Mizote A, Okazaki Y, Iqbal M, Okada S
Faculty of Medicine, Department of Pathological Research, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
Hum Exp Toxicol. 2008 Mar;27(3):207-14. doi: 10.1177/0960327107087795.
We have evaluated the effect of dietary antioxidant, antioxidant biofactor (a processed grain food), on iron nitrilotriacetate-induced renal tumorigenesis, hyperproliferative response, and oxidative damage. In tumorigenesis studies, iron nitrilotriacetate alone treatment resulted in a development of 75% renal cell tumor incidence, whereas, in the group of animals fed with antioxidant biofactor diet and treated with iron nitrilotriacetate, only 43% of renal cell tumor incidence was observed. In oxidative damage studies, the decrease in the level of renal glutathione and antioxidant enzymes induced by iron nitrilotriacetate was significantly reversed by antioxidant biofactor diet pretreatment in a dose-dependent manner (18-71% recovery, P < 0.05). Antioxidant biofactor diet pretreatment also resulted in a dose-dependent inhibition (35-49% inhibition, P < 0.05) of iron nitrilotriacetate-induced lipid peroxidation as measured by thiobarbituric acid reactive substances formation in renal tissues. Similarly, in hyperproliferation studies, antioxidant biofactor diet pretreatment showed a strong inhibition of iron nitrilotriacetate-induced renal ornithine decarboxylase activity (18-54% inhibition, P < 0.05). In addition, antioxidant biofactor fed diet pretreatment also protected the kidney tissues against observed histopathological alterations. From this data, it can be concluded that antioxidant biofactor diet can abrogate the toxic and tumor promoting effects of iron nitrilotriacetate and can serve as a potent chemopreventive agent to suppress oxidant-induced tissue injury and tumorigenesis.
我们评估了膳食抗氧化剂——抗氧化生物因子(一种加工谷物食品)对次氮基三乙酸铁诱导的肾肿瘤发生、过度增殖反应和氧化损伤的影响。在肿瘤发生研究中,单独使用次氮基三乙酸铁治疗导致肾细胞肿瘤发生率达75%,而在喂食抗氧化生物因子饮食并接受次氮基三乙酸铁治疗的动物组中,仅观察到43%的肾细胞肿瘤发生率。在氧化损伤研究中,抗氧化生物因子饮食预处理以剂量依赖方式(恢复率18 - 71%,P < 0.05)显著逆转了次氮基三乙酸铁诱导的肾谷胱甘肽水平和抗氧化酶的降低。抗氧化生物因子饮食预处理还导致次氮基三乙酸铁诱导的脂质过氧化呈剂量依赖性抑制(抑制率35 - 49%,P < 0.05),这通过肾组织中硫代巴比妥酸反应性物质的形成来衡量。同样,在过度增殖研究中,抗氧化生物因子饮食预处理显示出对次氮基三乙酸铁诱导的肾鸟氨酸脱羧酶活性有强烈抑制作用(抑制率18 - 54%,P < 0.05)。此外,喂食抗氧化生物因子饮食预处理还保护肾组织免受观察到的组织病理学改变的影响。根据这些数据,可以得出结论,抗氧化生物因子饮食可以消除次氮基三乙酸铁的毒性和促肿瘤作用,并可作为一种有效的化学预防剂来抑制氧化剂诱导的组织损伤和肿瘤发生。