Titlebook: Biochemistry of Chemical Carcinogenesis; R. Colin Garner,Jan Hradec Book 1989 Plenum Press, New York 1989 Colon.DNA.Glutamat.Glutamin.bioc

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https://doi.org/10.1007/978-3-663-13239-4omotion with repeated RPA treatment. The conversion step is characterized by its half-life of 10 to 12 weeks (in NMRI mice) and its independence from initiation. For conversion the mitogenic capacity of TPA appears to be necessary in addition to a specific effect of TPA (by which TPA differs qualita

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https://doi.org/10.1007/978-3-322-85825-2 dietary habits in inducing cancers of the digestive tract. Foods contain various types of mutagens and carcinogens, and contain both initiators and promoters of carcinogenesis. In general mutagens and carcinogens in food may be A. naturally occurring constituents especially in edible plants or spic

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Cervical-Spine

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,Normalkosten — Zuschlagss?tze,vary (CHO) cells is biphasic. During the treatment of cell and early afterwards ALS are induced in DNA; they are removed from DNA by a repair mechanism with a half-life of about 3 hours. Between the 3rd and 6th hour after treatment, secondary ALS developed the repair of which had a half-life of 9 to

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https://doi.org/10.1007/978-3-658-42234-9llular genome and may thus lead to malignant transformation. Besides DNA, carcinogens are known to react also with proteins and RNA. It has been stated that RNA has even a greater propensity for the covalent reaction with carcinogens than DNA. Of various species of RNA, tRNA seems to be most frequen

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https://doi.org/10.1007/978-3-658-42234-9her fail to do so or even assist in its renaturation. The carcinogenic metals tend to keep the DNA unravelled when its two strands are annealed from around 80. to 2.C as studied by U.V. spectrophotometry. Studies on the interactions of carcinogenic metals with nucleic acid based have further reveale

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Aufbau der modernen Kostenrechnung,cer among human populations and its prevalence in individuals with specific occupations and habits has provided important clues on the etiology of the disease. Studies on the metabolism of potent chemical carcinogens in different cell types have identified active derivatives of many of these compoun

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Jürgen Christmann,Hans-Wilhelm Witthoffetitively inhibited by .-methyl-.-nitrosourea which has been previously demonstrated to alkylate guanine. It thus appears that the lipid reacts with guanosine residues in the molecule of tRNA.. Initiator tRNA preparations pretreated with cholesteryl 14-methylhexadecanoate were charged significantly