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小鼠大脑中硫化氢的产生受睾酮和S-腺苷-L-甲硫氨酸的调节。

The production of hydrogen sulfide is regulated by testosterone and S-adenosyl-L-methionine in mouse brain.

作者信息

Eto Ko, Kimura Hideo

机构信息

National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8551, Japan.

出版信息

J Neurochem. 2002 Oct;83(1):80-6. doi: 10.1046/j.1471-4159.2002.01097.x.

Abstract

Hydrogen sulfide (H2S) is endogenously produced in the brain from L-cysteine by the enzyme cystathionine beta-synthase (CBS) and functions as a neuromodulator in the brain. H2S selectively enhances NMDA receptor-mediated responses and alters hippocampal long-term potentiation (LTP). The production of H2S is regulated by Ca2+/calmodulin-mediated pathways and is enhanced in response to neuronal excitation. In addition to this fast regulation, we describe here a slower form of the regulation of H2S production by testosterone and S-adenosyl-L-methionine (SAM), a CBS activator. Endogenous H2S in the mouse brain increases after birth, reaches a maximum level at 8 weeks and then decreases. Female brain contains less H2S than male brain at each age. A single administration of testosterone to female mice increases the endogenous H2S and SAM, which reach levels similar to those of male mice. In contrast, castration of male mice decreases the levels of testosterone, SAM and H2S in the brain. Administration of SAM once a day for 3 days increases the brain H2S without significantly changing the testosterone level. These observations suggest that testosterone can regulate the brain H2S level via changing the level of SAM.

摘要

硫化氢(H2S)在大脑中由L-半胱氨酸通过胱硫醚β-合酶(CBS)内源性产生,并在大脑中作为一种神经调节剂发挥作用。H2S选择性增强NMDA受体介导的反应并改变海马体长期增强效应(LTP)。H2S的产生受Ca2+/钙调蛋白介导的途径调节,并在神经元兴奋时增强。除了这种快速调节外,我们在此描述了一种由睾酮和CBS激活剂S-腺苷-L-甲硫氨酸(SAM)对H2S产生进行的较慢形式的调节。小鼠大脑中的内源性H2S在出生后增加,在8周时达到最高水平,然后下降。在每个年龄段,雌性大脑中的H2S含量都低于雄性大脑。对雌性小鼠单次注射睾酮会增加内源性H2S和SAM,使其达到与雄性小鼠相似的水平。相反,对雄性小鼠进行去势会降低大脑中睾酮、SAM和H2S的水平。连续3天每天注射一次SAM会增加大脑中的H2S,而不会显著改变睾酮水平。这些观察结果表明,睾酮可以通过改变SAM的水平来调节大脑中的H2S水平。

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