Mechanism of prostaglandin biosynthesis. III. Catechol amines and serotonin as coenzymes

Sih, Charles J.; Takeguchi, C.; Foss, Paul

doi:10.1021/ja00725a064

Cited by 85 publications

(21 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nicotine stimulates the release of catecholamines from the adrenal gland (Benowitz 1991) and the release of serotonin from gastrointestinal enterochromaffin cells (Racké and Schwörer 1992), which are thought to be the main source of platelet serotonin (Verbeuren 1989). Both catecholamines (Alanko et al 1992) and serotonin (Sih et al 1970) can increase eicosanoid synthesis. Nicotine increases the production of proinflammatory cytokines (Fischer and König 1994), which have been reported to augment the expression of 5-lipoxygenase and cyclooxygenases (Serhan et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Saareks

Ylitalo

Alanko

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

View full text Add to dashboard Cite

This study investigated the effects of smoking cessation with and without nicotine substitution on the excretion of major urinary metabolites of thromboxane A2 and prostacyclin, 11-dehydrothromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1alpha, respectively, as well as on the excretion of leukotriene E4 in man. Urine samples were obtained from 20 healthy non-smoking controls and from 60 healthy smoking volunteers before, and 3, 7 and 14 days after smoking cessation. Fifteen smokers quit smoking without nicotine substitution, 15 used nicotine chewing gum and 30 used nicotine patches as a substitution therapy. Urinary thiocyanate as well as cotinine and trans-3'-hydroxycotinine excretions were used as compliance and nicotine substitution indicators. 11-Dehydrothromboxane B2, 2,3-dinor-6-ketoprostaglandin F1alpha and leukotriene E4 excretion was about two, three and five times higher in smokers than in controls, respectively. Three days after smoking cessation without nicotine substitution, 11-dehydrothromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1alpha levels were lowered to 75% (P<0.01) and 80% (P<0.05) of the initial values, and after 14 days to 50% (P<0.01) and 60% (P<0.05), respectively. In 3 days leukotriene E4 excretion was dropped to 70% of the initial value (P<0.05), but no further decrease was observed during the study. In individuals using nicotine chewing gum or nicotine patches no significant changes were observed in the analytes during the 2-week follow-up. The increased systemic eicosanoid synthesis observed in smokers may be involved in the harmful cardiovascular effects of smoking. The fact that eicosanoid production remains at pre-cessation level in volunteers who quit smoking but use nicotine substitution may be involved in the risk of cardiovascular complications reported during nicotine replacement therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Saareks

Ylitalo

Alanko

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

View full text Add to dashboard Cite

show abstract

“…There is now accumulating evidence that the action of compounds of this type may be due to a nonenzymatic reduction of the prostaglandin endoperoxides K G , and PGH, which are the immediate unstable products of the activity of the fatty acid cyclo-oxygenase (33)(34)(35). The endogenous formation of PGF2, from the endoperoxides probably takes place nonenzymatically determined by the specific local reducing environment where the endoperoxide is formed.…”

Section: Species and Brain Regional Difirencesmentioning

confidence: 99%

The endogenous biosynthesis of prostaglandins by brain tissue in vitro

Wolfe¹,

Rostworowski²,

Pappius³

1976

Can. J. Biochem.

131

View full text Add to dashboard Cite

The capacity for biosynthesis of prostaglandin F2alpha (PGF2alpha) and prostaglandin E2 (PGE2) from endogenous precursors by brain tissue slices and homogenates was measured by a gas chromatography - mass fragmentography method using deuterated prostaglandins as internal standards. Mean biosynthesis in rat cerebral cortex slices incubated for 60 min was 60.2 ng PGF2alpha and 17.4 ng PGE2 per 100 mg of tissue. The corresponding values for homogenates were 78.1 ng and 28.9 ng. Synthetic capacity of cat cerebral cortex was considerably greater but that of human tissue was smaller than that found in rat brain. Cat cerebellum in contrast to other regions synthesized more PGE2 than PGF2alpha. The time-course of prostaglandin formation in slices was linear for the initial 60 min. Catabolism in cerebral tissues was found to be very small. Prostaglandins formed or added to the incubation media distributed between tissue and medium in a manner indicating some specific binding as well as nonspecific solubilization in tissue lipids. Norepinephrine, 3,4-L-dihydroxyphenylalanine, dopamine, adrenochrome and apomorphine greatly stimulated PGF2alpha formation probably through a nonenzymatic reduction of endoperoxides. Norepinephrine added to homogenates appeared to stabilize the fatty acid cyclo-oxygenase preventing it from inactivation. Indomethacin and Ketoprofen were potent inhibitors of biosynthesis. Paracetamol was found to be a less potent synthetase inhibitor than aspirin. The biosynthetic capacity of brain tissue in vitro appears to be orders of magnitude more than that of normal brain in situ.

show abstract

“…Many phenolic compounds, such as catecholamines (Sih et al 1970), hydroquinones (Markey et al 1987, Schreiber et al 1986), and 4-CB-HQ (Wangpradit et al 2009) have been shown to stimulate prostaglandin biosynthesis in vitro . However, the cosubstrate property of these exogenous compounds was not elucidated in any animal model.…”

Section: Discussionmentioning

confidence: 99%

PAMAM dendrimers as nano carriers to investigate inflammatory responses induced by pulmonary exposure of PCB metabolites in Sprague-Dawley rats

Wangpradit

Adamcakova‐Dodd

Heitz

et al. 2015

Environ Sci Pollut Res

View full text Add to dashboard Cite

Polychlorinated biphenyls (PCBs) persist and accumulate in the ecosystem depending upon the degree of chlorination of the biphenyl rings. Airborne PCBs are especially susceptible to oxidative metabolism, yielding mono- and di-hydroxy metabolites. We have previously demonstrated that 4-chlorobiphenyl hydroquinones (4-CB-HQs) acted as co-substrates for arachidonic acid metabolism by prostaglandin H synthase (PGHS) and resulted in an increase of prostaglandin production in vitro. In the present study, we tested the capability of 4-CB-HQ to act as a co-substrate for PGHS catalysis in vivo. 4-CB-2′,5′-HQ and BQ were administered intratracheally to male Sprague-Dawley rats (2.5 μmol/kg body weight) using nanosized polyamidoamine (PAMAM) dendrimers as carriers. We found that 24 hr post application, PGE2 metabolites in kidney of rats treated with 4-CB-2′,5′-HQ were significantly increased compared to the controls. The increase of PGE2 metabolites was correlated with increased alveolar macrophages in lung lavage fluid. The elevation of PGE2 synthesis is of great interest since it plays a crucial role in balancing homeostasis and inflammation where a chronic disturbance may increase risk of cancer. PAMAM dentrimers proved to be an effective transport medium and did not stimulate an inflammatory response themselves.

show abstract

Mechanism of prostaglandin biosynthesis. III. Catechol amines and serotonin as coenzymes

Cited by 85 publications

References 0 publications

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

Effects of smoking cessation and nicotine substitution on systemic eicosanoid production in man

The endogenous biosynthesis of prostaglandins by brain tissue in vitro

PAMAM dendrimers as nano carriers to investigate inflammatory responses induced by pulmonary exposure of PCB metabolites in Sprague-Dawley rats

Contact Info

Product

Resources

About