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PubMed1970

Activite succino-deshydrogenasique des microsomes et mode d'incorporation du succinate 2,3-(14)C dans les acides gras des microsomes de foie de rat in vitro.

The incorporations of 2,3-(14)C-succinate 2-(14)C-acetate into fatty acids of different cellular fractions of rat liver were studied. Acetate was incorporated mainly into supernatant and succinate into microsomal fatty acids. Mitochondria only could intensively decarboxylate pyruvate. Avidine inhibited fatty acid synthesis from succinate mainly in the supernatant. It is suggested that succinate is an important physiological precursor of fatty acids in the liver and that an active succino-dehydrogenase is present in microsomes.

Journal Article↗
PubMed1989

Induction of differentiated phenotypes in melanoma cells by a combination of an adenosine 3',5'-cyclic monophosphate stimulating agent and D-alpha tocopheryl succinate.

The purpose of this investigation was to identify those agents and combinations of agents that help convert murine melanoma cells to cells of differentiated (normal-like) phenotype in culture. The agents used were 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (R020-1724), which is an adenosine 3',5'-cyclic monophosphate (cAMP) phosphodiesterase inhibitor that has never been tested on melanoma cells in culture, and d-alpha tocopheryl succinate (vitamin E succinate), which has previously been shown to inhibit growth and induce morphological differentiation in melanoma cells. The results indicated that R020-1724 by itself inhibited growth, reduced survival, caused morphological differentiation and increased the melanin content (one of the biochemical differentiated functions) in melanoma cells. Vitamin E succinate had a similar effect on the melanoma cells, which supports past research on this vitamin. A combination of R20-1724 and vitamin E succinate had a significantly greater effect on the melanoma cells than either of the agents by themselves. The agents identified in this study may provide useful tools for studying the mechanisms of differentiation in melanoma cells.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1981

Effect of oestriol succinate on serum lipids.

The series comprises 70 women with climacteric symptoms; 14 of them were oophorectomized. The first group of patients received 4 mg of oestriol succinate per day or a placebo in a double-blind experiment. In the second part of the study oophorectomized women were given 8 mg of oestriol succinate per day or 16 mg/day divided into two doses. Serum total cholesterol, HDL-cholesterol and serum triglycerides were estimated before drug treatment and after drug administration for three and six months. Administration of 4-16 mg/day of oestriol succinate was without effect on serum total cholesterol. A significant increase of 25-30% in HDL-cholesterol was observed following administration of oestriol succinate (8 mg divided into two doses) with a rising tendency in total triglyceride value.

Adult↗
PubMed1996

Naphthalene-induced oxidative stress in rats and the protective effects of vitamin E succinate.

Quinone metabolites of naphthalene (NAP) are known to produce lipid peroxidation. However, the ability of naphthalene to induce oxidative stress in experimental animals has not been extensively investigated. Furthermore, the effects of vitamin E succinate [(+)-alpha-tocopherol acid succinate; VES] on naphthalene-induced oxidative stress and tissue damage were assessed. Female Sprague-Dawley rats were treated with a single oral dose of 1100 mg naphthalene/kg (0.50 LD50) in corn oil. Vitamin E succinate-treated rats received 100 mg VES/kg/day orally for 3 d before naphthalene treatment, and 40 mg VES/kg/d after NAP administration. Hepatic and brain tissues and urine samples were collected 0, 12, 24, 48, and 72 h after NAP treatment. Naphthalene treatment resulted in a 2.1-fold increase in lipid peroxidation in liver and brain mitochondria at the 24-h time point. Increases in hepatic and brain mitochondrial lipid peroxidation in VES plus NAP-treated rats were 39-46% less than NAP treated rats at 24 h. DNA-single strand breaks increased 3.0-fold in hepatic tissues in NAP treated rats, and increased only 1.6-fold in VES protected rats at the 24-h time point. Glutathione (GSH) decreased by 83 and 49% in hepatic and brain tissues, respectively, in NAP-treated rats at the 24-h time point, while GSH content in VES plus NAP-treated rats decreased 47 and 21% in hepatic and brain tissues, respectively, at this same time point. Microsomal membrane fluidity, a measurement of membrane damage, increased 1.9- and 1.7-fold in liver and brain tissues, respectively, in NAP-treated rats, and only 1.3- and 1.2-fold in NAP plus VES-treated rats at the 24-h time point. The urinary excretion of malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT), and acetone (ACON) was determined at 0-96 h after NAP administration. Between 12-24 h after NAP administration maximal excretion of the four urinary lipid metabolites was observed, with increases of 4.5-, 2.7-, 2.3-, and 2.8-fold for MDA, FA, ACT, and ACON, respectively, at the 24-h time point. VES reduced the NAP-induced excretion of these urinary metabolites by 28-49% 24 h after NAP administration. These results support the hypothesis that NAP induces oxidative stress and tissue damage, and that vitamin E succinate provides significant protection.

Animals↗
PubMed1995

Vitamin E succinate potentiates the inhibitory effect of prostaglandins on oral squamous carcinoma cell proliferation.

Previous studies have shown that prostaglandin E2 (PGE2) and vitamin E succinate can act in an additive manner to inhibit the proliferation of human oral squamous carcinoma cells (SCC-25). The initial studies on the additive anticancer activity of PGE2 and vitamin E succinate have been extended to include antineoplastic PGs, delta 12-PGJ2 and PGJ2. Treatment of oral squamous carcinoma cells (SCC-15) with delta 12-PGJ2, PGJ2, and vitamin E succinate, individually, caused significant concentration-dependent inhibition of cell proliferation to various degrees. PGJ2 was most potent and caused an inhibition that corresponded to 85.55% at 10(-5) M. Addition of 1 microM of vitamin E succinate to delta 12-PGJ2 or PGJ2 resulted in a significant increase in the inhibitory potency of the lower concentrations of the two PGs. These results suggest a novel role for a mixture of PGs and vitamin E as potent antitumor proliferative agents.

Antineoplastic Agents↗
PubMed2005

Economic implications of extended-release metoprolol succinate for heart failure in the MERIT-HF trial: a US perspective of the MERIT-HF trial.

BACKGROUND: The MERIT-HF trial demonstrated improved survival and fewer hospitalizations for worsening heart failure with extended-release (ER) metoprolol succinate in patients with heart failure. This study sought to estimate the economic implications of this trial from a US perspective. METHODS AND RESULTS: A discrete event simulation was developed to examine the course of patients with heart failure. Characteristics of the population modeled, probabilities of hospitalization and death with standard therapy, and risk reductions with ER metoprolol succinate were obtained from Metoprolol CR/XL Randomized Intervention Trial in Chronic Heart Failure (MERIT-HF) and evaluated in weekly cycles. Direct medical costs were estimated from US databases in 2001 US dollars. Uncertainty in inputs was incorporated and analyses were carried out to estimate events prevented total and net costs. The model predicts that ER metoprolol succinate will prevent approximately 7 deaths and 15 hospitalizations from heart failure per 100 patients over 2 years. Compared with standard therapy alone, this translates to a cost reduction between $395 and $1112 per patient, depending on whether the costs of hospitalizations for other causes are included. Savings were maintained in 90% of the simulations. CONCLUSION: This analysis predicts that the positive effect of ER metoprolol succinate on mortality and morbidity demonstrated in MERIT-HF leads to substantial savings.

Adrenergic beta-Antagonists↗
PubMed1986

Reversed-phase high-performance liquid chromatographic assay for the determination of potency and impurities in tazadolene succinate bulk drug and capsules.

A reversed-phase assay based on high-performance liquid chromatography with a water-acetonitrile-tetrahydrofuran (THF)-triethylamine (TEA)-perchloric acid (pH 2.5) mobile phase and a Zorbax C8 column has been validated for the determination of the purity of tazadolene succinate (I) [E-(+/-)-1-(2-benzylidenecyclohexyl)azetidine succinate, U-53996H] bulk drug, the potency of tazadolene succinate hard-filled capsule formulations and impurity levels in bulk drug. The system resolves E- and Z-isomers and other structurally related molecules. Retention of these compounds is mainly dependent on the amount of acetonitrile and THF in the mobile phase. An amine must be present in the mobile phase to bring about elution of I. The potency assay utilizes testosterone as internal standard. Potency assays exhibited relative standard deviations (R.S.D.) of less than 1%. Quantitative recovery from hard-filled capsules (HFC) is obtained by using a simple extraction procedure. Potential process impurities, potential degradation products, and formulation excipients are resolved. The assay is linear for tazadolene succinate concentrations equivalent to 50-150% of the assay concentration. Impurities can be quantitated to levels equivalent to about 0.1% by weight with R.S.D. less than 5%. The estimated limit of detection for I is about 2 ng for a 20 microliters injection.

Analgesics↗
PubMed1989

Purification and properties of two succinic semialdehyde dehydrogenases from Klebsiella pneumoniae.

Two forms of succinic semialdehyde dehydrogenase have been isolated in Klebsiella pneumoniae M5a1. The two enzymes could be separated by filtration on Sephacryl S-300 and their apparent molecular weights were approx. 275,000 and 300,000. The large enzyme is specific for NADP. The smaller enzyme, which is induced by growth on 3-hydroxyphenylacetic acid, 4-hydroxyphenylacetic acid, 3,4-dihydroxyphenylacetic acid and gamma-aminobutyrate, has been purified to 96% homogeneity by affinity chromatography. The NAD-linked succinic semialdehyde dehydrogenase was able to use NADP as cofactor. Its induction is coordinated with 3- and 4-hydroxylase, the enzymes which initiate degradation of 3- and 4-hydroxyphenylacetic acid. The NAD-linked form is also induced by exogenous succinic semialdehyde. The large enzyme is specific for NADP and has been isolated from a defective mutant which lacked the activity of the NAD-linked succinic semialdehyde dehydrogenase. Activity and stability conditions and true K m values for substrates and cosubstrates of the two enzymes were determined. Some aspects of the induction of the NAD-linked enzyme participating in the metabolism of 4-hydroxyphenylacetic and gamma-aminobutyrate were studied.

Enzyme Induction↗
PubMed2003

Stability-indicating methods for the determination of sumatriptan succinate.

Four stability-indicating methods were developed for the determination of sumatriptan succinate in the presence of its degradation products. The first method depends on the quantitative densitometric evaluation of thin-layer chromatography of sumatriptan succinate in the presence of its degradation products without any interference. Cyclohexane-dichloromethane-diethylamine (50:40:10 v/v/v) was used as a mobile phase and the chromatogram was scanned at 228 nm. This method determines sumatriptan succinate in the concentration range l-8 microg per spot with mean percentage recovery 100.52+/-1.23%. The second and third methods depend on the use of first-derivative (D(1)) and second-derivative (D(2)) spectrophotometry at 234 and 238 nm, respectively. These methods determine the drug in the concentration range 1.25-10 microg x ml(-1) with mean percentage recovery 99.91+/-1.01% and 99.96+/-1.13% for (D(1)) and (D(2)), respectively. The fourth method depends on the use of ratio derivative spectrophotometric technique. The amplitude in the first derivative of the ratio spectra at 235 nm was selected to determine the cited drug in the presence of its degradation products. Calibration graph is linear in the concentration range 1.25-10 microg x ml(-1) with mean percentage recovery 100.19+/-1.19%. The suggested methods were successfully applied for determining sumatriptan succinate in bulk powder, laboratory-prepared mixtures and pharmaceutical dosage forms (Imigran tablet) with good accuracy and precision. The results obtained by applying the proposed methods were statistically analyzed and compared with those obtained by the reported method.

Calibration↗
PubMedDate not supplied

An adduct of cis-diamminedichloroplatinum(II) and poly(ethylene glycol)poly(L-lysine)-succinate: synthesis and cytotoxic properties.

A noncovalent adduct of the antineoplastic drug cis-diamminedichloroplatinum (cDDP) and a biocompatible graft copolymer of poly(L-lysine) and methylpoly(ethylene glycol) succinate is described. Upon incubation of cDDP with [O-methylpoly(ethylene glycol)-O'-succinyl]-N- epsilon-poly(L-lysine)n-N-epsilon-succinate, n = 250-270, highly soluble, long circulating adducts were formed which contained 4.3% of platinum by weight. Approximately 60% of the polymer-associated drug was released during dialysis against saline or serum albumin containing saline, with a half-time of release of 63 h. The adducts showed a pronounced antineoplastic effect in BT-20 human adenocarcinoma cell cultures. In cell proliferation assays, the concentration of half-inhibition of [3H]thymidine uptake was 0.9 +/- 0.2 microM for the drug-copolymer adduct compared to 0.3 +/- 0.1 microM for free cDDP. The adduct showed a long blood half-life (ca. 14 h in rats) and accumulated in experimental mammary adenocarcinomas at 2.5-3.5% injected dose per gram of tissue. A control adduct of cDDP with the backbone portion of the copolymer, poly(L-lysine)-N-epsilon-succinate, had a short half-life in the bloodstream (ca. 30 min) and low accumulation (0.5% injected dose per gram) in tumor. A dual therapeutical effect of methylpoly(ethylene glycol)succinylpoly(L-lysine)-succinate as a carrier of cDDP is suggested: (1) as a carrier for systemic release of the active drug from the macromolecule while it circulates in the bloodstream and (2) as a carrier for on-site delivery which results from the release of the drug in the tumor as a consequence of accumulation of the copolymer in the tumor.

Adenocarcinoma↗
PubMed2001

Dimeric pig heart succinate-coenzyme A transferase uses only one subunit to support catalysis.

Pig heart succinate-coenzyme A transferase (succinyl-coenzyme A: 3-oxoacid coenzyme A transferase; E. C. 2.8.3.5.), a dimeric enzyme purified by affinity chromatography on Procion Blue MX-2G Sepharose, reacts with acetoacetyl-coenzyme A to form a covalent enzyme-coenzyme A thiolester intermediate in which the active site glutamate (E344) of both subunits each forms thiolester links with coenzyme A. Reaction of this dimeric enzyme-coenzyme A species with sodium borohydride leads to inactivation of the enzyme and reduction of the thiolester on both subunits to the corresponding enzyme alcohol, as judged by electrospray mass spectrometry. Reaction of the dimeric enzyme-coenzyme A intermediate with either succinate or acetoacetate, however, results in only one-half of the coenzyme A being transferred to the acceptor carboxylate to form either succinyl-coenzyme A or acetoacetyl-coenzyme A. Reaction of this latter enzyme species with borohydride caused no loss of enzyme activity despite the reduction of the remaining half of the enzyme-coenzyme A thiolester to the enzyme alcohol. That this catalytic asymmetry existed between subunits within the same enzyme dimer was demonstrated by showing that the enzyme species, created by successive reaction with acetoacetyl-coenzyme A and succinate, bound to Blue MX-2G Sepharose through the remaining available active site and could be eluted as a single chromatographic species by succinyl-coenzyme A. It is concluded that while both of the subunits of the succinate-coenzyme A transferase dimer are able to form enzyme-coenzyme A thiolester intermediates, only one subunit is competent to transfer the coenzyme A moiety to a carboxylic acid acceptor to form the new acyl-coenzyme A product. The possible structural basis for this catalytic asymmetry and its mechanistic implications are discussed.

Acyl Coenzyme A↗
PubMed2006

Pediatric erythromycins: a comparison of the properties of erythromycins A and B 2'-ethyl succinates.

The antibiotic erythromycin A is generally administered to children as a suspension of the pro-drug erythromycin A 2'-ethyl succinate. The success of the pro-drug depends on (a) elimination of the unacceptably bitter taste of free erythromycin, (b) its stability against stomach acid, and (c) its smooth (base-catalyzed) hydrolysis in the body to yield active erythromycin. We have investigated the rates and pathways of acid-catalyzed degradation and base-catalyzed hydrolysis of the 2'-ethyl succinates of erythromycins A and B. Esterification does not protect the drugs against acid-catalyzed degradation in solution; however, erythromycin B 2'-ethyl succinate is much more stable than the corresponding erythromycin A ester, degrading nearly 40 times more slowly. The rates of base-catalyzed hydrolysis in conditions mimicking the blood stream are similar for the two pro-drugs. We conclude that erythromycin B 2'-ethyl succinate is an attractive prospect as a pediatric erythromycin pro-drug.

Anti-Bacterial Agents↗
PubMed1983

Chloramphenicol serum concentration falls during chloramphenicol succinate dosing.

Chloramphenicol succinate and chloramphenicol kinetics were examined on two occasions at steady state, separated by 2 to 17 days, in 10 pediatric patients on the same intravenous dose of chloramphenicol succinate. The steady-state peak serum concentration of chloramphenicol succinate fell from an average of 77.1 micrograms/ml during the first study to 42.2 micrograms/ml during the second. The steady-state peak serum concentration of chloramphenicol also decreased from an average of 27.8 micrograms/ml to 24.9 micrograms/ml. There was a marked decrease in the steady-state trough serum concentration of chloramphenicol, which averaged 8.4 micrograms/ml during the first and 5.3 micrograms/ml at the time of the second study. Mean area under the serum concentration-time curve (AUC) of chloramphenicol succinate decreased from 59.7 micrograms . hr/ml to 24.0 micrograms . hr/ml. The AUC of chloramphenicol averaged 105.7 micrograms . hr/ml at the time of the first and decreased to 79.5 micrograms . hr/ml during the second study. Mean percent decrease in the AUC of chloramphenicol was about 28% and occurred most substantially in patients with high AUCs during the first study. Mean elimination chloramphenicol half-life was 3.0 hr during the first study and fell to 2.3 hr at the time of the second study. Our data indicate that chloramphenicol serum concentration should be monitored frequently, especially in patients not responsive to a set dose.

Adolescent↗
PubMed1987

Results of a 5 years prospective study of estriol succinate treatment in patients with climacteric complaints.

In a prospective study 911 patients were treated over a period of 5 years (M = 2.2) or a total of 2007 treatment years with estriol succinate oral (Synapause, 2-12 mg per day). The treatment was very effective in the removal of all typical climacteric complaints and of the atrophic genital changes caused by estrogen deficiency. Subjective side effects were seldom seen and without practical importance for the treatment. Objective, grave side effects were only few: one superficial phlebo-thrombosis, 2 cases of thrombophlebitis, one carcinoma in situ of the portio vaginalis uteri and 2 mammary cancers were seen. The carcinoma had probably no causal relationship to the treatment. Embolies, myocardial infarctions, cerebrovascular and liver-gall bladder complications did not occur during treatment. The rate of uterine bleedings was low. The incidence of all complications was not increased by estriol succinate; but was even lower than expected. Endometrial and ovarian cancers were not seen. Estriol succinate is accordingly a very effective and well tolerated preparation against climacteric complaints, exerting no significant side effects. It is remarkable that it does not proliferate the endometrium when given in one dose a day. Estriol succinate can therefore be characterized as the estrogen to be favoured for the treatment of postclimacteric women, who do not want to have uterine bleedings any longer.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1997

Antiproliferative effect of intravitreal alpha-tocopherol and alpha-tocopheryl-acid-succinate in a rabbit model of PVR.

PURPOSE: To evaluate the antiproliferative properties of alpha-tocopherol and alpha-tocopheryl-acid-succinate in a rabbit model of proliferative vitreoretinopathy. METHODS: Fifty-seven rabbits underwent gas-compression vitrectomy and gas/fluid exchange. Group 1 (n = 8): 50 micrograms alpha-tocopherol in 1 ml of 0.5% ethanol in balanced salt solution; Group 2 (n = 8): 50 micrograms alpha-tocopheryl-acid-succinate in 1 ml of 0.5% ethanol in balanced salt solution; Groups 3 (n = 4) and 4 (n = 2): 1 ml 0.5% ethanol in balanced salt solution; Groups 5 (n = 12) and 8 (n = 9): alpha-tocopherol in 1 ml silicone oil (12 mg/ml); Group 6 (n = 9): 1 ml silicone oil; Group 7 (n = 5): 1 ml balanced salt solution. Groups 1-3, and 5-7 also received fibroblasts and platelet-rich plasma injection. Fundus evaluation was performed during a four-week period. The eyes were enucleated for gross examination on day 28. Histopathology was performed on Group 4. RESULTS: Alpha-tocopherol and alpha-tocopheryl-acid-succinate in saline solution delayed development of proliferative vitreoretinopathy, compared to the control group (statistically significant during the first week, Mann Whitney, p < 0.05). The alpha-tocopherol in the silicone-oil group delayed development of proliferative vitreoretinopathy, compared to the silicone-oil group during the second to fourth weeks (no statistically significant difference, p > 0.05). CONCLUSIONS: Alpha-tocopherol and alpha-tocopheryl-acid-succinate in saline solution showed retardation of proliferative vitreoretinopathy traction retinal detachments. In silicone oil, alpha-tocopherol is slowly released and decreases the severity of proliferative vitreoretinopathy, especially during the second week of follow-up.

Animals↗
PubMed2001

Prostaglandin E2 is involved in the increase of cytochrome P-450 2B1 expression by alpha-tocopheryl succinate in primary rat hepatocytes in the presence of phenobarbital.

The modulation of cytochrome P-450 2B1 expression by alpha-tocopheryl succinate and whether prostaglandin E2 is involved in this modulation in primary rat hepatocytes in the presence of phenobarbital were investigated. A primary rat hepatocyte culture model that faithfully reproduces the phenobarbital response observed in vivo was used. Intracellular alpha-tocopherol content was dose dependently increased by alpha-tocopheryl succinate incubation. Hepatocytes were demonstrated to have prostaglandin E2-synthesizing capability. alpha-Tocopheryl succinate inhibited prostaglandin E2 synthesis by hepatocytes and increased cytochrome P-450 2B1 expression in the presence of phenobarbital; however, it had little effect on intracellular cAMP level. To mimic the exogenous source of prostaglandin E2 from nonparenchymal cells, various concentrations of prostaglandin E2 were added to the cell culture. High doses of exogenous prostaglandin E2 (100 and 1,000 nM) inhibited the cytochrome P-450 2B1 expression in the presence of phenobarbital compared with low doses (1 and 10 nM); however, the presence of high doses of prostaglandin E2 had no effect on intracellular cAMP level. Forskolin significantly increased intracellular cAMP level and inhibited cytochrome P-450 2B1 expression in the presence of phenobarbital. The results of this study indicate that alpha-tocopheryl succinate increases cytochrome P-450 2B1 expression via its inhibition of prostaglandin E2 synthesis in the presence of phenobarbital; however, changes in intracellular cAMP level are not related to cytochrome P-450 2B1 expression.

Animals↗
PubMed1991

RRR-alpha-tocopheryl succinate enhances T cell mitogen-induced proliferation and reduces suppressor activity in spleen cells derived from AEV-infected chickens.

RRR-alpha-tocopheryl succinate was demonstrated to be a potent in vitro modulator of retrovirus-induced immune abnormalities. Spleen cells from avian erythroblastosis virus (AEV)-infected chickens exhibit suppressed T cell mitogen-induced proliferative responses and elevated levels of suppressor T cell activity. In vitro addition of RRR-alpha-tocopheryl succinate resulted in amelioration of these abnormalities. Antioxidants including Trolox (a water-soluble analogue of RRR-alpha-tocopherol with antioxidant properties) and a combination of butylated hydroxyanisole and butylated hydroxytoluene were able to restore immune functions to levels similar to those achieved with RRR-alpha-tocopheryl succinate treatment. Aspirin, an irreversible inhibitor of cyclooxygenase activity, was capable of ameliorating some of the AEV-induced immune dysfunctions. These studies suggest a role for the antioxidant functions of RRR-alpha-tocopheryl succinate in modulation of retrovirus-induced immune abnormalities.

Alpharetrovirus↗
PubMed1988

Effect of alpha tocopheryl succinate on adenylate cyclase activity in murine neuroblastoma cells in culture.

Alpha tocopheryl succinate treatment (6-8 micrograms/ml), which inhibited the growth of murine neuroblastoma (NBP2) cells (46 +/- 3%), reduced basal and prostaglandin (PG)E1- and PGA2-stimulated adenylate cyclase (AC) activity in vitro. It also inhibited sodium fluoride (NaF)- and forskolin-stimulated AC activity, suggesting that the effect of vitamin E succinate on AC activity is mediated via stimulatory GTP-binding protein (Gs) and catalytic subunit. Vitamin E succinate-induced reduction of AC activity is not strictly related to inhibition of cell growth. This is substantiated by the finding that, although retinoic acid and butylated hydroxyanisole reduced the growth by over 50%, they did not inhibit AC activity. On the other hand, 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (R020-1724, 200 micrograms/ml), which inhibited growth (73 +/- 3%) and induced differentiation in NB cells, increased basal and PGE1-stimulated AC activity. Vitamin E succinate treatment also reduced PGE1- and PGA2-AC activity in murine fibroblasts (L-cells) without inhibiting growth.

Adenylyl Cyclases↗