Effects of endocrine disruptors on the formation of prostaglandin and arachidonoyl-CoA formed from arachidonic acid in rabbit kidney medulla microsomes

Fujimoto, Y; Usa, K; Sakuma, S

HERO ID

675168

Reference Type

Journal Article

Year

2005

Language

English

PMID

16181777

HERO ID 675168
In Press No
Year 2005
Title Effects of endocrine disruptors on the formation of prostaglandin and arachidonoyl-CoA formed from arachidonic acid in rabbit kidney medulla microsomes
Authors Fujimoto, Y; Usa, K; Sakuma, S
Journal Prostaglandins Leukotrienes and Essential Fatty Acids
Volume 73
Issue 6
Page Numbers 447-452
Abstract Under physiological conditions, small amounts of free arachidonic acid (AA) are released from membrane phospholipids, and cyclooxygenase (COX) and acyl-CoA synthetase (ACS) competitively act on this fatty acid to form prostaglandins (PGs) and arachidonoyl-CoA (AA-CoA). To explore the possible actions of endocrine disruptors on the metabolic fate of free AA into these two pathways, we investigated the effects of nonylphenol (NP), bisphenol A (BPA), di-n-butyl phthalate (DBP), benzyl-n-butyl phthalate (BBP) and di-2-ethylhexyl phthalate (DEHP) on the formation of PG and AA-CoA from 5 microM AA (close to the physiological concentration of the substrate) in rabbit kidney medulla microsomes. The kidney medulla microsomes were incubated with 5 microM [(14)C]-AA in 0.1 M Tris/HCl buffer (pH 8.0) containing cofactors of COX (reduced glutathione and hydroquinone) and cofactors of ACS (ATP, MgCl(2) and CoA). After incubation, PG (as total PGs) and AA-CoA were separated by selective extraction using petroleum ether and ethyl acetate. NP (1-200 microM) strongly enhanced the AA-CoA formation with a coincident decrease in the PG formation. BPA, DBP, BBP and DEHP failed to show any effect on the PG and AA-CoA formation up to 200 microM. Experiments utilizing 60 microM AA as the substrate concentration indicated that, under a low concentration of AA, NP decreases PG formation by inhibiting the COX activity, and reduces the AA flow into the COX pathway through inhibition on the COX activity, increasing availability of the substrate for the ACS and leading to enhanced AA-CoA formation. These results firstly show that NP has the potential to disturb the balance of PG and AA-CoA formations under normal physiological conditions.
Doi 10.1016/j.plefa.2005.08.002
Pmid 16181777
Wosid WOS:000233369300006
Url https://search.proquest.com/docview/68761053?accountid=171501
Is Certified Translation No
Dupe Override No
Comments Source: Web of Science WOS:000233369300006
Is Public Yes
Language Text English
Keyword Acyl Coenzyme A/ biosynthesis; Alkanes/pharmacology; Animals; Arachidonic Acid/ metabolism; Dibutyl Phthalate/pharmacology; Diethylhexyl Phthalate/pharmacology; Endocrine Disruptors/ pharmacology; Kidney Medulla/drug effects/ metabolism/ultrastructure; Male; Microsomes/drug effects/metabolism; Phenol/pharmacology; Phenols/pharmacology; Phthalic Acids/pharmacology; Prostaglandins/ biosynthesis; Rabbits
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