Protection against chemical-induced lung injury by inhibition of pulmonary cytochrome P-450
Autor: | R D, Verschoyle, D, Dinsdale |
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Rok vydání: | 1990 |
Předmět: |
Lung Diseases
Terpenes Health Toxicology and Mutagenesis Organothiophosphates Public Health Environmental and Occupational Health Administration Oral Organothiophosphorus Compounds Naphthalenes Xylenes Rats Cytochrome P-450 Enzyme System Cytochrome P-450 CYP2B1 Carcinogens Cytochrome P-450 CYP1A1 Animals Female Oxidoreductases Toxins Biological Research Article |
Zdroj: | Environmental Health Perspectives |
ISSN: | 1552-9924 0091-6765 |
DOI: | 10.1289/ehp.85-1568337 |
Popis: | Protection afforded by trialkyl phosphorothionates against the lung injury caused by trialkyl phosphorothiolates probably results from the inhibition by the P = S moiety of the thionates, of one or more pulmonary cytochrome P-450 isozymes. The aromatic hydrocarbons p-xylene and pseudocumene also protect against this injury and inhibit some P-450 isozymes, but by a different mechanism. OOS-Trimethylphosphorothionate and p-xylene were compared as protective agents against the effect of OOS-trimethylphosphorothiolate and two other lung toxins ipomeanol and 1-nitronaphthalene that are known to be activated by cytochrome P-450. The effects of these protective compounds, in vivo, on pulmonary cytochrome P-450 activity were also determined. Both compounds inhibited pentoxyresorufin O-deethylase activity, but not ethoxyresorufin O-deethylase. The phosphorothionate was most effective against lung injury caused by the phosphorothiolates and 1-nitronaphthalene, whereas p-xylene was much more effective against ipomeanol. beta-Naphthoflavone, which induces pulmonary ethoxyresorufin O-deethylase activity, did not protect against phosphorothiolate or 1-nitronaphthalene injury, and it was only marginally effective in decreasing the toxicity of ipomeanol. Images FIGURE 1. A FIGURE 1. B |
Databáze: | OpenAIRE |
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