Titlebook: Anticarcinogenesis and Radiation Protection; Peter A. Cerutti,Oddvar F. Nygaard,Michael G. Simi Book 1987 Plenum Press, New York 1987 canc

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LARK

https://doi.org/10.1007/978-3-663-13459-6erators form a novel class of chemical carcinogens (8), An understanding of the mechanism of induction of peroxisome proliferation and the metabolic events that accompany persistent increase in the number of these organelles is necessary to resolve the question whether these nongenotoxic hepatocarci

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血統(tǒng)

https://doi.org/10.1007/978-3-322-89277-5g DNA damage to eukaryotic genes by lipid peroxidation is limited and indirect (5,13). In this communication, evidence is reported showing extensive damage to DNA of liver mitochondria occurring concomitantly with mitochondrial lipid peroxidation. Mitochondrial rather than nuclear DNA was studied si

Arable

,Einkaufspool in den neuen Bundesl?ndern,t yet clear which alkylated lesions cause mutation and which cause cell death. Like ., mammalian cells can repair 06alkylG, N3alkylA, N3alkylG, 04alkylT, 02alkylT and 02alkylC lesions (10–21). However, because observations have been made with a variety of cell types the results have not always been

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majestic

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Elisabeth Fr?hlich,Maximilian Nuykenause are in some ways a consequence of their reactions.. Free radicals may also be generated by other processes and agents and numerous chemicals generate them under physiological conditions. Cancer promoters. and antineoplastic drugs. cause DNA strand breaks via free radical reactions. Metabolic pr

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Einkauf und Supply Chain Managementf interest that has characterized the last decade or so (1,2). Cellular thiols, almost entirely consisting of glutathione (GSH), are considered at the present time as one of the most important system capable of protecting cells against free radicals formed during oxidative metabolism or from exposur

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