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PubMed1986

Mechanisms of lipid peroxidation dependent upon cytochrome P-450 LM2.

A mechanism of lipid peroxidation dependent on the oxidase activity of cytochrome P-450 LM2 in reconstituted membrane vesicles has been investigated. The rate of lipid peroxidation, determined as the formation of thiobarbituric-acid-reactive substances, was inhibited by CO. It increased concomitantly to the production of O-2 and H2O2, when cytochrome P-450 LM2 was incorporated into vesicles containing NADPH-cytochrome-P-450 reductase, until a 1:1 molar ratio between the enzymes was reached. Also the formation of lipid hydroperoxides was dependent on the presence of cytochrome P-450 LM2 in the membranes. This lipid peroxidation was not inhibited by hydroxyl radical scavengers and not specifically inhibited by scavengers of singlet oxygen. By contrast, superoxide dismutase was a very potent scavenger of the lipid peroxidation. A half-maximal effect at 3 ng/ml enzyme was registered, whereas a 100-fold higher concentration was necessary in order to inhibit O-2 formation as detected by succinylated cytochrome c or pyrogallol. The reason for this difference might be inherent in different types of kinetics in the interaction of O-2 with different scavengers or might possibly indicate that SOD scavenges another type of reactive oxygen, different from O-2, generated by cytochrome P-450 LM2. Iron chelators inhibited the P-450-dependent lipid peroxidation, whereas iron chelate interacted with NADPH-cytochrome-P-450 reductase in the membranes giving rise to reductase-dependent lipid peroxidation. Neither superoxide dismutase nor EDTA at high concentrations, inhibited CCl4-initiated lipid peroxidation, indicating the point of action of these compounds at the initiation step in the cytochrome-P-450-LM2-dependent lipid peroxidation. Superoxide generated by pyrogallol, in three times the amount produced by P-450 LM2, could not bring about lipid peroxidation. It is suggested that the cytochrome-P-450-dependent lipid peroxidation mechanism might be of importance for intracellular oxidative damage under certain conditions.

Carotenoids↗

PubMed1983

Microelectrode recording of the effects of agonists and antagonists on alpha-adrenoceptors on rat somatic nerve terminals.

The effects of apomorphine, catechol, clonidine, isoprenaline, (-)-and (+/-)-noradrenaline, phenylephrine, pyrogallol and xylazine were investigated on the frequency and amplitude of miniature endplate potentials (m.e.p.ps) and, with the exception of apomorphine, catechol and pyrogallol, on the amplitude of endplate potentials (e.p.ps) in the rat phrenic nerve diaphragm preparation. Clonidine, (-)-noradrenaline, phenylephrine and xylazine (each at 1.5 X 10(-5)M) increased m.e.p.p. frequency but not amplitude. The other drugs were ineffective, except isoprenaline (1.5 X 10(-5)M) which enhanced m.e.p.p. amplitude but not frequency. The increase in m.e.p.p. frequency was inhibited by phentolamine, prazosin and yohimbine (each 1.5 X 10(-9)M). Prazosin and yohimbine alone each reduced m.e.p.p. frequency but failed to abolish m.e.p.ps even at high concentrations (10(-3)M). Clonidine, (-)-noradrenaline, phenylephrine and xylazine (each 3 X 10(-6)M) enhanced e.p.p. amplitude; this enhancement was blocked by prazosin and by yohimbine (each 3 X 10(-6)M). In preparations fatigued by prolonged continuous nerve stimulation (5 Hz, 0.05 ms for 30 min), (-)-noradrenaline (3.3 X 10(-4)M) restored m.e.p.p. frequency. The results indicate that adrenoceptors on somatic nerve terminals interact with both alpha 1- and alpha 2-agonists and antagonists and show different characteristics from those at autonomic neuroeffector junctions. The alpha-adrenoceptors on somatic nerve terminals may have an ancilliary physiological role in influencing but not controlling transmitter release.

Adrenergic alpha-Antagonists↗

PubMed1995

Comparison of the pharmacological profile of S-nitrosothiols, nitric oxide and the nitrergic neurotransmitter in the canine ileocolonic junction.

1. In organ bath experiments, hydroquinone (30-100 microM) and hydroxocobalamin (30-100 microM) concentration-dependently inhibited the relaxations induced by NO (0.3-30 microM) but not those by nitroglycerin (GTN, 1 microM) in the canine ileocolonic junction (ICJ). Hydroxocobalamin reduced the relaxation to low frequency (2 Hz) stimulation of the non-adrenergic, non-cholinergic (NANC) nerves, whereas hydroquinone only reduced the NANC nerve-mediated relaxations to electrical stimulation at 16 Hz, 0.5 ms. 2. Relaxations to S-nitroso-L-cysteine (CysNO, 1-30 microM), or S-nitroso-N-acetyl-D,L-penicillamine (SNAP, 1-30 microM) were not inhibited by hydroquinone (30-100 microM), hydroxocobalamin (30-100 microM), pyrogallol (30-100 microM) or L-cysteine (1-3 microM). Hydroquinone (100 microM) only reduced the relaxation to 10 microM CysNO. Hydroxocobalamin, but not hydroquinone, pyrogallol or L-cysteine, potentiated the relaxations to the lowest concentration (1 microM) of S-nitrosoglutathione (GSNO, 1-30 microM). 3. In the superfusion bioassay, hydroquinone (100 microM) and hydroxocobalamin (1 microM) concentration-dependently inhibited the biological activity of authentic NO (1-4 pmol) to the same extent as that of the transferable nitrergic factor, released from the canine ICJ in response to NANC nerve stimulation (8-16 Hz, 2 ms). Responses to GTN (10 pmol) or adenosine 5'-triphosphate (10 nmol) were not affected. 4. In conclusion, the nitrosothiols CysNO, SNAP and GSNO relax the canine ileocolonic junction, but these relaxations, pharmacologically, behave differently from the NANC nerve-mediated relaxations. From the bioassay experiments, we conclude that the nitrergic factor, released in response to NANCnerve stimulation of the canine ICJ, behaves pharmacologically like NO but not like a nitrosothiol.Therefore, we suggest NO, and not CysNO, SNAP or GSNO as the inhibitory NANC neurotransmitter in the canine ICJ.

Animals↗

PubMed1993

Role of the L-arginine/nitric oxide pathway in relaxation of isolated human penile cavernous tissue and circumflex veins.

In human penile corpus cavernosum strips, pre-contracted by noradrenaline, electrical stimulation of nerves evoked non-adrenergic, non-cholinergic (NANC) relaxant responses which could be inhibited by tetrodotoxin 10(-6) M, NG-nitro-L-arginine (L-NNA) 10(-7)-10(-4) M, and oxyhaemoglobin 10(-5) M, but not by methylene blue (MB) 10(-5) M. Acetylcholine-induced relaxations were also inhibited by L-NNA 10(-4) M and oxyhaemoglobin 10(-5) M, but were unaffected by pyrogallol 10(-4) M, MB 10(-5) M, and tetrodotoxin 10(-6) M. MB 5 x 10(-4)-10(-4) M significantly reduced the responses to both electrical stimulation and to acetylcholine. Nitric oxide (NO) 10(-7)-10(-4) M and sodium nitroprusside 10(-9)-10(-4) M caused concentration-dependent relaxations. The NO-induced relaxations were inhibited by oxyhaemoglobin 10(-5) M, and the concentration-response curve for sodium nitroprusside was shifted to the right by MB 10(-5) M. The response to sodium nitroprusside was unaffected by L-NNA 10(-4) M, oxyhaemoglobin 10(-5) M, and pyrogallol 10(-4) M. In circumflex veins, pre-contracted by noradrenaline, no NANC-mediated relaxation was found in response to electrical stimulation; acetylcholine caused endothelium-dependent relaxations, which were insensitive to L-NNA 10(-4) M and oxyhaemoglobin 10(-5) M. NO and sodium nitroprusside caused concentration-dependent relaxations; the concentration-response curves for NO and sodium nitroprusside were shifted to the right by oxyhaemoglobin 10(-5) M. Removal of the endothelium left the NO- and sodium nitroprusside-induced relaxations unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1982

On the preferred rotameric conformation for dopamine agonist action: an illusory quest.

Putative dopamine agonists from the 2-aminotetrahydronaphthalene and trans-octahydrobenzo (f) and (g) quinoline series were shown to inhibit the spontaneous locomotor activity of mice. Marked potency differences were observed between the alpha-and beta-rotameric conformations, compounds having the alpha-rotameric conformation having the greater potency. Thus, 2-di-n-propylmino-5,6-dihydroxytetrahydronaphthalene was 339 times more potent than the 6, 7-dihydroxy isomer, and 2-n-propylamino-5,6-dihydroxy-compound was respectively 79 times and 179 times more than 6,7-hydroxy-and 7,8-dihydroxycompounds. trans-7,8-dihydroxy-1-n-propyl-1,2,3,4,a,9,10,10b-octahydrobenzo(f)quinoline was 11 times more potent than the beta-rotamer, the 6,7-dihydroxy compound, and within the trans-octahydrobenzo(g)quinoline series the alpha-rotameric N-propyl derivative was 467 times more potent than the beta-rotamer, and the alpha-rotameric greater than N-H analogue was 46 fold more potent than the beta-rotamer. Thus, the alpha-rotamer appears the more potent in causing the present functional dopaminergic change. The dopaminergic nature of the response was indicated by its sensitivity to spiroperidol but not to yohimbine or prazosin. The possibility that a difference in behavioural potency between the alpha- and beta-rotamers may reflect a differential metabolism by catechol-O-methyl transferase was assessed by administration of different agonists after pyrogallol pretreatment. This potentiated the activity of 2-di-n-propylamino-6,7-dihydroxytetrahydro-naphthalene but not that of the 5,6-dihydroxy analogue. However, changes in the effects of N-propyl derivatives of trans-octahydrobenzo (f) and (g)quinoline were not marked and, in all experiments, pyrogallol treatment failed by orders of magnitude to shift the dose-response curves of the beta-rotamers to indicate a comparable potency to the rotameric forms.

Animals↗

PubMed1970

The metabolism of (3H)noradrenaline released by electrical stimulation from the isolated nictitating membrane of the cat and from the vas deferens of the rat.

1. The noradrenaline (NA) stores of the isolated medial muscle of the cat's nictitating membrane were labelled with [(3)H]NA and the tissue was set up in an isolated organ bath for field stimulation. The tritiated NA and its metabolites released spontaneously and by field stimulation were determined by scintillation counting following chromatographic separation.2. NA represented 11.8 +/- 1.0% of the total radioactivity of the spontaneously released tritiated compounds. The rest was accounted for by NA metabolites: (a) normetanephrine (NMN), 35%; (b) 4-hydroxy-3-methoxymandelic acid (VMA), 20%; (c) 3,4-dihydroxyphenylglycol (DOPEG), 10%; (d) 3,4-dihydroxymandelic acid (DOMA), 10%; (e) 4-hydroxy-3-methoxyphenylglycol (MOPEG), 14%.3. Field stimulation at 25 shocks/sec with supramaximal stimuli of 1 msec duration increased the outflow of NA six to eightfold and that of NMN, DOPEG and VMA two to threefold. The increase in outflow of DOMA and MOPEG was small. NA represented 35.8 +/- 4.1% of the total increase in radioactivity.4. After pargyline pretreatment field stimulation increased the outflow of NA and NMN. Stimulation in the presence of pyrogallol raised the release of NA, DOMA and DOPEG. Neither pargyline nor pyrogallol affected the total release induced by stimulation.5. Cocaine 0.3 mug/ml. increased the release due to stimulation at 4 shocks/sec but not at 25 shocks/sec. Cocaine did not affect the metabolism of the released transmitter.6. Phenoxybenzamine (10 mug/ml.) increased release by stimulation at 4 and 25 shocks/sec. Metabolism of the released transmitter was prevented in the presence of phenoxybenzamine.7. Phentolamine (3 mug/ml.), like phenoxybenzamine, blocked responses to field stimulation, but failed to modify release and subsequent metabolism of NA liberated by field stimulation.8. The main NA metabolites in the rat vas deferens were DOPEG, DOMA and MOPEG. Stimulation at 4 shocks/sec resulted in an increased outflow of NA and of DOPEG. Fifty per cent of the total increase of radioactive compounds was accounted for by NA metabolites.9. These experiments show that for the calculation of the actual output of transmitter it is important to include the metabolites and not to rely on the determination of [(3)H]NA alone.

Animals↗

PubMedDate not supplied

Protective effects of phenolic compounds on CCl4-induced toxicity in isolated rat hepatocytes.

The protective effects of a series of phenolic compounds, phenolic acids and flavonoids on the cytotoxicity of CCl4 in rat hepatocytes were studied. A number of flavones, 7,8-dihydroxy-flavone, luteolin and hypolaetin-8-glucoside, flavonols, morin, quercetin, robinetin and gossypin, phenolic acids, gallic, caffeic and chlorogenic acids, as well as the flavane (+)-catechin significantly inhibited alanine amine transferase (ALT) release. Catechol groups are determinant for the protective activity of flavonoids and cinnamic acid derivatives, as well as the resorcinol or pyrogallol moieties in the B ring of flavonoids. In benzoic acid derivatives a pyrogallol group is required. This feature is associated with the inhibition of ALT spontaneous release.

Animals↗

PubMed1976

Reactivation mechanisms of thiamine with thermostable factors.

It was observed, in vitro, that the water extract of the fermented-tea customarily chewed by Thai people has a similar thermostable thiamine-inactivating factor to that found in the water extract of fern. It was also observed that the percentage of thiamine disulfide formed from thiamine with some flavones, catechol, pyrogallol, caffeic acid, dihydroxyphenylalanine, and hemin is greater at pH 7.5 than at pH 7.0. With some flavonoids, such as quercetin, rutin, and 6,7,4'-trihydroxyisoflavone, and pyrogallol, hemin, catechol and caffeic acid at pH 7.5, around 30-100% of thiamine is changed into thiamine disulfide. Water extract of shiitake, okra, coffee, black tea and fukinoto have only weak activities of thermostable thiamine-inactivating factors as a large percentage of thiamine disulfide is formed from thiamine even at pH 7.0. 2-Methyl-4-amino-5-aminomethylpyrimidine was isolated from the reaction mixture of 1 g thiamine with 20 mg catechol (1:0.5 mole) at pH 7.0, 45 degrees C, and identified with the synthesized pyrimidine.

Antimetabolites↗

PubMed1990

[Antibacterial and anti-hemolysin activities of tea catechins and their structural relatives].

Among catechins tested, (-)epigallocatechin (EGC), (-)epicatechin gallate (ECg), (-) epigallocatechin gallate (EGCg) inhibited the growth of Staphylococcus aureus, Vibrio cholerae O1 classical Inaba 569B and El Tor Inaba V86. S. aureus was more sensitive than V. cholerae O1 to these compounds. EGCg showed also a bactericidal activity against V. cholerae O1 569B. Pyrogallol showed a stronger antibacterial activity against S. aureus and V. cholerae O1 than tannic and gallic acid. Rutin or caffein had no effect on them. ECg and EGCg showed the most potent anti-hemolysin activity against S. aureus alpha-toxin, Vibrio parahaemolyticus thermostable direct hemolysin (Vp-TDH) and cholera hemolysin. Among catechin relatives, only tannic acid had a potent anti-hemolysin activity against alpha-toxin. These results suggest that the catechol and pyrogallol groups are responsible for the antibacterial and bactericidal activities, while the conformation of catechins might play an important role in the anti-hemolysin activity.

Antitoxins↗

PubMed1989

Dioxygenase and peroxidase activities of soybean lipoxygenase: synergistic interaction between linoleic acid and hydrogen peroxide.

The interaction of H2O2 with soyabean lipoxygenase was investigated in the presence of linoleic acid. Dioxygenase activity was significantly higher at pH 9.0 than at pH 6.0. H2O2 at concentrations less than 1.0 nM stimulated linoleic acid oxidation synergistically and the magnitude of synergism was higher at pH 9.0. Linoleic acid dependent peroxidase activity towards benzidine, guaiacol, tetramethylbenzidine (TMBD) and tetramethylphenylenediamine (TMPD) was higher at pH 9.0, whereas pyrogallol and ABTS oxidation rates were higher at pH 6.0. H2O2 supported oxidation of benzidine, guaiacol, pyrogallol and ABTS was higher at pH 6.0, whereas TMPD, TMBD exhibited higher oxidation rates at pH 9.0. H2O2 in the presence of linoleic acid produced synergism in xenobotic metabolism and depending upon the substrate in question upto 11-fold increase in oxidation rate was noted.

Drug Synergism↗

PubMed1982

High performance liquid chromatographic determination of vitamin D in fortified milks, margarine, and infant formulas.

Fortified milks were saponified overnight at room temperature with 1% ethanolic pyrogallol and KOH. The digest was extracted with hexane after adding water and ethanol, and the extract was washed consecutively with 5% KOH, water, and 55% aqueous ethanol to remove polar lipids. After evaporation, the residue was first chromatographed on a column of 5 micrometer silica. A fraction containing vitamin D was collected, evaporated, and rechromatographed on a reverse phase column for the separation and quantitation of vitamins D2 and D3. Recovery was 96-99% and the coefficient of variation was 3% (8 replicates). Infant formula was diluted and then saponified and extracted as in the analysis of milk. Margarine was saponified by shaking overnight with 1% ethanolic pyrogallol and 80% KOH. Water and ethanol were added to the digest before extraction. Extracts from formula and margarine were chromatographed as milk except, before HPLC, the extract was dissolved in isopropanol-hexane (1 + 99) and passed through 5 cm alumina in a Pasteur pipet, and the concentration of isopropanol in the first high performance liquid chromatographic (HPLC) solvent system was halved to improve the separation of vitamin D from other absorbing lipids. Usually several peaks were obtained during the final HPLC analysis, and the identification of vitamins D2 and D3 was less certain than in the analysis of milk. The coefficients of variation for formula and margarine were 6% (5 replicates) and 9% (6 replicates), respectively.

Animals↗

PubMed1998

[Contact eczema caused by pine wood].

A 34 year-old woman, working with pine wood treated with sodium hydroxide and pyrogallol, developed dermatitis on arms, face and neck. Patch testing showed allergic reaction to colophony and pine wood, but not to sodium hydroxide or pyrogallol. Pine wood contains colophony. Since avoiding pine wood, she has had no further attack of dermatitis.

Adult↗

PubMed1992

Automated analysis of rabbit sperm motility and the effect of chemicals on sperm motion parameters.

Appropriate software settings and optimum procedures were determined for the measurement of the motion parameters of rabbit spermatozoa by the CellSoft (Cryo Resources Ltd., Montgomery, NY) computer-assisted digital image analysis system. The system was used to follow motion parameter changes occurring in spermatozoa incubated for 6 hr with or without exposure to chemicals. Mean amplitude of lateral head displacement (AALH) increased over the 6 hr period, while curvilinear velocity (Vc) first increased and then decreased. Values for linearity (Lin), or beat cross frequency (BCF), were unchanged. The majority of spermatozoa progressed linearly, with rapid rotation of the sperm head, but subpopulations of spermatozoa with different swimming patterns appeared after 1-3 hr of incubation. Percentage motile sperm and Vc were most sensitive to the action of the compounds (pyrogallol, hydroquinone, ammonium oxalate, triethyl phosphite, and pinocolyl alcohol), while BCF was least affected. The decline in percentage of motile sperm was dependent on duration of exposure and chemical concentration. Mean Vc of the sperm population decreased rapidly upon chemical exposure and remained at a low value until motility ceased. The initial decrease in Vc was dependent on the concentration of the added compound. Motion-based indices--motility concentration (MCI50), motility time (MTI50), and velocity (VI)--were defined and used as toxicological endpoints. The rank order of these indices, the end point of the neutral red in vitro assay for cytotoxicity, and LD50 values for the five compounds were the same, suggesting that chemical inhibition of sperm motility may be useful as a method for the in vitro assessment of chemical cytotoxicity.

Animals↗

PubMed1975

Catechol-O-methyl transferase and monoamine oxidase activities in brains of mice susceptible and resistant to audiogenic seizures.

The activities of catechol-O-methyl transferase (COMT), monoamine oxidase (MAO), and a methanol forming enzyme were studied in whole brain homogenates and in livers obtained from DBA/2J, C57B1/6J, and F1 hybrid mice. DBA/2J mice are extremely susceptible to audiogenic seizures, whereas C57B1/6J mice are resistant to sound-induced convulsions. C57B1/6J mice were found to have significantly higher brain levels of COMT, while MAO activities were not different in animals of these genotypes. No methanol forming activity was detected in animals of either strain. No differences were found in hepatic activities of either COMT or MAO. Pyrogallol was shown to protect DBA/2J animals against audiogenic seizures.

Acoustic Stimulation↗

PubMed1994

Oxidative stress induces NF kappa B DNA binding and inducible NOS mRNA in human epithelial cells.

Free radicals generated by a partial reduction of O2 pose a serious threat to tissues and vital organs and cells. The major site of interaction between the lung and inhaled oxidants is the epithelium. We have examined the effect of pyrogallol, an O2- generator, on the ability of human epithelial cells to produce active DNA binding proteins and inducible nitric oxide synthase (iNOS) mRNA in cultured A549 epithelial cells. NF kappa B binding in the nuclei of these cells was determined by electrophoretic mobility shift assays. iNOS mRNA was measured using reverse transcription of PCR. There was a time- and concentration-dependent induction of NF kappa B binding, followed by a time and dose dependent increase in iNOS mRNA levels. These results suggest that in airways the initial response to oxidative stress may be to induce NF kappa B-responsive genes, such as iNOS, which may play an important role in defending the airway against oxidative stress.

Amino Acid Oxidoreductases↗

PubMed1990

CGP 28014, a new inhibitor of cerebral catechol-O-methylation with a non-catechol structure.

CGP 28014 (N-(2-pyridone-6-yl)-N',N'-di-n-propylformamidine) or its methanesulfonate salt CGP 28014 A was suspected to be a catechol-O-methyl-transferase (COMT) inhibitor because it was found to reduce the levels of homovanillic acid (HVA) and to increase those of 3,4-dihydroxyphenylacetic acid (DOPAC) in the rat striatum, after oral or intraperitoneal administration. These effects were maintained after repeated administration. The compound was only weakly active as a COMT inhibitor in vitro. However, its effect on striatal HVA and DOPAC was not prevented by pretreatment with the inhibitor of microsomal drug metabolizing enzymes in the liver, proadifen, indicating that, if CGP 28014 acts as a prodrug, its conversion to the active compound is not by oxidative metabolism in the liver. Also, there was no evidence that conversion to 2-amino-6-hydroxypyridine could explain its effects. The in vivo effect of CGP 28014 was substantiated in two additional in vivo test systems. Thus, it inhibited the accumulation of 3-methoxytyramine in the rat striatum after MAO inhibition by clorgyline, and the formation of O-methyl-DOPA from exogenously administered DOPA. It proved to be equipotent or nearly so with tropolone, and also showed a similar duration of action. Similar to tropolone, it increased S-adenosylmethionine levels in the striatum. Pyrogallol, on the other hand, decreased them, because being a substrate of COMT, it consumes methyl groups. This suggests that CGP 28014 does not inhibit COMT because it is a substrate of the enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

PubMed1986

Enhanced superoxide dismutase activity of pulsed cytochrome oxidase.

The superoxide dismutase (SOD) activity of beef heart cytochrome oxidase, both in the resting (as isolated) and pulsed (reduced and reoxidized) states, has been investigated using their ability to inhibit the autoxidation rate of pyrogallol and epinephrine. Resting oxidase showed variable SOD activity, while in the pulsed state the SOD activity of cytochrome oxidase (CcO) increased by an order of magnitude. These results are discussed in terms of a physiological role for the pulsed oxidase.

Animals↗

PubMed1983

Inhibitors of prostaglandin synthesis block the induction of staphylococcal enterotoxin B-activated T-suppressor cells.

A variety of arachidonic acid metabolites possess the ability to modulate immune cell function. Various inhibitors of arachidonic acid metabolism were compared with regard to their effects on T-suppressor (Ts) cell function. Using staphylococcal enterotoxin B (SEB) to activate Lyt-2+ Ts cells, it was shown that indomethacin and 5,8,11,14-eicosatetraynoic acid (ETYA) inhibit the induction phase, but not the expression phase, of suppressor cell activity. Agents which inhibit thromboxane synthetase or lipoxygenase activities (imidazole, nordihydroguaiaretic acid, and pyrogallol) were not found to affect Ts cell induction. Since inhibitors of prostaglandin synthesis are thought to induce lower levels of cyclic adenosine monophosphate, an attempt to overcome the indomethacin inhibition of Ts cell induction by modulating cyclic adenosine monophosphate levels was made. It was found that theophylline and isoproterenol are not able to overcome the inhibition by indomethacin of Ts cell activity. These results strongly suggest that induction of Ts cells by SEB is dependent on the synthesis of products of the prostaglandin synthetase pathway.

5,8,11,14-Eicosatetraynoic Acid↗