metabolism of 3-methylindole by the lung
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metabolism of 3-methylindole by the lung by Keith Allen Cummins

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Published .
Written in English

Subjects:

  • Lungs -- Diseases.

Book details:

Edition Notes

Statementby Keith Allen Cummins.
The Physical Object
Paginationix, 57 leaves :
Number of Pages57
ID Numbers
Open LibraryOL16419215M

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Metabolism and bioactivation of 3-methylindole (3MI) were investigated in human liver microsomes. The metabolism of two deuterium-labeled analogues of 3MI permitted a relatively unambiguous identification of multiple metabolites and glutathione (GSH) adducts of reactive intermediates. A total of eight oxidized metabolites were detected, five of which were assigned as previously identified 3 Cited by:   Metabolism and Bioactivation of 3-Methylindole by Clara Cells, Alveolar Macrophages, and Subcellular Fractions from Rabbit Lungs Author links open overlay panel Thorntonmanning J.R. Nichols W.K. Manning B.W. Skiles G.L. Yost by:   Bioactivation of 3-methylindole (3MI), a highly selective pneumotoxin in goats, was investigated in human lung and liver tissues in order to provide information about the susceptibility of humans to 3MI toxicity. Human lung microsomes were prepared from eight organ transplantation donors and liver microsomes from one of the donors were utilized. The 3MI turnover rate with human lung Cited by:   3-Methylindole (3MI) is the causative agent of a naturally occurring lung disease in cattle. The effects of 3MI on the prostaglandin H synthase (PHS) .

Metabolic Activation and Toxicity of Chemical Agents to Lung Tissue and Cells Book • Browse book content CHAPTER 10 - THE METABOLIC BASIS OF 3-METHYLINDOLE-INDUCED PNEUMOTOXICITY. Tammy M. Bray and James B. Kirkland. Pages 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 m 2 /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, ; Witschi and Cote, , ). The book is a vital source of information for readers interested in studying the metabolism of the lung. Show less Lung Metabolism: Proteolysis and Antiproteolysis Biochemical Pharmacology Handling of Bioactive Substances focuses on studies on the response of the lung relative to the management of bioactive substances. Lung Metabolism: Proteolysis and Antiproteolysis Biochemical Pharmacology Handling of Bioactive Substances focuses on studies on the response of the lung relative to the management of bioactive substances. Divided into three sections with 35 chapters, the book focuses first on proteolysis and antiproteolysis in the lung.

  3-Methylindole (3MI) is a highly selective pneumotoxicant that is present in abundant amounts (as high as µg/cigarette) present in cigarette smoke. Several human cytochrome P enzymes that are expressed in lung, such as CYP1A1, CYP2F1, CYP2A13, and CYP4B1 catalyze the dehydrogenation of 3MI to the reactive intermediate 3.   3-Methylindole (3MI) is a preferential pneumotoxicant found in cigarette smoke. A number of lung-expressed human cytochrome P enzymes, including 1A1, 2F1, and 2A13, catalyze the metabolism of 3MI to reactive intermediates that fragment DNA – measured with the Comet assay to assess DNA damage – in a cytochrome Pdependent manner in primary normal human lung cells . Abstract. 3-Methylindole (3MI) is constitutively produced by anaerobic bacterial fermentation of tryptophan in mammalian intestines. In the case of ruminants excessive 3MI production causes selective pulmonary toxicity which can be fatal (Carlson and Yost, ; Yost, ). 3-Methylindole (3MI) is a preferential pneumotoxicant found in cigarette smoke. A number of lung-expressed human cytochrome P enzymes, including 1A1, 2F1, and 2A13, catalyze the metabolism of 3MI to reactive intermediates that fragment DNA, measured with the Comet assay to assess DNA damage, in a cytochrome Pdependent manner in primary normal human lung cells in culture, but .