Krishna G, Nath J, Ong T
Cancer Res. 1986 Jun;46(6):2670-4.
Ascorbic acid (vitamin C) is known to act as an antimutagen and anticarcinogen in several test systems. However, there is no report of its effect on carcinogen-induced chromosomal damage in vivo in animals. The present study was performed to determine whether or not ascorbic acid affects sister chromatid exchanges (SCEs) induced by cyclophosphamide (CPA) and mitomycin C (MMC) in bone marrow and spleen cells in mice. The results indicate that ascorbic acid per se did not cause a significant increase in SCEs in mice. However, increasing concentrations of ascorbic acid caused decreasing levels of CPA- and MMC-induced SCEs in both cell types in vivo. At the highest concentration of ascorbic acid, 6.68 g/kg, approximately 75 and 40% SCE inhibition in both cell types was noted for CPA and MMC, respectively. Likewise, under in vivo/in vitro conditions (exposure of animals to experimental chemicals followed by culturing of cells), ascorbic acid caused a dose-related decrease in CPA- and MMC-induced SCEs, up to a dose of 3.34 g/kg At this concentration, approximately 50% CPA- and MMC-induced SCE inhibition was observed in both cell types studied. Thus, ascorbic acid acts as an anti-SCE agent in both in vivo and in vivo/in vitro conditions in mice.
已知抗坏血酸（维生素C）在多个测试系统中作为抗诱变剂和抗癌剂发挥作用。然而，尚无关于其对动物体内致癌物诱导的染色体损伤影响的报道。进行本研究以确定抗坏血酸是否会影响环磷酰胺（CPA）和丝裂霉素C（MMC）在小鼠骨髓和脾细胞中诱导的姐妹染色单体交换（SCE）。结果表明，抗坏血酸本身并未导致小鼠SCE显著增加。然而，在体内，抗坏血酸浓度增加导致两种细胞类型中CPA和MMC诱导的SCE水平降低。在抗坏血酸最高浓度6.68 g/kg时，两种细胞类型中CPA和MMC诱导的SCE抑制率分别约为75%和40%。同样，在体内/体外条件下（动物接触实验化学品后培养细胞），抗坏血酸导致CPA和MMC诱导的SCE呈剂量相关下降，直至剂量为3.34 g/kg。在此浓度下，在所研究的两种细胞类型中均观察到约50%的CPA和MMC诱导的SCE抑制。因此，在小鼠体内和体内/体外条件下，抗坏血酸均作为抗SCE剂发挥作用。
