• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Biochemical Journal >Role of haem in the induction of cytochrome P-450 by phenobarbitone. Studies in chick embryos in ovo and in cultured chick embryo hepatocytes.
【2h】

Role of haem in the induction of cytochrome P-450 by phenobarbitone. Studies in chick embryos in ovo and in cultured chick embryo hepatocytes.

机译：血红素在苯巴比妥诱导细胞色素P-450的作用。在卵内的鸡胚和培养的鸡胚肝细胞中的研究。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The role of haem synthesis during induction of hepatic cytochrome P-450 haemoproteins was studied in chick embryo in ovo and in chick embryos hepatocytes cultured under chemically defined conditions. 1. Phenobarbitone caused a prompt increase in the activity of 5-aminolaevulinate synthase, the rate-limiting enzyme of haem biosynthesis, and in the concentration of cytochrome P-450. This induction response occurred without measurable initial destruction of the haem moiety of cytochrome P-450. 2. When intracellular haem availability was enhanced by exogenous haem or 5-aminolaevulinate, phenobarbitone-medicated induction of cytochrome P-450 was not affected in spite of the well known repression of 5-aminolaevulinate synthase by haem. These data are consistent with the concept that haem does not regulate the synthesis of cytochrome P-450 haemoproteins. 3. Acetate inhibited haem biosynthesis at the level of 5-aminolaevulinate formation. When intracellular haem availability was diminished by treatment with acetate, phenobarbitone-medicated induction was decreased. 4. This inhibitory effect of acetate on cytochrome P-450 induction was reversed by exogenous haem or its precursor 5-aminolaevulinate. These data suggest that inhibition of haem biosynthesis does not decrease synthesis of apo-cytochrome P-450. Moreover, they indicate that exogenous haem can be incorporated into newly formed aop-cytochrome P-450.
机译：研究了血红素合成在卵内鸡胚和在化学条件下培养的鸡胚肝细胞中诱导肝细胞色素P-450血红蛋白过程中的作用。 1.苯巴比妥引起5-氨基油酰戊酸合酶，血红素生物合成的限速酶和细胞色素P-450浓度的活性迅速增加。该诱导反应的发生没有细胞色素P-450的血红素部分的可测量的初始破坏。 2.当细胞内血红素的可用性通过外源血红素或5-氨基油酰戊酸增加时，尽管众所周知血红素能抑制5-氨基油酰戊酸合酶，但苯巴比妥酮对细胞色素P-450的诱导作用并未受到影响。这些数据与血红素不能调节细胞色素P-450血红蛋白合成的概念一致。 3.乙酸盐抑制了血红素的生物合成，形成了5-氨基戊酸盐。当通过乙酸盐处理减少了细胞内血红素的可用性时，苯巴比妥治疗的诱导降低。 4.乙酸盐对细胞色素P-450诱导的这种抑制作用被外源血红素或其前体5-氨基乙酰戊酸酯所逆转。这些数据表明，抑制血红素的生物合成不会减少脱辅基细胞色素P-450的合成。而且，它们表明可以将外源血红素掺入新形成的载脂细胞色素P-450中。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号