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阿片受体功能可能通过氧化还原机制进行调节。

Opiate receptor function may be modulated through an oxidation-reduction mechanism.

作者信息

Marzullo G, Hine B

出版信息

Science. 1980 Jun 6;208(4448):1171-3. doi: 10.1126/science.6246583.

DOI:10.1126/science.6246583
PMID:6246583
Abstract

Cupric ion, a thiol oxidant, caused naloxone-reversible analgesia when injected intracerebroventricularly in mice; its potency was close to that of morphine. Dithiothreitol, a thiol reductant, reversed the analgesia induced by cupric ion and antagonized analgesia induced by morphine. Oxidized dithiothreitol had no effect. These findings, together with evidence for redox modification of opiate receptor binding in vitro, suggest that a mechanism of oxidation-reduction of thiols may modulate opiate receptor function.

摘要

铜离子是一种硫醇氧化剂,当向小鼠脑室内注射时会引起纳洛酮可逆性镇痛;其效力与吗啡相近。二硫苏糖醇是一种硫醇还原剂,可逆转铜离子诱导的镇痛作用,并拮抗吗啡诱导的镇痛作用。氧化型二硫苏糖醇则无此作用。这些发现,连同体外阿片受体结合的氧化还原修饰证据,表明硫醇的氧化还原机制可能调节阿片受体功能。

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Opiate receptor function may be modulated through an oxidation-reduction mechanism.阿片受体功能可能通过氧化还原机制进行调节。
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2
Opiate analgesia: evidence for mediation by a subpopulation of opiate receptors.
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Suppression of GABA(B) receptor function in vivo by disulfide reducing agent, DL-dithiothreitol (DTT).二硫键还原剂DL-二硫苏糖醇(DTT)对体内GABA(B)受体功能的抑制作用。
Psychopharmacology (Berl). 2004 Jul;174(2):283-90. doi: 10.1007/s00213-003-1737-y.
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Anti-Rho(D) IgG binds to band 3 glycoprotein of the human erythrocyte membrane.抗Rho(D)免疫球蛋白与人红细胞膜的带3糖蛋白结合。
Proc Natl Acad Sci U S A. 1981 May;78(5):2898-902. doi: 10.1073/pnas.78.5.2898.
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Changes in the redox state of neuroblastoma cells after manganese exposure.
Arch Toxicol. 1983 Sep;54(1):53-9. doi: 10.1007/BF00277815.
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Opioids stimulate sarcolemmal NAD(P)H-vanadate dehydrogenase activity.阿片类药物刺激肌膜烟酰胺腺嘌呤二核苷酸(磷酸)钒酸盐脱氢酶活性。
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Copper complexes of non-steroidal antiinflammatory agents: analgesic activity and possible opioid receptor activation.
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Effect of latent iron deficiency on metal levels of rat brain regions.潜在铁缺乏对大鼠脑区金属水平的影响。
Biol Trace Elem Res. 1989 Nov;22(2):141-52. doi: 10.1007/BF02916645.