The effects of selenium (Na_2SeO_3) on aflatoxin B_1 (AFB_1)-induced hepatic neoplasia were studied in the rat. Putative preneoplastic foci and nodules composed of basophilic, eosinophilic, and clear cells developed e...The effects of selenium (Na_2SeO_3) on aflatoxin B_1 (AFB_1)-induced hepatic neoplasia were studied in the rat. Putative preneoplastic foci and nodules composed of basophilic, eosinophilic, and clear cells developed early. Basophilic foci were seen first; in the later stages basophilic and eosinophilic nodules predominated. At each stage the AFB_1 + Se groups showed fewer and smaller foci and nodules than the AFB_1 -Se group. The number of foci in the AFB_1 + 3 ppm Se group and their mean area were smaller than those in the 6 ppm Se + AFB_1 group. At the end of the experiment hepatocellular carcinoma (HCC) was found in 11/18 rats (61%) of the AFB_1-Se group. HCC was not found in either of the groups given AFB_1 +Se. We conclude that Se had an inhibitory effect on the initiation and promotion stages of AFB_1-induced preneoplastic foci and nodules. Se also prevented progression of these nodules to HCC even after cessation of AFB_1 administration. The inhibitory effect of Se at 3 ppm was greater than at 6 ppm. The 6 ppm Se group also showed evidence of toxicity. 1990 Academic Press.Inc.展开更多
There is very convincing evidence that a high dietary level of selenium substantially reduces the incidence of a wide variety of animal cancers. The human epidemiological evidence is less clear cut, but overall sugges...There is very convincing evidence that a high dietary level of selenium substantially reduces the incidence of a wide variety of animal cancers. The human epidemiological evidence is less clear cut, but overall suggests that selenium may be protective: the evidence is strongest in men in relation to gastro-intestinal cancers. There is evidence that dietary selenium compounds reduce the formation of DNA adducts by carcinogens. Selenium compounds also inhibit growth in vitro and induce apoptosis. In general, there is a good correlation between the effectiveness of selenium compounds in chemoprevention and growth inhibition, implying that the mechanisms of growth inhibition and chemoprevention may be similar and that a major factor in the chemopreventive effects of selenium compounds in vivo is their ability to retard outgrowth of pre-malignant cells. Various hypotheses have been advanced as to how selenium compounds might prevent tumour cellgrowth. One is that they cause apoptosis by inducing oxidative stress. However, we have shown that the most potent selenium compound, selenodiglutathione (SDG), a natural metabolite of selenite, does not induce oxidative stress, at least not in the sarne way as other oxidants such as H2O2 and diamide. Firstly, a partially selenium-resistant variant cell line does not show increased resistance to H2O2. Moreover, SDG does not induce widespread tyrosine phosphorylation, including MAP and SAN kinases, like other oxidants such as H2O2 and diamide and its effects are not reversed by pretreatment with the tyrosine kinase inhibitor, herbimycin. Our experiments with the selenium-resistant variant suggest that a novel selenium-binding protein may be involved in growth inhibition by selenium展开更多
This study determined the effects of selenium on the growth of Fusorium strains and the effects of products extracted from the fungal cultures on relevant indicators of chondrocytes injury.
文摘The effects of selenium (Na_2SeO_3) on aflatoxin B_1 (AFB_1)-induced hepatic neoplasia were studied in the rat. Putative preneoplastic foci and nodules composed of basophilic, eosinophilic, and clear cells developed early. Basophilic foci were seen first; in the later stages basophilic and eosinophilic nodules predominated. At each stage the AFB_1 + Se groups showed fewer and smaller foci and nodules than the AFB_1 -Se group. The number of foci in the AFB_1 + 3 ppm Se group and their mean area were smaller than those in the 6 ppm Se + AFB_1 group. At the end of the experiment hepatocellular carcinoma (HCC) was found in 11/18 rats (61%) of the AFB_1-Se group. HCC was not found in either of the groups given AFB_1 +Se. We conclude that Se had an inhibitory effect on the initiation and promotion stages of AFB_1-induced preneoplastic foci and nodules. Se also prevented progression of these nodules to HCC even after cessation of AFB_1 administration. The inhibitory effect of Se at 3 ppm was greater than at 6 ppm. The 6 ppm Se group also showed evidence of toxicity. 1990 Academic Press.Inc.
文摘There is very convincing evidence that a high dietary level of selenium substantially reduces the incidence of a wide variety of animal cancers. The human epidemiological evidence is less clear cut, but overall suggests that selenium may be protective: the evidence is strongest in men in relation to gastro-intestinal cancers. There is evidence that dietary selenium compounds reduce the formation of DNA adducts by carcinogens. Selenium compounds also inhibit growth in vitro and induce apoptosis. In general, there is a good correlation between the effectiveness of selenium compounds in chemoprevention and growth inhibition, implying that the mechanisms of growth inhibition and chemoprevention may be similar and that a major factor in the chemopreventive effects of selenium compounds in vivo is their ability to retard outgrowth of pre-malignant cells. Various hypotheses have been advanced as to how selenium compounds might prevent tumour cellgrowth. One is that they cause apoptosis by inducing oxidative stress. However, we have shown that the most potent selenium compound, selenodiglutathione (SDG), a natural metabolite of selenite, does not induce oxidative stress, at least not in the sarne way as other oxidants such as H2O2 and diamide. Firstly, a partially selenium-resistant variant cell line does not show increased resistance to H2O2. Moreover, SDG does not induce widespread tyrosine phosphorylation, including MAP and SAN kinases, like other oxidants such as H2O2 and diamide and its effects are not reversed by pretreatment with the tyrosine kinase inhibitor, herbimycin. Our experiments with the selenium-resistant variant suggest that a novel selenium-binding protein may be involved in growth inhibition by selenium
基金funded by the Natural Science Basic Research Plan of Shaanxi Province,China(2014JM4170)the Department of disease control of Shaanxi Health and Family Planning Commission,China(2010/2012)
文摘This study determined the effects of selenium on the growth of Fusorium strains and the effects of products extracted from the fungal cultures on relevant indicators of chondrocytes injury.
