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Biomedical subjects

I A Tavares

Publications and source records attributed to I A Tavares.

At least 55 records · Page 3Linked to original sources
PubMed1989

Stimulation of gastric and colonic mucosal eicosanoid synthesis by plantain banana.

Extracts of plantain banana (Musa sapientum Linn var. paradisiaca) were studied on the accumulation of eicosanoids in incubates of human gastric and colonic mucosa. The ethanolic extract caused a concentration-dependent increase in the eicosanoid accumulation but the water extract was ineffective. Since all the eicosanoids studied tended to increase, banana may act by increasing the availability of arachidonate. In control tissues the accumulation of PGE and TXB2 in the incubates decreased with time while that of 6-keto-PGF1 alpha increased (colon only, studied).

Eicosanoids↗
PubMed1988

Delayed-release mesalazine (5-aminosalicylic acid): coat dissolution and excretion in ileostomy subjects.

1. Delayed-release mesalazine has been formulated to deliver 5-aminosalicylic acid to the colon. We have therefore studied the ileostomy excretion and coat dissolution of this preparation. 2. Following ingestion of a single tablet 88% (range 69-114%) of the 400 mg dose appeared unchanged in the ileosomy effluent over the subsequent 12 h. 3. Ileostomy effluent pH appeared to be a major determinant of 5-aminosalicylic acid release. 4. In vitro studies revealed rapid coat dissolution above pH 7.0, slow dissolution between pH 6.0 and 7.0 and non-dissolution at pH 2.0 and 4.0.

Adult↗
PubMed1987

Eicosanoid formation by mammalian intestine. Effects of some intestinal secretagogues.

Intestinal tissues of man, rat, mouse, guinea-pig and rabbit were preincubated with laxatives, homogenised, and incubated with [14C]arachidonic acid. After extraction into chloroform, the eicosanoids were separated by thin layer chromatography. Metabolism of [14C]arachidonic acid into prostaglandins (PGs), and the lipoxygenase products LTB4 and 5-HETE, was stimulated by ricinoleic acid (100 micrograms/ml) or phenolphthalein (100 micrograms/ml), and to a lesser extent by picosulphate (125 micrograms/ml) and sulfosuccinate (200 micrograms/ml). Mannitol (500 micrograms/ml) had no effect. Indomethacin (1 microgram/ml) inhibited the stimulation of PG formation. The dual pathway inhibitor BW755C (1 microgram/ml) reduced the formation of prostaglandins, LTB4 and 5-HETE. In some experiments on rat colon, prostanoids were separated from lipoxygenase products, characterised by their chromatographic mobility and quantitated (relative amounts PGE2 greater than PGF2 alpha greater than TXB2 greater than PGD2). Their formation was enhanced by ricinoleic acid (100 micrograms/ml) and inhibited by either indomethacin or BW 755C (1 microgram/ml). The present results indicate that mammalian isolated gut tissue can convert [14C]arachidonic acid into both cyclo-oxygenase and lipoxygenase products, and support the suggestion that eicosanoids may participate in the laxative effect of some secretagogues.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1987

Inhibition of prostanoid synthesis by human gastric mucosa.

Non-steroidal anti-inflammatory drugs (NSAIDs) damage the gastric mucosa, and an important part of this effect is probably due to inhibition of prostaglandin synthesis. We have therefore studied various drugs for their ability to reduce prostaglandin and thromboxane formation by human isolated gastric mucosa. The overall relative potencies for inhibiting the endogenous production of PGE, 6-keto-PGF1 alpha and thromboxane B2 by mucosal pieces was generally: indomethacin = naproxen greater than ibuprofen greater than piroxicam; diflunisal, the prodrug sulindac, and the analgesic paracetamol usually had small or variable effects. This rank order was mainly similar to the inhibition of gastric microsomal PGE2 formation from exogenous arachidonic acid, the relative potencies being: indomethacin greater than naproxen greater than ibuprofen = piroxicam = diflunisal; again sulindac and paracetamol had little or no effect. The relative propensity of NSAIDs to cause gastric mucosal damage is controversial, but aspirin and indomethacin may be worst, and ibuprofen seems to be among the safest. Potency as an inhibitor of prostaglandin synthesis correlates better with the reported propensity for damage than does potency x dose. For reasons that are given in the discussion, this may indicate that gastric mucosal damage by NSAIDs with short or moderate half-lives is due largely to locally absorbed drug. Whereas inhibition of prostaglandin synthesis is probably the major cause of the damage, the simultaneous reduction of thromboxane formation might be advantageous for gastric mucosal integrity. Various implications arise from our hypotheses concerning the design of anti-inflammatory drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1987

Tamoxifen inhibits 5-lipoxygenase in human polymorphonuclear leucocytes.

Breast cancer patient survival is increased by tamoxifen, and we therefore need to understand how this drug exerts its effect. We describe a novel action of tamoxifen, the inhibition of LTB4 and 5-HETE production from [14C]-arachidonic acid by human polymorphonuclear leucocytes.

Arachidonate Lipoxygenases↗
PubMed1985

The role of calcium in eicosanoid production induced by ricinoleic acid or the calcium ionophore A23187.

Rat isolated intestine incubated in Krebs solution converted exogenous [14C]-arachidonic acid into products that chromatographed with prostaglandins, leukotriene B4 and 5-hydroxy-eicosatetraenoic acid. Accumulation of these products was increased by the laxative ricinoleic acid (0.34 mM) or the calcium ionophore A23187 (7.6 microM). In the presence of the calcium antagonists TMB-8 (0.43 microM) or verapamil (0.2 microM) the mean effects of ricinoleic acid or the calcium ionophore were smaller. Stimulation of arachidonic acid metabolism by ricinoleic acid therefore seems likely to involve a calcium-dependent mechanism.

Animals↗
PubMed1985

Effects of isoxicam and other non-steroidal anti-inflammatory drugs on arachidonic acid metabolism by rat peritoneal leucocytes.

Inhibition of prostaglandin formation from [14C]arachidonic acid by rat peritoneal leucocytes occurred with nonsteroidal anti-inflammatory drugs, their order of potency being indomethacin greater than piroxicam greater than naproxen greater than ibuprofen greater than isoxicam. At the lowest concentration tested (1 microgram ml-1), indomethacin markedly increased the accumulation of lipoxygenase products in the cell incubates. Naproxen, ibuprofen or piroxicam 1 or 10 micrograms ml-1 resulted in smaller increases of lipoxygenase products, and there was only a small rise with these concentrations of isoxicam.

Animals↗
PubMed1984

The biological activities of phthalate esters on rat gastric muscle.

Monoethylhexyl phthalate, at concentrations that can occur in blood stored in plastic bags (0.1-0.5 mg/ml), reduced contractions of rat isolated gastric fundus to PGE2 and acetylcholine; the diethyl compound was less effective. In contrast, dibutyl phthalate (1 and 10 micrograms/ml) and, to a lesser extent di-isobutyl phthalate, increased the muscle tone. These results are discussed in relation to blood transfusion, and to structural similarities between phthalates and prostaglandins.

Animals↗
PubMed1984

The effect of garlic extracts on contractions of rat gastric fundus and human platelet aggregation.

Garlic has been extracted and separated chromatographically into various fractions which show different degrees of activity as inhibitors of platelet aggregation and smooth muscle. The most potent smooth muscle inhibitor fraction had little activity on platelet aggregation, but microgram ml-1 concentrations greatly reduced the contractions of rat gastric fundus to prostaglandin E2 and acetylcholine. Material in this fraction may contribute to some of the claimed therapeutic effects of garlic involving smooth muscle. Its identity is not known, but is different from allyl sulphide, dimethyl sulphide and diallyl disulphide. These compounds eluted earlier on liquid chromatography than the most active fraction, and they showed only modest inhibitory activity against prostaglandin E2 and acetylcholine on rat fundus.

Acetylcholine↗
PubMed1977

4,4'-dimethylcholesta-7,9,14-trienol is an intermediate in the demethylation of dihydroagnosterol.

1. 4,4'-Dimethylcholesta-7,9,14-trienol is an intermediate in the metabolism of dihydroagnosterol to cholesterol by rat liver homogenate. 2. This triene is reduced by a rat liver microsomal preparation in the presence of NADPH to give 4,4'-dimethylcholesta-7,9-dienol under anaerobic conditions. 3. Reduction of the triene in the presence of [4-3H2]NADPH resulted in the incorporation of 3H into the product. 4. Under aerobic conditions the triene is converted into cholesterol by a rat liver homogenate.

Animals↗