Ren J G, Li J F, Zheng R L
Lanzhou University, Lanzhou 730000, P. R. China.
Shi Yan Sheng Wu Xue Bao. 1998 Sep;31(3):273-82.
The human hepatoma cells SMMC-7721 were treated with different concentrations of ascorbic acid (50-800 mumol/L) and FeSO4 (2.5-40 mumol/L) system to generate oxidative stress at various degrees. The oxidative stress induced by the system were mainly contributed to hydroxyl radical. All the various degrees of oxidative stress in this study are able to inhibit the proliferation of hepatoma cells. While low levels of oxidative stress may cause hepatoma cells lost some malignant features, such as aggregation of Con-A to the cell surface, alpha-fetoprotein, gamma-glutamyltransepeptidase and tyrosine-alpha-ketoglutarate transaminase, all of the 4 indices tended to cell differentiation, coloning efficiency potential decreased significantly, and apoptotic cells appeared. The numbers of apoptotic cells increased with the increasing of oxidative stress. The apoptotic cells exhibited non-adherent, smaller, chromatin condensed around the periphery of the nucleus in the shape of crescent, nuclear fragmentations but with intact cellular membrane, and DNA degraded to around 21.2 kbp fragment. All of the results showed that there is possibility to inhibit hepatoma cells growth, to promote differentiation and apoptosis, and therefore to initiate reverse transformation via strict regulation of oxidative stress.
将人肝癌细胞SMMC - 7721用不同浓度的抗坏血酸（50 - 800 μmol/L）和硫酸亚铁（2.5 - 40 μmol/L）体系处理，以产生不同程度的氧化应激。该体系诱导的氧化应激主要由羟基自由基引起。本研究中所有不同程度的氧化应激均能抑制肝癌细胞的增殖。低水平的氧化应激可能导致肝癌细胞丧失一些恶性特征，如刀豆球蛋白A在细胞表面的聚集、甲胎蛋白、γ - 谷氨酰转肽酶和酪氨酸 - α - 酮戊二酸转氨酶，这4项指标均倾向于细胞分化，克隆效率潜能显著降低，并出现凋亡细胞。凋亡细胞数量随氧化应激程度的增加而增多。凋亡细胞表现为不贴壁、体积较小、染色质浓缩于细胞核周边呈新月形、核碎裂但细胞膜完整，且DNA降解为约21.2 kbp的片段。所有结果表明，通过严格调控氧化应激，有可能抑制肝癌细胞生长、促进其分化和凋亡，从而启动逆转。
