Visser O, van den Berg J W, Koole-Lesuis H, Voortman G, Wilson J H
Department of Internal Medicine II, Erasmus University Rotterdam, The Netherlands.
Toxicology. 1991 Mar 25;67(1):75-83. doi: 10.1016/0300-483x(91)90165-w.
Experiments were carried out to investigate the possibility of inducing porphyria in human hepatocytes and HepG2 cells in culture. After treatment with hexachlorobenzene, 3-methylcholanthrene, phenobarbital or dimethyl sulfoxide, protoporphyrin was the predominating porphyrin accumulating in presence of delta-aminolevulinic acid. The typical uroporphyrin accumulation, as is seen in hexachlorobenzene-induced porphyria in vivo, was absent. In HepG2 cells, the activities of uroporphyrinogen decarboxylase and porphobilinogen deaminase were not influenced by cytochrome P-450 inducers, hexachlorobenzene or dimethyl sulfoxide during 48 h of culture. Therefore, the use of these cells in the study of porphyria cutanea tarda does not seem promising.
开展了实验以研究在培养的人肝细胞和HepG2细胞中诱导卟啉症的可能性。在用六氯苯、3-甲基胆蒽、苯巴比妥或二甲基亚砜处理后，在δ-氨基-γ-酮戊酸存在的情况下，原卟啉是积累的主要卟啉。未出现体内六氯苯诱导的卟啉症中所见的典型尿卟啉积累。在HepG2细胞中，在48小时培养期间，尿卟啉原脱羧酶和胆色素原脱氨酶的活性不受细胞色素P-450诱导剂、六氯苯或二甲基亚砜的影响。因此，将这些细胞用于迟发性皮肤卟啉症的研究似乎没有前景。
