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首页> 外文期刊>Journal of applied toxicology >Biochemical and ultrastructural alterations in the rat ventral prostate due to repetitive alcohol drinking.
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Biochemical and ultrastructural alterations in the rat ventral prostate due to repetitive alcohol drinking.

机译：重复饮酒导致大鼠腹侧前列腺的生化和超微结构改变。

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Previous studies showed that cytosolic and microsomal fractions from rat ventral prostate are able to biotransform ethanol to acetaldehyde and 1-hydroxyethyl radicals via xanthine oxidase and a non P450 dependent pathway respectively. Sprague Dawley male rats were fed with a Lieber and De Carli diet containing ethanol for 28 days and compared against adequately pair-fed controls. Prostate microsomal fractions were found to exhibit CYP2E1-mediated hydroxylase activity significantly lower than in the liver and it was induced by repetitive ethanol drinking. Ethanol drinking led to an increased susceptibility of prostatic lipids to oxidation, as detected by t-butylhydroperoxide-promoted chemiluminiscence emission and increased levels of lipid hydroperoxides (xylenol orange method). Ultrastructural alterations in the epithelial cells were observed. They consisted of marked condensation of chromatin around the perinuclear membrane, moderate dilatation of the endoplasmic reticulum and an increased number of epithelial cells undergoing apoptosis. The prostatic alcohol dehydrogenase activity of the stock rats was 4.84 times lower than that in the liver and aldehyde dehydrogenase activity in their microsomal, cytosolic and mitochondrial fractions was either not detectable or significantly less intense than in the liver. A single dose of ethanol led to significant acetaldehyde accumulation in the prostate. The results suggest that acetaldehyde accumulation in prostate tissue might result from both acetaldehyde produced in situ but also because of its low aldehyde dehydrogenase activity and its poor ability to metabolize acetaldehyde arriving via the blood. Acetaldehyde, 1-hydroxyethyl radical and the oxidative stress produced may lead to epithelial cell injury.
机译：先前的研究表明，来自大鼠腹侧前列腺的胞质和微粒体部分能够分别通过黄嘌呤氧化酶和非P450依赖性途径将乙醇生物转化为乙醛和1-羟乙基。将Sprague Dawley雄性大鼠饲喂含乙醇的Lieber和De Carli饮食28天，并与成对喂养的对照进行比较。发现前列腺微粒体级分显示CYP2E1介导的羟化酶活性显着低于肝脏，并且是由反复饮酒诱导的。乙醇摄入导致前列腺脂质对氧化的敏感性增加，这可以通过叔丁基过氧化氢促进的化学发光性检测和脂质过氧化氢水平的升高来检测（二甲酚橙法）。观察到上皮细胞的超微结构改变。它们包括染色质在核周膜周围的明显凝结，内质网的中等扩张和上皮细胞凋亡的增加。储备大鼠的前列腺醇脱氢酶活性比肝脏低4.84倍，其微粒体，胞质和线粒体组分中的醛脱氢酶活性比肝脏中低，或者检测不到。单剂量乙醇导致前列腺中大量乙醛积聚。结果表明，乙醛在前列腺组织中的积累可能是由于原位产生的乙醛引起的，也可能是由于其乙醛脱氢酶活性低和代谢经由血液到达的乙醛的能力差所致。乙醛，1-羟乙基自由基和产生的氧化应激可能导致上皮细胞损伤。

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