By Daniel Acosta
Focusing completely on toxicity to the cardiovascular process, this fourth version of a bestseller emphasizes mechanistic features of toxicity, reading the mobile and molecular results of chemical substances in additional element. Revised and extended, this version includes a new bankruptcy at the hostile results of environmental chemical substances at the cardiovascular process. moreover, the e-book comprises an summary at the opposed results of smoking and secondary smoke. This finished textual content additionally offers new details at the cardiovascular toxicity of antimicrobials, which come with anti-virals and different brokers, in addition to antibacterial brokers and endotoxins.
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Additional info for Cardiovascular Toxicology, Fourth Edition (Target Organ Toxicology Series)
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5). A number of factors may contribute to the more advanced stages of membrane injury. Cellular and organellar membranes consist of a phospholipid bilayer containing cholesterol and glycoproteins. The phospholipid bilayer is maintained by a balance between phospholipid degradation and synthesis. In myocardial ischemia, progressive phospholipid degradation occurs, probably as a result of the activation of one or more phospholipases secondary to an increase of cytosolic calcium or possibly other metabolic derangements (4–6).
Apoptosis in heart failure. Prog Cardiovasc Dis 1998; 40:549–562. 15. Bishopric NH, Andreka P, Slepak T, et al. Molecular mechanisms of apoptosis in the cardiac myocyte. Curr Opin Pharmacol 2001; 1:141–150. 16. Bergmann MW, Loser P, Dietz R, et al. Effect of NF-kappa B Inhibition on TNFalpha-induced apoptosis and downstream pathways in cardiomyocytes. J Mol Cell Cardiol 2001; 33:1223–1232. 17. Green PS, Leeuwenburgh C. Mitochondrial dysfunction is an early indicator of doxorubicin-induced apoptosis.
Cardiovascular Toxicology, Fourth Edition (Target Organ Toxicology Series) by Daniel Acosta