Sakagami H, Asano K, Fukuchi K, Gomi K, Ota H, Kazama K, Tanuma S, Kochi M
First Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.
Anticancer Res. 1991 Jul-Aug;11(4):1533-8.
Intravenous administration of sodium benzylideneascorbate (SBA) rapidly necrotized inoperable human lung cancer, and induced degeneration of 3'-methyl-4-dimethylaminoazobenzene-induced rat hepatocellular carcinoma (vacuolar, eosinophilic degeneration, nuclear debris) without affecting the serum glutamic oxaloacetic transaminase, gamma-glutamyl transpeptidase and total protein levels. Cultured normal human lung and skin fibroblasts, and human glioma and glioblastoma cell lines were relatively resistant to SBA, when compared to human myelogenous leukemic cell lines. SBA had no apparent host immunopotentiation activity such as stimulation of cytokine action or production; activation of monocyte or polymorphonuclear cells; or modulation of poly (ADP-ribose) glycohydrolase activity. The data suggest that the antitumor activity of SBA might be produced by direct action of authentic SBA or its metabolized form(s), rather than by immunopotentiation of the hosts.
静脉注射亚苄基抗坏血酸钠（SBA）可使无法手术切除的人类肺癌迅速坏死，并诱导3'-甲基-4-二甲基氨基偶氮苯诱发的大鼠肝细胞癌发生变性（空泡变性、嗜酸性变性、核碎片），且不影响血清谷氨酸草酰乙酸转氨酶、γ-谷氨酰转肽酶和总蛋白水平。与人类骨髓白血病细胞系相比，培养的正常人肺和皮肤成纤维细胞以及人类神经胶质瘤和胶质母细胞瘤细胞系对SBA相对耐药。SBA没有明显的宿主免疫增强活性，如刺激细胞因子作用或产生；激活单核细胞或多形核细胞；或调节聚（ADP-核糖）糖水解酶活性。数据表明，SBA的抗肿瘤活性可能是由真实的SBA或其代谢形式的直接作用产生的，而不是通过宿主的免疫增强作用。
