One theory is that it's an autoimmune reaction attacking the body's glutamic acid decarboxylase (GAD) protein.

一种理论认为这是一种攻击人体谷氨酸脱羧酶（GAD）蛋白的自身免疫反应。

Afterwards, hydroxymethylbilane is converted to Uroporphyrinogen III and catalyzed to coproporphrinogen III, via uroporphyrinogen III co-synphase and uroporphyrinogen decarboxylase respectively.

之后，羟甲基胆色烷转化为尿卟啉原III，并分别通过尿卟啉原Ⅲ共合酶与尿卟啉原脱羧酶催化形成粪卟啉原Ⅲ。

Afterwards, hydroxymethylbilane is converted to uroporphyrinogen III and catalyzed to coproporphyrinogen III via uroporphyrinogen III cosynthase and uroporphyrinogen decarboxylase, respectively.

之后，羟甲基胆素通过尿卟啉原III协同合成酶转化为尿卟啉原III，再由尿卟啉原脱羧酶催化为粪卟啉原III。

This is exactly why levodopa is administered with carbidopa, a dopa decarboxylase inhibitor that isn't able to cross the blood-brain barrier.

这也就是左旋多巴要和卡比多巴共用的原因；卡比多巴是一种不能通过血脑屏障的多巴脱羧酶抑制剂。

Because of this, Levodopa must be administered with another agent called Carbidopa, which inhibits dopamine decarboxylase and thus reduces metabolism of Levodopa in the periphery.

因此，左旋多巴必须与另一种叫做卡比多巴的药物一起使用抑制多巴胺脱羧酶，从而减少左旋多巴在外周的代谢。

Dopamine itself can't cross the blood-brain barrier, but its precursor levodopa can, and once in the brain, levodopa is converted to dopamine by dopa decarboxylase, most importantly within the remaining nigrostriatal neurons.

多巴胺本身不能通过血脑屏障，但它的前体左旋多巴可以，一旦进入脑中，左旋多巴就会被多巴脱羧酶转换为多巴胺，尤其是在残存的黑质纹状体神经元内。

In the second step, the L-dopa formed by tyrosine hydroxylation is quickly decarboxylated by another enzyme called aromatic L-amino acid decarboxylase (AADC), to the neurotransmitter dopamine.

在第二步中，由酪氨酸羟基化形成的L-多巴通过酶快速脱羧另一种称为芳香族L-氨基酸脱羧酶（AADC）的神经递质多巴胺。

Peripheral dopa decarboxylase also exists, which can metabolize levodopa into dopamine before it gets through the blood brain barrier, and—via additional enzymes— metabolize it into other catecholamines like epinephrine, which can cause unwanted side effects like arrhythmias.

体内还有外周多巴脱羧酶，可以在左旋多巴穿过血脑屏障前将其转换为多巴胺；然后，通过其他酶将其转换为其他儿茶酚胺，如肾上腺素，它可以导致不良的副作用，如心律失常。