Part I. The role of metabolism in N-methylthiobenzamide-induced pneumotoxicity. Part II. The role of the sympathetic nervous system in methylcyclopentadienyl manganese tricarbonyl-induced pneumotoxicity

Thesis/Dissertation · Sun Jan 01 00:00:00 EST 1984

OSTI ID:6101350

Penney, D A

Part I. This is an investigation of the role of metabolism in the induction of lung injury by N-methylthiobenzamide (NMTB). N-methylthiobenzamide S-oxide (NMTBSO), a metabolite of NMTB, was prepared and found to produce lung injury that was qualitatively identical to that of NMTB. 1-methyl-1-phenyl-3-benzoylthiourea (MPBTU) protected rodents from lethal doses of either NMTB or NMTBSO. MPBTU also blocked the increases in pulmonary /sup 14/C-thymidine incorporation induced by these compounds. Both NMTB and NMTBSO were found to undergo oxidation when incubated with either lung or liver microsomes and an NADPH-generating system. The in vitro microsomal oxidation of NMTB and NMTBSO was markedly inhibited by addition of MPBTU. These data suggest that oxidation of NMTB is required for the expression of NMTB-induced pneumotoxicity. Part II. Methylcyclopentadienyl Manganese Tricarbonyl (MMT) has been used as an antiknock additive in unleaded gasoline. Rats treated with MMT exhibit severe convulsions accompanied by hemorrhagic pulmonary edema. The purpose of this study was to investigate the possible role of neurogenic mechanisms in MMT-induced hemorrhagic pulmonary edema.

• Research Organization: Kansas Univ., Lawrence (USA)
• OSTI ID: 6101350
• Resource Relation: Other Information: Thesis (Ph. D.)
• Country of Publication: United States
• Language: English

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