By James C. Fishbein
Advances in Molecular Toxicology good points the newest advances in the entire subspecialties of the huge sector of molecular toxicology. Toxicology is the examine 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 take place themselves as pollution. no longer strictly constrained to documenting those examples the sequence can be all for the complicated internet of chemical and organic occasions that supply upward thrust to toxin-induced signs and affliction. the recent applied sciences which are being harnessed to research and comprehend those occasions can also be reviewed by way of top employees within the box. Advances in Molecular Toxicology will record growth in all features of those speedily evolving molecular facets of toxicology with a view towards designated elucidation of either growth at the molecular point and on advances in technological techniques hired * leading edge reports through prime staff within the self-discipline. * extensive dissection of molecular points of curiosity to a extensive variety of scientists, physisicans and any scholar within the allied disciplines. * cutting edge purposes of technological options within the chemistry, biochemistry and molecular medication.
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Additional info for Advances in Molecular Toxicology, Vol. 2
Wetterhahn, In vitro reaction of the carcinogen chromate with cellular thiols and carboxylic acids, J. Am. Chem. Soc. 107 (1985) 4282–4285. M. E. Wetterhahn, Ascorbate is the principal reductant of chromium(VI) in rat liver and kidney ultrafiltrates, Carcinogenesis 12 (1991) 1733–1737. M. E. Wetterhahn, Ascorbate is the principal reductant of chromium(VI) in rat lung ultrafiltrates and cytosols and mediates chromium-DNA binding in vitro, Carcinogenesis 13 (1992) 1319–1324. E. K. L. Melnick, In vitro steady-state levels of hydrogen peroxide after exposure of male F344 rats and female B6C3F1 mice to hepatic peroxisome proliferators, Carcinogenesis 7 (1986) 1871–1876.
S. Food and Drug Administration, including hepatobiliary dysfunction and cholestasis [13–17]. S. market in 2004. Previously, in a black-box warning in the drug’s label, the rate of liver failure was estimated as about 1 case in 250,000 patients per year. This rate was about four-fold the background rate for liver failure and in contrast to no significant hepatotoxicity associated with other serotonin reuptake inhibitors. A liver biopsy from a patient with hepatic injury associated with nefazodone treatment revealed centrilobular necrosis consistent with a metabolism-related toxic liver injury.
Gasparutto, J. Cadet, A. Favier, J. Ravanant, Characterization of lysineguanine cross-links upon one-electron oxidation of a guanine-containing oligonucleotide in the presence of a trilysine peptide, J. Am. Chem. Soc. 128 (2006) 5703–5710. CHAPTER 2 Drug-Induced Hepatotoxicity: Learning from Recent Cases of Drug Attrition Axel Pa¨hlerÃ and Christoph Funk Contents 1. 1. 2. Clinical attrition due to hepatotoxicity 2. 1. 2. 3. Contributing risk factors 3. 1. 2. Reducing the potential of drug candidates to induce intrahepatic cholestasis 4.
Advances in Molecular Toxicology, Vol. 2 by James C. Fishbein