Pulmonary biosynthesis and metabolism of prostaglandins and related substances.
Author(s) -
Thomas E. Eling,
A.I. Ally
Publication year - 1984
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.8455159
Subject(s) - arachidonic acid , intracellular , prostaglandin , metabolism , biosynthesis , substrate (aquarium) , enzyme , lung , microsome , chemistry , biochemistry , in vivo , in vitro , incubation , prostaglandin h2 , biology , medicine , ecology , microbiology and biotechnology
On passage through the lung vascular bed, prostaglandins are removed from the circulation by a transport carrier and subsequently inactivated by intracellular enzymes. However, PGI2 is not inactivated by the lung in vivo. Although PGI2 is an excellent substrate for the intracellular enzymes in vitro, PGI2 is not a substrate for the carrier system. Thus, the transport carrier determines which circulating prostaglandin is inactivated by the pulmonary vascular bed. Also, the lung has a high capacity for forming prostaglandins from arachidonic acid. Considerable differences exist between species in relation to amount and specific prostaglandin formed as determined by incubation of 11C-PGH2 with pulmonary microsomes. The pulmonary biosynthesis and metabolism of these prostaglandins and related substances are discussed.
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