Ren J G, Zheng R L, Shi Y M, Gong B, Li J F
State Key Laboratory of Arid Agroecology, Lanzhou University, Lanzhou, 730000, P.R. China.
Cell Biol Int. 1998;22(1):41-9. doi: 10.1006/cbir.1998.0226.
The effects of oxidative stress (ascorbic acid-ferrous system) on the proliferation, differentiation and apoptosis of the human hepatoma cell SMMC-7721 were studied. Oxidative stress significantly inhibited cell proliferation and induced morphological differentiation. Whatever the indices related with cell malignancy, such as alpha-fetoprotein and c-glutamyltranspeptidase or the index related with cell differentiation, such as tyrosine-alpha-ketoglutarate transaminase, all inclined evidently to normalization. The tumour's clonogenic potential decreased significantly. Moreover, together with differentiation, the phenomenon of apoptosis was found by the appearance of apoptotic bodies, detached cells, and apoptotic morphological feature. Although, their DNA was not degraded into oligonucleosomal fragmentation, the DNA was cut into larger fragments (about 21.2 kbp) of a size associated with chromatin loops. These findings indicated that oxidative stress can induce both differentiation and apoptosis simultaneously in tumour cells. All the results showed that oxidative stress may initiate the tumour cells reverse transformation. The possible mechanism of the differentiation and apoptosis induced by oxidative stress may be related to the lipid peroxidation of cell membrane.
研究了氧化应激（抗坏血酸 - 亚铁体系）对人肝癌细胞SMMC - 7721增殖、分化和凋亡的影响。氧化应激显著抑制细胞增殖并诱导形态分化。无论与细胞恶性相关的指标，如甲胎蛋白和γ - 谷氨酰转肽酶，还是与细胞分化相关的指标，如酪氨酸 - α - 酮戊二酸转氨酶，均明显趋于正常化。肿瘤的克隆形成潜力显著降低。此外，随着分化的出现，通过凋亡小体、脱落细胞以及凋亡形态特征的出现发现了凋亡现象。虽然其DNA未降解为寡核小体片段，但DNA被切割成与染色质环相关大小的较大片段（约21.2 kbp）。这些发现表明氧化应激可在肿瘤细胞中同时诱导分化和凋亡。所有结果表明氧化应激可能引发肿瘤细胞的逆向转化。氧化应激诱导分化和凋亡的可能机制可能与细胞膜的脂质过氧化有关。
