Galbraith R A, Sassa S, Fujita H
Rockefeller University Hospital, New York, NY 10021.
Biochem Biophys Res Commun. 1988 Jun 16;153(2):869-74. doi: 10.1016/s0006-291x(88)81176-8.
Dimethyl sulfoxide (DMSO) treatment of human HepG2 hepatoma cells increases the activity and the concentration of delta-aminolevulinic acid dehydratase (ALAD) to a comparable degree. Results of experiments with transcriptional inhibitors suggest that the increase in ALAD reflects de novo synthesis of the enzyme resulting from transcriptional activation. Commitment to increased ALAD activity in HepG2 cells is seen after 18 hr and complete by 48 hr. In contrast to the effects on ALAD, DMSO decreases the activities of porphobilinogen deaminase and uroporphyrinogen decarboxylase.
用二甲基亚砜（DMSO）处理人肝癌HepG2细胞，可使δ-氨基-γ-酮戊酸脱水酶（ALAD）的活性和浓度提高到相当程度。转录抑制剂实验结果表明，ALAD的增加反映了转录激活导致的该酶从头合成。在18小时后可观察到HepG2细胞中ALAD活性增加，并在48小时时达到完全增加。与对ALAD的影响相反，DMSO会降低胆色素原脱氨酶和尿卟啉原脱羧酶的活性。
