Enwonwu C O
Lancet. 1984 Oct 27;2(8409):956-8. doi: 10.1016/s0140-6736(84)91168-1.
Impaired activity of the liver microsomal mixed-function-oxidase (MFO) system is characteristic of protein malnutrition. It explains the accumulation of aflatoxin (AFB1) in livers of kwashiorkor victims, whose staple foods are usually heavily contaminated with this fungal toxin. Dietary rehabilitation of such children with high-protein foods not only increases the activity of the liver MFO system but also stimulates DNA replication and rapid regeneration of liver cells. Under such circumstances highly reactive metabolites of AFB1, such as the AFB1-epoxide, can produce malignant transformation of the cells by binding covalently with genetic macromolecules. Alternating cycles of food shortage and sufficiency, which usually characterise impoverished communities, and liver-cell hyperplasia stimulated by the non-genetic cytotoxic effects of AFB1 or parasitic infestation promote rapid replication of the transformed cells.
肝脏微粒体混合功能氧化酶（MFO）系统活性受损是蛋白质营养不良的特征。这解释了夸休可尔症患者肝脏中黄曲霉毒素（AFB1）的蓄积现象，这些患者的主食通常受到这种真菌毒素的严重污染。用高蛋白食物对这类儿童进行饮食康复治疗，不仅能提高肝脏MFO系统的活性，还能刺激DNA复制和肝细胞的快速再生。在这种情况下，AFB1的高活性代谢产物，如AFB1-环氧化物，可通过与遗传大分子共价结合而导致细胞发生恶性转化。食物短缺与充足交替循环的情况通常是贫困社区的特征，而AFB1的非遗传细胞毒性作用或寄生虫感染所刺激的肝细胞增生会促进转化细胞的快速复制。
