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Structure and activation of ipomeanol and paraquat.
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Other toxic lung furans, such as the atmospheric contaminants 2-methylfuran and 3methylfuran, may exert their toxicity through the formation of reactive metabolites, probably reactive aldehydes.
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Systemic administration of compounds such as the herbicide paraquat (Figure 18.4), bleomycin (a cancer therapeutic agent), and nitro urantoin (an antibiotic used for urinary tract infections) initiate a progression of degenerative and potentially lethal lesions in the lung by a mechanism known as redox cycling. These compounds are reduced by cytochrome P450 reductase and NADPH, forming a free radical. Although the free radical could potentially react with tissue macromolecules, one molecule of oxygen is reduced to superoxide that can then be converted to other toxic oxygen species. These reactive compounds may cause peroxidation of cellular membranes. The speci c toxicity of paraquat to the lung results from the uptake of this compound by the polyamine transport system in the lung as well as from the high pulmonary oxygen tension. Nitro urantoin, however, is not actively accumulated in the lung, and its tissue speci city probably results from the high pulmonary oxygen tension.
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There are two important defense mechanisms against inhaled particles. The rst of these involves the mucociliary escalator and consists of the trapping of particles in mucus followed by the upward movement of the mucus brought about by the upward beating of cilia on the airway epithelial airway cells. The material is then either swallowed or expectorated. The second mechanism is macrophage mediated. Macrophages engulf particles and either deposit them on the mucociliary escalator or enter the lymphatic system. Toxicants may also be detoxi ed by xenobiotic-metabolizing enzymes such as cytochrome P450 or the avin-containing monooxygenase. It should be borne in mind, however, that these enzymes may also activate toxicants to more reactive, and potentially more toxic, metabolites.
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Bond, J. A. Metabolism and elimination of inhaled drugs and airborne chemicals from the lungs. Pharmacol. Toxicol. 72: 36 47, 1993. Cho, M., C. Chichester, C. Plopper, and A. Buckpitt. Biochemical factors important in Clara cell selective toxicity in the lung. Drug Metabol. Rev. 27: 369 386, 1995. Dahl, A. R., and J. L. Lewis. Respiratory tract uptake of inhalants and metabolism of xenobiotics. An. Rev. Pharmacol. Toxicol. 32: 383 407, 1993. Foth, H. Role of the lung in accumulation and metabolism of xenobiotic compounds-implications for chemically induced toxicity. Crit. Rev. Toxicol. 25: 165 205, 1995. Henderson, R. J., and K. J. Nikula. Respiratory tract toxicity. In Introduction to Biochemical Toxicology, 3rd ed., E. Hodgson and R. C. Smart, eds. New York: Wiley-Interscience, 2001. Wheeler, C. W., T. M. Guenthner. Cytochrome P450-dependent metabolism of xenobiotics in human lung. J. Biochem. Toxicol. 6: 163 169, 1991. Witschi, H. R., and J. A. Last. Toxic responses of the respiratory system. In Casarett and Doull s Toxicology: The Science of Poisons, 6th ed., C. D. Klaassen, ed. New York: McGraw-Hill, 2001, pp. 515 534.
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A properly functioning immune system is essential to good health. It defends the body against infectious agents and in some cases tumor cells. Individuals with immune de ciencies resulting from genetic defects, diseases (e.g., AIDS, leukemia), or drug therapies are more susceptible to infections and certain types of cancer, the consequences of which can be life-threatening. On the other hand, the immune system may react to foreign substances that would otherwise be relatively innocuous, such as certain chemicals, pollens, and house dust. The resulting allergic reactions can produce an array of pathologies, ranging from skin rashes and rhinitis to more life-threatening asthmatic and anaphylactic reactions. A crucial part of immune function is the ability to distinguish endogenous components (self) from potentially harmful exogenous components (non-self). Failure to make this distinction results in autoimmune disease. Immunotoxicology is the study of undesired effects resulting from the interactions of xenobiotics with the immune system (Figure 19.1). There is evidence that some xenobiotics can cause immune suppression. Xenobiotics can also interact with the immune system to either cause or exacerbate allergic disease. Finally there is growing concern that xenobiotics could have some involvement in autoimmune disease. This chapter provides a brief overview of the immune system, chemicals associated with immune suppression and immune pathologies, and approaches to testing for these effects.
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