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作者复习近20年来北美及欧洲一系列有关精神分裂症生化变化及病因方面的文献,提出一种关于精神分裂症病因机制的假说:分裂症是色氨酸代谢的疾病,是由能引起烟酸生成减少和/或致精神病性代谢物贮积的广泛生化障碍而致病.假说的根据一、色氨酸代谢异常色氨酸(α-氨基-β-吲哚丙酸)是唯一含有吲哚核的、不能在人组织中产生的特殊氨基酸.在人类其正常降解途径有二,即:与吲哚核分开的色氨酸-烟酸代谢途径(下简称T-N途径),和保持吲哚核的其他途径.正常情况下,70～75%色氨酸通过T-N途径代谢为烟酸,并进一步转为烟酰胺.此二者均为NAD(辅酶I)及NADP(辅酶Ⅱ)的组成成分.辅酶Ⅰ、Ⅱ在还原反应中是氢的供给者,在氧化反应中是氢的受体;此外,也是线粒体的组成成分(线粒体是细胞能量的主要来源及细胞呼吸的主要场所).已知人体中有100个以上的反应需要此二辅酶.其次,少部分色氨酸在保
The author reviews the recent 20 years in North America and Europe, a series of biochemical changes and etiology of schizophrenia literature, put forward a hypothesis about the etiology of schizophrenia: schizophrenia is a tryptophan metabolism disease is caused by niacin Resulting in a reduction in and / or the release of psychotropic metabolites of a wide range of biochemical disorders and pathogenic hypothesis based on the abnormal tryptophan metabolism of tryptophan (α-amino-β-indole propionic acid) is the only containing indole Nuclear, can not be produced in human tissue special amino acids in humans its normal pathways for degradation of two, namely: separate from the indole nuclear tryptophan - nicotinic acid metabolism (hereinafter referred to as TN pathway), and to maintain indole Of the other pathways.70-75% tryptophan is normally metabolized to nicotinic acid via the TN pathway and further to nicotinamide, both of which are components of NAD (coenzyme I) and NADP (coenzyme II). Coenzymes I and II are suppliers of hydrogen in the reduction reaction and hydrogen receptors in the oxidation reaction, and are also the components of mitochondria (mitochondria are the main source of cell energy and the main site of cellular respiration) There are more than 100 reactions in need of these two supplements Secondly, a small number of tryptophan in Bulgaria