Arachidonate release from rat liver mitochondria in endotoxin shock

Conde, Gillian; García‐Barreno, Pedro; Torres-Suárez, Ana Isabel

doi:10.1016/0014-5793(80)80135-9

Cited by 15 publications

(5 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Endotoxin has been shown in many different systems to cause the liberation of arachidonic acid (Conde, Garcia-Barreno & Suarez, 1980) and prostaglandins (Skarnes & Harper, 1972;Bult, Rampart, Van Hove & Herman, 1979;Bult, Beetens & Herman, 1980). Skarnes & Harper (1972) demonstrated increased levels of prostaglandins and inhibition of diarrhoea by indomethacin in a model involving the same dose and type of endotoxin as used in the present study.…”

Section: Discussionsupporting

confidence: 54%

Inhibition of Arachidonic Acid Release as the Mechanism by Which Glucocorticoids Inhibit Endotoxin‐induced Diarrhoea

Doherty¹

1981

British J Pharmacology

View full text Add to dashboard Cite

Dexamethasone blocked endotoxin‐induced diarrhoea in mice, but not that induced by arachidonic acid or prostaglandin E2. Indomethacin blocked endotoxin and arachidonic acid‐induced diarrhoea, but not that induced by prostaglandin E2. Codeine blocked all three forms of diarrhoea. The above data, when considered in relation to literature reports that endotoxin induces prostaglandin synthesis, suggest that dexamethasone blocks diarrhoea by preventing the release of arachidonic acid, the substrate for prostaglandin biosynthesis. The activities of indomethacin and dexamethasone in castor oil diarrhoea support the above conclusion and their inactivity in 5‐hydroxytryptophan‐induced diarrhoea confirms the absence of ‘codeine‐like’ direct effects on the gut. Other glucocorticoids (hydrocortisone, prednisolone) were also able to block endotoxin diarrhoea, but oestradiol, testosterone and progesterone did not. The inhibitory action of dexamethasone on endotoxin diarrhoea could not be blocked by the protein synthesis inhibitor, cycloheximide, nor by the glucocorticoid receptor antagonist, progesterone. Thus, involvement of glucocorticoid receptor‐mediated gene activation could not be demonstrated.

show abstract

Section: Discussionsupporting

confidence: 54%

Inhibition of Arachidonic Acid Release as the Mechanism by Which Glucocorticoids Inhibit Endotoxin‐induced Diarrhoea

Doherty¹

1981

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Also, there is now general agreement that, in the liver, endotoxemia causes hepatocyte mitochondrial alterations that can be characterized by both morphologic and functional alterations [ 19,20].…”

Section: Introduction 2 Experimentalmentioning

confidence: 99%

“…However, it is generally accepted that liver exerts a LPS clearance function with the participation of both Kupffer cells [14][15][16][17] and parenchymal cells [18]. Also, there is now general agreement that, in the liver, endotoxemia causes hepatocyte mitochondrial alterations that can be characterized by both morphologic and functional alterations [ 19,20].…”

Section: Introduction 2 Experimentalmentioning

confidence: 99%

The binding of Escherichia coli endotoxin to isolated rat hepatocytes

1981

View full text Add to dashboard Cite

“…We found a decreased PG-formation from arachidonic acid after 2 days of fasting. This points to a difference in the metabolism of arachidonic acid as compared to non-essential fatty acids, which has been proposed by several investigators [3,4,7].…”

Section: Discussionmentioning

confidence: 84%

Prostaglandin formation and platelet aggregation during fasting and linoleic acid intake

Adam¹,

Wolfram²,

Zöllner³

1985

Res. Exp. Med.

View full text Add to dashboard Cite

Prostaglandin formation, estimated by the determination of tetranorprostanedioic acid (TNPDA) in the urine, and platelet aggregation were investigated in seven healthy volunteers each day during fasting, and in three of them additionally during intake of carbohydrates (328kcal/day) or safflor oil (328 kcal, 20 g linoleic acid). Monitoring TNPDA in 8-h fractions of the urine showed a reduction during the night (23.00-07.00) by 70% on the average. During Days 1 and 2 of fasting the amount of TNPDA in 24-h urine was the same as under a conventional diet. On Day 3, TNPDA decreased in all experimental subjects to 162 micrograms/day on the average and was not changed by carbohydrate intake. A linoleic acid intake of 20 g/day increased TNPDA in 24-h urine to pre-experimental levels measured under free diet. Platelet aggregation did not change during the experiment. No relationship between prostaglandin formation and lipolysis in man was found.

show abstract

Arachidonate release from rat liver mitochondria in endotoxin shock

Cited by 15 publications

References 22 publications

Inhibition of Arachidonic Acid Release as the Mechanism by Which Glucocorticoids Inhibit Endotoxin‐induced Diarrhoea

Inhibition of Arachidonic Acid Release as the Mechanism by Which Glucocorticoids Inhibit Endotoxin‐induced Diarrhoea

The binding of Escherichia coli endotoxin to isolated rat hepatocytes

Prostaglandin formation and platelet aggregation during fasting and linoleic acid intake

Contact Info

Product

Resources

About