Abstract
Damage to lung tissue can result from exposure to a variety of chemicals in the internal and external environment. Chemicals gain access to the lung through the large alveolar surface areas (1 m2/kg body wt.), in the case of inhaled agents, and the extensive perfusion of the lung with blood in the case of blood-borne chemicals (Witschi, 1976; Witschi and Cote, 1976, 1977). Chemicals that cause acute lung damage in man and animals include oxidants, heavy metals, and a variety of foreign chemicals present in cigarette smoke, diet, environmental pollution, and other sources. These chemicals can cause pulmonary injury by (1) direct effects, in which the parent compound is the toxic agent, or (2) after metabolic activation to toxic intermediates, metabolites, or products. Examples of chemicals in which the parent compound is the toxic agent include oxidants such as oxygen, ozone, and nitrogen dioxide (Witschi and Cote, 1977; Mustafa and Tierney, 1978). These chemicals generate free radicals, such as superoxide, singlet oxygen, or hydroxyl radicals, that cause lipid peroxidation and oxidation of other cellular components resulting in cytotoxicity to lung cells (McCord, 1979; Bus and Gibson, 1979).
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Carlson, J.R., Bray, T.M. (1983). Nutrition and 3-Methylindole-Induced Lung Injury. In: Draper, H.H. (eds) Advances in Nutritional Research. Advances in Nutritional Research. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-9937-7_3
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