Xu Juan, Zhou Jing, Sheng Jianchun, Fang Yong, Li Feng, Sun Guiju, Hu Qiuhui
College of Food Science and Technology, Nanjing Agricultural University, Nanjing 210095, Institute of Supervision and Inspection on Product Quality, Lianyungang Bureau of Quality and Technical Supervision, Lianyungang 222000, People's Republic of China.
J Agric Food Chem. 2008 May 28;56(10):3869-75. doi: 10.1021/jf073063a. Epub 2008 Apr 25.
Previously, the antioxidant activity of Se-enriched green tea extracts has been studied in vitro. In the present study, an in vivo micronuclei test was employed to assess the antimutagenic effect of microsized Se-enriched green tea powder (MSTP) in mice bone marrow. Pretreatments of MSTP, micrometer-sized regular tea powder (MRTP), selenite, and MRTP + selenite were given by gavage for 29 consecutive days prior to cyclophoshamide (CP) treatment. Certain key antioxidant enzymes were also investigated to elucidate the mechanism of antimutagenic effect. Results indicated that MSTP and MRTP or selenite alone did not significantly induce micronuclei at either concentration, confirming its nonmutagenicity. In the CP-treated groups, significant suppressions in the micronuclei were recorded following pretreatment with MSTP, MRTP, and selenite administration. The antimutagenic effect of MSTP was evidently observed by significant reduction in the frequencies of micronuclei in bone marrow cells when compared to a positive control group. The administration of MSTP, selenite, and MRTP + selenite also increased the levels of selenium concentration, glutathione peroxidase (GPx), and superoxide dismutase (SOD) enzymes in both blood and liver. However, no pronounced differences in activities of GPx and SOD were found among MSTP, selenite, and MRTP + selenite. The present findings demonstrate that the antimutagenic potential of MSTP could not be solely related to the enhancment of antioxidant enzymes of GPx and SOD.
此前，已对富硒绿茶提取物的抗氧化活性进行了体外研究。在本研究中，采用体内微核试验评估微米级富硒绿茶粉（MSTP）对小鼠骨髓的抗诱变作用。在环磷酰胺（CP）处理前，连续29天通过灌胃给予MSTP、微米级普通茶粉（MRTP）、亚硒酸盐以及MRTP + 亚硒酸盐进行预处理。还研究了某些关键抗氧化酶以阐明抗诱变作用的机制。结果表明，单独的MSTP、MRTP或亚硒酸盐在任何浓度下均未显著诱导微核，证实其无诱变性。在CP处理组中，用MSTP、MRTP和亚硒酸盐预处理后，微核率显著降低。与阳性对照组相比，骨髓细胞微核频率显著降低，明显观察到MSTP的抗诱变作用。给予MSTP、亚硒酸盐和MRTP + 亚硒酸盐还提高了血液和肝脏中硒浓度、谷胱甘肽过氧化物酶（GPx）和超氧化物歧化酶（SOD）的水平。然而，在MSTP、亚硒酸盐和MRTP + 亚硒酸盐之间，GPx和SOD的活性没有明显差异。目前的研究结果表明，MSTP的抗诱变潜力不能仅仅归因于GPx和SOD抗氧化酶的增强。
