Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Chemical carcinogens metabolism

Covalent binding of chemical carcinogens to cellular macromolecules, DNA, RNA and protein, is wel1-accepted to be the first step in the tumor initiation process ( 1, 2). Most carcinogens, including polycyclic aromatic hydrocarbons (PAH), require metabolic activation to produce the ultimate electrophilic species which react with cellular macromolecules. Understanding the mechanisms of activation and the enzymes which catalyze them is critical to elucidating the tumor initiation process. [Pg.293]

Wattenberg LW. 1975. Effects of dietary constituents on the metabolism of chemical carcinogens. Cancer Res 35(11) 3326—3331. [Pg.50]

A snbstantial body of experimental evidence indicates that the formation of a covalent bond between chemical carcinogens and cellnlar macromolecnles represents the first critical step in the multistage process, eventually leading to tumor formation (see Geacintov et al. 1997, references therein). Most chemical carcinogens are not active on their own, but require metabolic activation to produce reactive intermediates capable of binding covalently with target macromolecnles, particularly with deoxyribonucleic acid (DNA), and thereby, initiate cancer. [Pg.186]

Nitrosamines, like many other classes of chemical carcinogens must undergo metabolic transformation to be converted into elect-... [Pg.133]

Miller, E.C. and Miller, J.A., "The Metabolism of Chemical Carcinogens to Reactive Electrophiles and Their Possible Mechanisms of Action in Carcinogenesis", Am. Cliem. Soc. Monograph, 1976, 173, 737-762. [Pg.150]

There are almost no data available concerning the pharmacokinetics (i.e., the uptake, distribution, metabolisms, and excretion) of chemical carcinogens in humans. Nevertheless, it is possible to make limited assumptions about the pharmacokinetics of carcinogens, based on the results of animal studies conducted with various chemicals, notably polycyclic hydrocarbons such as benzo[a]p3nene. [Pg.36]

As discussed in detail in Section 5, with chemical carcinogens, the route of exposure can be an important determinant of the site of cancer induction, particularly with direct-acting carcinogens which may act at the initial point of contact. For the majority of carcinogens, however, which require metabolic activation, the location in the body of activating enzymes is thought to be the major determinant of the site of carcinogenesis. [Pg.68]

Weisburger, J.H. and Wiluams, G.M. (1975). Metabolism of chemical carcinogens, page 185 in Cancer A Comprehensive Theatise VoL I., Becker,... [Pg.160]

The review of all structural classes of chemical carcinogens and SAR analyses of the effects of chemical reactivity, molecular geometry, and metabolism on... [Pg.378]

Woo, Y.-T., Arcos, J.C. and Lai, D.Y. (1988) Metabolic and chemical activation of carcinogens an overview, in Chemical Carcinogens Activation Mechanisms, Structural and Electronic Factors, and Reactivity (eds P. Politzer and F.J. Martin), Elsevier, Amsterdam, pp. 1-31. [Pg.405]

Miller EC, Miller JA. The metabolism of chemical carcinogens to reactive electrophiles and their possible mechanism of action in carcinogenesis. In Searle CE, ed. Chemical Carcinogens. Washington D.C. American Chemical Society, 1976. A seminal article by the original authors of this important concept. [Pg.291]

There is some evidence that the form of the chemical carcinogen that ultimately reacts with cellular macromolecules must contain a reactive electrophilic center, that is. an electron-deficient atom that can attack the numerous electron-rich centers in polynucleotides and proteins. As examples, significant electrophilic centers include free radicals, carbonium ions, epoxides, the nitrogen in esters of hydroxylamines and hydroxamic acids, and some metal cations. It is believed that carcinogens, which in themselves are not electrophiles, are metabolized to electrophilic derivatives that then become the ultimate" carcinogens. [Pg.296]

Most chemical carcinogens are not active on their own, but require metabolic activation to produce reactive intermediates capable of binding covalently to target macromolecules, in particular DNA, and thereby initiate cancer. [Pg.181]

In the 1940s and 1950s the pioneering studies of James and Elizabeth Miller provided early evidence for in vivo conversion of chemical carcinogens to reactive metabolites. They found that reactive metabolites of the aminoazo dye A, /V-dimcthyl-4-aminoazobenzene (DAB), a hepatocarcinogen in rats, would bind covalently to proteins and nucleic acids. The term, metabolic activation, was coined by the Millers to describe this process. Moreover they demonstrated that covalent binding of these chemicals was an essential part of the carcinogenic process. [Pg.149]

Gonzalez, F. J., and H. V. Gelboin. Role of human cytochromes P450 in the metabolic activation of chemical carcinogens and toxins. Drug Metabol. Rev. 26 165-183, 1994. [Pg.161]


See other pages where Chemical carcinogens metabolism is mentioned: [Pg.62]    [Pg.62]    [Pg.313]    [Pg.86]    [Pg.626]    [Pg.23]    [Pg.55]    [Pg.17]    [Pg.192]    [Pg.198]    [Pg.304]    [Pg.355]    [Pg.5]    [Pg.1361]    [Pg.154]    [Pg.4]    [Pg.33]    [Pg.1361]    [Pg.10]    [Pg.12]    [Pg.12]    [Pg.31]    [Pg.42]    [Pg.43]    [Pg.44]    [Pg.47]    [Pg.157]    [Pg.376]    [Pg.376]    [Pg.382]    [Pg.382]    [Pg.385]    [Pg.223]    [Pg.335]    [Pg.406]   
See also in sourсe #XX -- [ Pg.37 ]




SEARCH



Carcinogen metabolism

Carcinogenic Chemicals metabolic reactions

Carcinogenic chemicals

Carcinogens, chemical

Chemical carcinogenicity

Chemical carcinogenity

Metabolic Activation of Chemical Carcinogens and DNA Adduct Formation

Metabolic carcinogenicity

Metabolic carcinogens

© 2024 chempedia.info