物,12-和15-羟基二十碳四烯酸(及其相应的氢过氧化物)可诱导卵母细胞成熟(约1微摩尔)。本文讨论了脂肪酸诱导卵母细胞成熟的可能作用方式。