Testosterone and prolactin stimulation of mitochondrial aconitase in pig prostate epithelial cells
Testosterone and prolactin stimulation of mitochondrial aconitase in pig prostate epithelial cells
复制标题
DOI：
10.1016/s0090-4295(96)00217-8
复制
发表时间：
1996-10-01
期刊：
影响因子：
2.1
通讯作者：
Franklin, RB
中科院分区：
文献类型：
--
作者：
Costello, LC;Liu, Y;Franklin, RB
目标.包括人类在内的许多动物前列腺的功能是积累和分泌大量柠檬酸盐。该功能源自前列腺分泌上皮细胞的代谢特性。这些细胞具有独特的限制性线粒体乌头酸酶（m-乌头酸酶），其使柠檬酸盐氧化最小化，从而允许柠檬酸盐积累。遗憾的是，前列腺间乌头酸酶的特性及其调节方式尚未确定。然而，激素睾酮和催乳素显著参与调节前列腺柠檬酸盐的产生。因此，这是合理的假设，这些激素可能参与调节的m-乌头酸酶和柠檬酸氧化。使用新鲜制备的猪前列腺上皮细胞，我们试图确定睾酮和催乳素治疗对m-乌头酸酶水平，m-乌头酸酶活性水平和柠檬酸盐利用率的影响。将上皮细胞与睾酮（10（-9）M）、催乳素（1 μ g/mL）或载体（对照）孵育3小时。两种激素的应用都导致m-顺乌头酸酶水平显着增加。相反，这两种激素对猪精囊细胞的间乌头酸酶水平没有任何影响，而精囊细胞也是柠檬酸产生细胞。此外，这两种激素对丙酮酸脱氢酶Ela没有任何影响。这些发现表明，睾酮和催乳素调节前列腺m-乌头酸酶是一个高度特异性的影响。沿着间乌头酸酶水平的增加，两种激素也增加间乌头酸酶活性和前列腺细胞对柠檬酸盐的利用。这些研究表明，睾酮和催乳素可以调节特定前列腺上皮细胞的m-乌头酸酶和随后的柠檬酸盐氧化。这种独特的顺乌头酸酶关系在其他哺乳动物细胞中没有观察到。
Objectives. The function of the prostate gland in many animals, including humans, is to accumulate and secrete large quantities of citrate. This function derives from the metabolic characteristics of the prostate secretory epithelial cells. These cells possess a uniquely limiting mitochondrial aconitase (m-aconitase) that minimizes citrate oxidation and thus permits citrate to accumulate. Unfortunately, the characteristics of prostate m-aconitase and its manner of regulation have not been established. The hormones testosterone and prolactin, however, are significantly involved in regulating prostate citrate production. Thus it is reasonable to hypothesize that these hormones may be involved in the regulation of both m-aconitase and citrate oxidation.Methods. Using freshly prepared pig prostate epithelial cells, we attempted to determine the effects of testosterone and prolactin treatment on the level of m-aconitase enzyme, on the level of m-aconitase activity, and on citrate utilization. The epithelial cells were incubated for 3 hours with either testosterone (10(-9) M), prolactin (1 mu g/mL), or vehicle (control).Results. Both hormone applications caused a marked increase in the level of m-aconitase. In contrast, neither hormone had any effect on the m-aconitase level of pig seminal vesicle cells, which are also citrate-producing cells. Moreover, neither hormone had any effect on pyruvate dehydrogenase Ela. These findings suggest that testosterone and prolactin regulation of prostate m-aconitase is a highly specific effect. Along with the increase in the level of m-aconitase enzyme, both hormones also increased m-aconitase activity and prostate-cell utilization of citrate.Conclusions. These studies demonstrate that testosterone and prolactin can regulate m-aconitase and subsequent citrate oxidation of specific prostate epithelial cells. This unique aconitase relationship is not observed in other mammalian cells.