Bräutigam M, Kittner B, Herken H
Eur J Pharmacol. 1986 Aug 7;127(1-2):143-6. doi: 10.1016/0014-2999(86)90217-7.
It was reported that R(-)apomorphine and other catechols are potent inhibitors of dihydropteridine reductase in vitro. It was suggested that decreased levels of tetrahydrobiopterin may represent a mechanism by which R(-)apomorphine inhibits catecholamine synthesis in vivo. This paper demonstrates that tetrahydrobiopterin levels are not affected either in vitro (PC12 cells) or in vivo (rat liver and corpus striatum) by treatment with R(-)apomorphine, whereas DOPA (3,4-dihydroxyphenylalanine) production (PC12 cells, corpus striatum) is reduced. This indicates that R(-)apomorphine does not inhibit DOPA production by reducing 6(R)-L-erythro-tetrahydrobiopterin) levels.
据报道，R(-)阿扑吗啡和其他儿茶酚在体外是二氢蝶啶还原酶的有效抑制剂。有人提出，四氢生物蝶呤水平降低可能是R(-)阿扑吗啡在体内抑制儿茶酚胺合成的一种机制。本文证明，用R(-)阿扑吗啡处理后，无论是在体外（PC12细胞）还是在体内（大鼠肝脏和纹状体），四氢生物蝶呤水平均未受到影响，而多巴（3,4-二羟基苯丙氨酸）生成（PC12细胞、纹状体）减少。这表明R(-)阿扑吗啡不是通过降低6(R)-L-赤藓糖四氢生物蝶呤水平来抑制多巴生成的。
