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雌二醇可诱导雌性大鼠肾脏中I类乙醇脱氢酶的活性及信使核糖核酸的产生。

Estradiol induces class I alcohol dehydrogenase activity and mRNA in kidney of female rats.

作者信息

Qulali M, Ross R A, Crabb D W

机构信息

Department of Medicine, Indiana University School of Medicine, Indianapolis 46202-5121.

出版信息

Arch Biochem Biophys. 1991 Aug 1;288(2):406-13. doi: 10.1016/0003-9861(91)90213-3.

Abstract

Rat kidney contains alcohol dehydrogenase (ADH) activity which appears to be similar or identical to the class I ADH expressed in liver. Both tissues contain a 1.6-kb transcript which hybridizes with an ADH cDNA under stringent conditions. Kidney ADH activity is responsive to estradiol. The enzyme activity in the kidneys of sham-operated and ovariectomized animals was the same. Treatment of either group of animals by intramuscular injection of estradiol (1 mg/kg body wt/day) for 10 days induced ADH activity in kidney two- to threefold, whether the activity was expressed as U/g tissue, U/g protein, or U/mg DNA. Estradiol induced kidney ADH mRNA in both ovariectomized and sham-operated rats approximately twofold. Thus, induction of ADH mRNA accounts for the increase in ADH activity. In situ hybridization indicated that the ADH mRNA was present in the inner cortex and medulla of the kidney. Methylation patterns of the ADH gene were examined. The gene resides in a methylated region of chromatin without any of the typical features of a HpaII tiny fragment (HTF) island. Two MspI sites flanking the transcription start site are undermethylated in liver compared with kidney and spleen. This suggests that methylation of this gene may play a role in the tissue-specific expression of ADH.

摘要

大鼠肾脏含有乙醇脱氢酶(ADH)活性,该活性似乎与肝脏中表达的I类ADH相似或相同。两种组织都含有一个1.6 kb的转录本,在严格条件下可与ADH cDNA杂交。肾脏ADH活性对雌二醇有反应。假手术和去卵巢动物肾脏中的酶活性相同。对两组动物中的任一组通过肌肉注射雌二醇(1 mg/kg体重/天)持续10天,均可使肾脏中的ADH活性增加2至3倍,无论该活性是以U/g组织、U/g蛋白还是U/mg DNA来表示。雌二醇使去卵巢和假手术大鼠的肾脏ADH mRNA均增加约两倍。因此,ADH mRNA的诱导导致了ADH活性的增加。原位杂交表明,ADH mRNA存在于肾脏的内皮质和髓质中。对ADH基因的甲基化模式进行了检查。该基因位于染色质的甲基化区域,没有任何典型的HpaII微小片段(HTF)岛的特征。与肾脏和脾脏相比,转录起始位点两侧的两个MspI位点在肝脏中甲基化程度较低。这表明该基因的甲基化可能在ADH的组织特异性表达中起作用。

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