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肾上腺切除术可增强肝脏中血红素加氧酶的诱导作用及细胞色素P-450的降解。

Adrenalectomy enhances the induction of heme oxygenase and the degradation of cytochrome P-450 in liver.

作者信息

Sardana M K, Sassa S, Kappas A

出版信息

J Biol Chem. 1980 Dec 10;255(23):11320-3.

PMID:6893709
Abstract

The induction of hepatic heme oxygenase in response to cobaltous chloride (CoCl2) administration was examined in normal, sham-operated, and adrenalectomized rats. The basal level of heme oxygenase was elevated about 2-fold in adrenalectomized rats as compared to normal controls or sham-operated animals. The extent of heme oxygenase induction by CoCl2 was also increased about 2-fold above normal in adrenalectomized animals and was accompanied by an enhanced breakdown of cytochrome P-450. The initial decline (approximately 2 h) and the late rebound increase (approximately 16 h) of delta-aminolevulinate synthase activity caused by the metal administration were, however, similar for all three groups of animals. Hydrocortisone is known to restore the impaired inducibility of delta-aminolevulinate synthase by allylisopropylacetamide in adrenalectomized rats. In this study, treatment with hydrocortisone prevented the exaggerated metal induction of heme oxygenase but did not affect the associated initial decline or the late rebound of delta-aminolevulinate synthase. These data indicate that hydrocortisone and adrenalectomy can significantly influence the extent of the induction of heme oxygenase produced by CoCl2, but that both the initial decline and the rebound induction of delta-aminolevulinate synthase associated with this metal treatment are apparently independent of these endocrine controls.

摘要

在正常大鼠、假手术大鼠和肾上腺切除大鼠中,研究了给予氯化钴(CoCl₂)后肝血红素加氧酶的诱导情况。与正常对照组或假手术动物相比,肾上腺切除大鼠的血红素加氧酶基础水平升高了约2倍。肾上腺切除动物中,CoCl₂诱导血红素加氧酶的程度也比正常水平增加了约2倍,同时细胞色素P - 450的分解增强。然而,对于所有三组动物,金属给药引起的δ-氨基乙酰丙酸合酶活性的初始下降(约2小时)和后期反弹增加(约16小时)是相似的。已知氢化可的松可恢复肾上腺切除大鼠中烯丙基异丙基乙酰胺对δ-氨基乙酰丙酸合酶诱导能力的损害。在本研究中,氢化可的松治疗可防止金属对血红素加氧酶的过度诱导,但不影响δ-氨基乙酰丙酸合酶相关的初始下降或后期反弹。这些数据表明,氢化可的松和肾上腺切除术可显著影响CoCl₂产生的血红素加氧酶诱导程度,但与这种金属处理相关的δ-氨基乙酰丙酸合酶的初始下降和反弹诱导显然与这些内分泌控制无关。

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