Advances in Molecular Toxicology by James C. Fishbein (Eds.)

By James C. Fishbein (Eds.)

Advances in Molecular Toxicology positive factors the most recent advances in all the subspecialties of the large sector of molecular toxicology. Toxicology is the research of toxins, and this sequence info the learn of the molecular foundation in which an unlimited array of brokers encountered within the human setting and produced through the human physique itself appear themselves as pollutants. no longer strictly restricted to documenting those examples, the sequence can also be curious about the complicated internet of chemical and organic occasions that provide upward thrust to toxin-induced indicators and illness. the hot applied sciences which are being harnessed to research and comprehend those occasions can be reviewed through top employees within the box. Advances in Molecular Toxicology will record development in all facets of those quickly evolving molecular features of toxicology with a view towards precise elucidation of either development at the molecular point and on advances in technological methods hired. * state of the art studies via best employees within the self-discipline. * In-depth dissection of molecular facets of curiosity to a extensive variety of scientists, physicians and any pupil within the allied disciplines. * innovative functions of technological suggestions in chemistry, biochemistry and molecular drugs.

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G. V. M. M. S. Lloyd, Error prone translesion synthesis past -hydroxy-propanodeoxyguanosine, the primary acrolein-derived adduct in mammalian cells, J. Biol. Chem. 277 (2002) 18257–18265. I. P. Pfeifer, A. Besaratinia, Lack of mutagenicity of acrolein-induced DNA adducts in mouse and human cells, Cancer Res. 67 (2007) 11640–11647. T. Wang, S. Zhang, Y. S. Tang, Mutagenicity and sequence specificity of acrolein-DNA adducts, Chem. Res. Toxicol. 22 (2009) 511–517. C. A. Harkin, Mutations at G:C base pairs predominate after replication of peroxyl radical-damaged pSP189 plasmids in human cells, Mutagenesis 14 (1999) 135–140.

01 Figure 4 HAA formation as a function of (A) cooking time and (B) temperature. Adapted fromTuresky et al. [6] with permission. of the exocyclic amine groups of the HAAs to produce the genotoxic N-hydroxy-HAA metabolites [50–52]. Hepatic P450 1A2 and extrahepatic P450s 1A1 and 1B1 are the principal P450s that catalyze this reaction. The N-hydroxy-HAA metabolites can directly react with DNA, but the penultimate carcinogenic species are thought to be acetate or sulfate esters of the N-hydroxy-HAAs, esters that are produced by N-acetyltransferases (NATs) or sulfotransferases (SULTs) expressed in liver or extrahepatic tissues [53,54].

Kensler, Nrf2 signaling: An adaptive response pathway for protection against environmental toxic insults, Mutat. Res. 659 (2008) 31–39. [82] K. I. Tong, M. Yamamoto, Molecular mechanism activating Nrf2-Keap1 pathway in regulation of adaptive response to electrophiles, Free Radic. Biol. Med. 36 (2004) 1208–1213. D. Hayes, M. McMahon, NRF2 and KEAP1 mutations: Permanent activation of an adaptive response in cancer, Trends Biochem. Sci. 34 (2009) 176–188. [83] R. Tirumalai, T. H. Mai, S. Biswal, Acrolein causes transcriptional induction of phase II genes by activation of Nrf2 in human lung type II epithelial (A549) cells, Toxicol.

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