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The estimation of 5-hydroxytryptamine (serotonin) in biological tissues.生物组织中5-羟色胺(血清素)的测定。
J Biol Chem. 1955 Jul;215(1):337-44.
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Metabolism of 5-hydroxytryptamine (serotonin) by monoamine oxidase.
Proc Soc Exp Biol Med. 1955 May;89(1):36-8. doi: 10.3181/00379727-89-21707.
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A SENSITIVE METHOD FOR SPECTROPHOTOFLUOROMETRIC ASSAY OF CATECHOLAMINES.一种用于儿茶酚胺分光光度荧光测定的灵敏方法。
Int J Neuropharmacol. 1964 Dec;3:643-9. doi: 10.1016/0028-3908(64)90089-9.
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TYROSINE HYDROXYLASE. THE INITIAL STEP IN NOREPINEPHRINE BIOSYNTHESIS.酪氨酸羟化酶。去甲肾上腺素生物合成的起始步骤。
J Biol Chem. 1964 Sep;239:2910-7.
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EFFECTS OF DISULFIRAM ON TISSUE NOREPINEPHRINE CONTENT AND SUBCELLULAR DISTRIBUTION OF DOPAMINE, TYRAMINE AND THEIR BETA-HYDROXYLATED METABOLITES.双硫仑对组织去甲肾上腺素含量以及多巴胺、酪胺及其β-羟化代谢产物亚细胞分布的影响
Life Sci (1962). 1964 Jul;3:769-75. doi: 10.1016/0024-3205(64)90032-3.
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INHIBITION OF DOPAMINE-BETA-HYDROXYLASE BY DISULFIRAM.双硫仑对多巴胺-β-羟化酶的抑制作用
Life Sci (1962). 1964 Jul;3:763-7. doi: 10.1016/0024-3205(64)90031-1.
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Metabolism of norepinephrine-H3 released by tyramine and reserpine.由酪胺和利血平释放的去甲肾上腺素-H3的代谢
J Pharmacol Exp Ther. 1962 Dec;138:351-9.
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The action of carbon disulphide on cerebral monoamine oxidase.二硫化碳对脑单胺氧化酶的作用。
Med Lav. 1961 Jan;52:1-10.
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Biochemical mechanisms in chronic carbon disulfide poisoning.慢性二硫化碳中毒的生化机制
Am Ind Hyg Assoc J. 1959 Aug;20(4):303-23. doi: 10.1080/00028895909343722.
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Interaction of drugs with norepinephrine in the brain.
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二硫化碳暴露对大鼠脑内儿茶酚胺的影响。

The effects of carbon disulphide exposure on brain catecholamines in rats.

作者信息

Magos L

出版信息

Br J Pharmacol. 1970 May;39(1):26-33. doi: 10.1111/j.1476-5381.1970.tb09552.x.

DOI:10.1111/j.1476-5381.1970.tb09552.x
PMID:5420143
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1703024/
Abstract
  1. Rats exposed to 2.0 mg/1. carbon disulphide (CS(2)) in the inspired air for 2 days, 4 h a day, showed a 13% decrease in their brain noradrenaline concentration and a 16% increase in their brain dopamine concentration.2. After exposure for 5 or 10 days there was a further decrease in the concentration of noradrenaline in the brain, but brain dopamine returned to the control level.3. In animals treated intraperitoneally with 2.0 mg/kg reserpine and exposed 2 and 3 days later to 2.0 mg/1. CS(2) for 4 h per day, the brain dopamine concentration showed a 77% increase compared with the unexposed reserpinized animals, but the noradrenaline concentration remained unchanged.4. The dopamine concentrations in the adrenals after 10 days' exposure to 2.0 mg/1. CS(2) were 67% to 100% higher than in the control animals. In reserpinized rats, 2 days' exposure to CS(2) nearly trebled the dopamine content of adrenals.5. Exposure to CS(2) had no effect on the tyrosine concentration in the brain, and there was no change in the brain monoamine oxidase (MAO) activity. Tyrosine in the brain showed a 30 to 96% increase in concentration and MAO activity, using kynuramine as substrate, showed an approximately 5% increase 0.5 to 2 h after the subcutaneous administration of 500 mg/kg sodium diethyldithiocarbamate.6. CS(2) at 10(-2)M or lower concentrations had no inhibitory effect on the brain MAO activity in vitro. Diethyldithiocarbamate inhibited MAO at 10(-2)M, but not at 10(-3)M or lower concentrations.
摘要
  1. 每天吸入含2.0毫克/升二硫化碳(CS₂)的空气4小时,持续2天的大鼠,其脑内去甲肾上腺素浓度降低了13%,脑内多巴胺浓度升高了16%。

  2. 暴露5天或10天后,脑内去甲肾上腺素浓度进一步降低,但脑内多巴胺恢复到对照水平。

  3. 腹腔注射2.0毫克/千克利血平,2天和3天后每天吸入2.0毫克/升CS₂,持续4小时的动物,与未暴露于CS₂的利血平处理动物相比,脑内多巴胺浓度升高了77%,但去甲肾上腺素浓度保持不变。

  4. 暴露于2.0毫克/升CS₂ 10天后,肾上腺中的多巴胺浓度比对照动物高67%至100%。在利血平化的大鼠中,暴露于CS₂ 2天使肾上腺中的多巴胺含量增加了近两倍。

  5. 暴露于CS₂对脑内酪氨酸浓度没有影响,脑内单胺氧化酶(MAO)活性也没有变化。皮下注射500毫克/千克二乙基二硫代氨基甲酸钠后0.5至2小时,脑内酪氨酸浓度升高了30%至96%,以犬尿胺为底物时MAO活性升高了约5%。

  6. 浓度为10⁻²M或更低的CS₂在体外对脑MAO活性没有抑制作用。二乙基二硫代氨基甲酸盐在10⁻²M时抑制MAO,但在10⁻³M或更低浓度时不抑制。