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STUDIES of alterations in enzyme activity levels in lung tissues resulting from inhalation of noxious agents have revealed that these changes tend to occur early and may precede clinical signs of tissue damage. Kilroe-Smith and Breyer1 found that succinodehydrogenase and succinoxidase activity levels were increased and cytochrome c oxidase levels decreased in guinea pig lung exposed to silica dust before the usual increase in collagen formation occurred. A single exposure of rats and mice to ozone resulted in lower alkaline phosphatase and succinic dehYdrogenase activity in the lung and elevated levels in serum.2 However, intermittent exposures (one to three times weekly) induced elevated lung and serum alkaline phosphatase. The conditions of exposure as well as the type of irritant apparently plays a part in the enzyme response. The work of Scheel et alB indicates that alkaline phosphatase and 5'-nucleotidase activity levels were depressed following in vivo ozone exposure. Oxygen consumption of the whole animal was depressed by the ozone exposure. Oxygen consumption, lactic dehydrogenase (LDH) and aldolase enzyme levels were determined in this laboratory in lung, liver, kidney and spleen tissue homogenate following acute and chronic exposure of guinea pigs to nitrogen dioxide and were found to be elevated in all tissues.4 The existence of characteristic tissue patterns is well
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Buckley et al. (1967) studied this question.
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