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PubMed1995

Stimulation of the Alternative Pathway by Succinate and Malate.

Stimulation of the cyanide-resistant oxidation of exogenous NADH in potato (Solanum tuberosum L. cv Bintje) tuber callus mitochondria was obtained with succinate, malate, and pyruvate. Half-maximal stimulation was observed at a succinate or malate concentration of 3 to 4 mM, which is considerably higher than that found for pyruvate (0.128 mM). No effect of succinate or malate addition was found when duroquinone was the electron acceptor. Duroquinol oxidation via the alternative pathway was poor and not stimulated by organic acids. Under stimulating conditions, no swelling or contraction of the mitochondria could be observed. Conversely, variation of the osmolarity did not affect the extent of stimulation. However, the assay temperature had a significant effect: no stimulation occurred at temperatures below 16 to 20[deg]C. Membrane fluidity measurements showed a phase transition at about 17[deg]C. Ubiquinone reduction levels were not significantly higher in the presence of succinate and malate, but the kinetics of the alternative oxidase were changed in a way comparable to that found for stimulation by pyruvate. At low temperatures the alternative oxidase displayed "activated" kinetics, and a role for membrane fluidity in the stimulation of the alternative pathway by carboxylic acids is suggested.

Journal Article↗
PubMed1968

Properties of succinate oxidation in tomato fruit mitochondria.

Mitochondria from tomato fruit (Lycopersicon esculentum Mill.) exhibited a respiratory control ratio of 2.5 and an ADP:O ratio of 1.3 for succinate oxidation for 24 hours after isolation. They also showed a delay in response to the first addition of ADP. The addition of ATP and ADP before succinate eliminated the delayed response as did chelation of endogenous cations with ethylenediaminetetraacetic acid. The addition of ATP after succinate resulted in a longer delay in response than that obtained with ADP. Exogenous oxaloacetate in low concentration inhibited respiration in states 3 and 4 with succinate and resulted in delayed response to ADP. The function of adenine nucleotide during the delay in response may be to promote the metabolism of oxaloacetate or to decrease the affinity of oxaloacetate to its site of inhibition.

Journal Article↗
PubMed1973

Regulation of Succinate Dehyrogenase in Higher Plants: I. Some General Characteristics of the Membrane-bound Enzyme.

The spectrophotometric phenazine methosulfate assay of succinate dehydrogenase was adapted to use with cauliflower (Brassica oleracea) and mung bean (Phaseolus aureus) mitochondria with suitable modifications to overcome the permeability barrier to the dye. Procedures in the literature for the isolation and sonic disruption of mitochondria from these sources were modified to assure maximal yield and stability of the enzyme. In tightly coupled mung bean mitochondria, as isolated, about half of the succinate dehydrogenase is in the deactivated state, and the enzyme is further extensively deactivated on sonication or freeze-thawing. In cauliflower mitochondria most of the enzyme is in the deactivated form, and little or no further deactivation occurs on sonication or freeze-thawing. Incubation of mitochondria from either source with succinate leads to full activation of the enzyme. The energy of activation for the conversion of the deactivated to the activated form in membranal preparations under the influence of substrate is about 30,000 cal/mole, essentially the same value as in animal tissues. Activation of the enzyme also occurs under the influence of a variety of other agents, among which the action of anions as activators is documented in the present paper. Activation is accompanied by the release of very tightly bound oxaloacetate. As in animal tissues, the enzyme appears to contain covalently bound flavin (histidyl 8alpha-FAD), and the turnover number is 19,400 moles of succinate oxidized/mole of histidyl flavin at pH 7.5, 38 C.

Journal Article↗
PubMed1979

Citrate and succinate uptake by potato mitochondria.

The uptake of [(14)C]citrate and [(14)C]succinate was studied in potato mitochondria (Solanum tuberosum var. Russet Burbank) using cellulose pore filtration and was found to occur by the same mechanisms as described for mammalian mitochondria. Potato mitochondria, in the absence of respiration, have a very low capacity for uptake by exchange with endogenous anions, taking up only 2.4 nanomoles citrate and 2.0 nanomoles succinate per milligram protein. Maximum citrate uptake of over 17 nanomoles per milligram protein occurs in the presence of inorganic phosphate, a dicarboxylic acid, and an external energy source (NADH), conditions where net anion accumulation proceeds, mediated by the interlinking of the inorganic phosphate, dicarboxylate, and tricarboxylate carriers. Maximum succinate uptake in the absence of respiratory inhibitors requires only added inorganic phosphate.Compounds which inhibit respiration (antimycin), the exchange carriers (mersalyl and benzylmalonate), or the establishment of the membrane proton motive force (uncouplers) reduce substrate accumulation. A potent inhibitor of the citrate carrier in animal mitochondria, 1,2,3-benzenetricarboxylic acid, does not inhibit citrate uptake in potato mitochondria. Citrate uptake is reduced by concurrent ADP phosphorylation and this reduction is sensitive to oligomycin. The initiation of state 3 after a 3-minute substrate state results in a reduction of the steady-state of citrate uptake by approximately 50%. Accumulation of succinate initially is inhibited by increasing sucrose concentration in the reaction medium from 50 to 400 millimolar.Limited substrate uptake is one of the factors responsible for the often observed depressed initial state 3 respiration rates in many mitochondrial preparations. Since nonlimiting levels of substrate in the matrix cannot be attained by energy-independent exchange, a dependence on respiration for adequate uptake results. Substrate limitation therefore occurs in the matrix for the period of time needed for energy-dependent accumulation of nonlimiting levels.

Journal Article↗
PubMed1982

Effect of butanedioic Acid mono (2,2-dimethylhydrazide) on the activity of membrane-bound succinate dehydrogenase.

Mitochondria isolated from hypocotyls of five-day-old bean (Phaseolus vulgaris L. ;Black Valentine') seedlings rapidly oxidized succinate, malate, and NADH. Oxidation rates, respiratory control, and ADP:O ratios obtained with saturating concentrations of all three substrates indicated that the mitochondria were tightly coupled. The mitochondrial preparation was then employed to investigate the respiration-inhibiting effects of butanedioic acid mono (2,2-dimethyl-hydrazide) (daminozide) a plant growth retardant having structural similarity to an endogenous respiratory substrate (succinate). Daminozide markedly inhibited the activity of membrane-bound succinate dehydrogenase. Inhibition was of the competitive type (apparent K(i), 20.2 millimolar) with respect to succinate. Although not excluding other hypotheses, the results support an active role for daminozide in the suppression of respiration as an important metabolic site of its action as a plant growth regulator.

Journal Article↗
PubMed2004

Protective effects of vitamin A and vitamin E succinate against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced body wasting, hepatomegaly, thymic atrophy, production of reactive oxygen species and DNA damage in C57BL/6J mice.

The protective effect of vitamin A and vitamin E succinate against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced acute toxicity and measures of oxidative stress was studied. Ten mice were treated with either vitamin A (50 mg/kg every other day for eight days) or vitamin E succiante (150 mg/kg/day followed by a dose of 40 mg/kg/day for five additional days). Half of each of the above groups of animals received TCDD on day 4. Five mice received corn oil or TCDD alone. After five days of TCDD treatment, antioxidant combination treatment with vitamin A and TCDD or vitamin E succinate and TCDD resulted in a significant reduction in indicators of acute toxicity including the decrease in total body and thymus weight as compared to TCDD alone (P<0.05). The combination treatment produced also a significant reduction in the increase in liver weight as compared to TCDD only (P<0.05). Following one day of treatment with 50 microg TCDD/kg, vitamin A and vitamin E succinate produced a significant decrease in the production of superoxide anion by peritoneal lavage cells (P<0.05) and in DNA-single strand breaks in the same cells (P<0.05) as assessed by the reduction of cytochrome c and the alkaline elution technique, respectively. A significant decrease in DNA-single strand breaks in peritoneal lavage cells was observed following 5 days treatment with 50 microg TCDD/kg (P<0.05). The results indicate a potential role for oxidative stress in the acute toxicity of TCDD and a protective effect for vitamin A and vitamin E succinate in the overall toxicity of TCDD including measures of oxidative stress.

Animals↗
PubMed1982

Succinate-Induced Morphology of Rhizobium trifolii 0403 Resembles That of Bacteroids in Clover Nodules.

Morphological changes which accompany nutrient enrichment of Rhizobium trifolii 0403 were studied. Assays of cell number and size coupled with scanning electron microscopy and immunofluorescence microscopy showed that succinate induces cells to stop dividing in vitro and to swell either in the cell center or at one cell pole. The extent and frequency of in vitro cell swelling were in direct relation to the concentration of succinate added to the enrichment medium. The in vitro swelling of cells in 16.6 mM succinate plus Casamino Acids, glucose, and yeast extract closely resembled that of bacteroids of R. trifolii 0403 in nitrogen-fixing nodules of white clover. We hypothesize that succinate may be involved in the transformation of vegetative bacteria into the bacteroid morphology found in nitrogen-fixing nodules.

Journal Article↗
PubMed1990

Decreased expressions of c-myc and H-ras oncogenes in vitamin E succinate induced morphologically differentiated murine B-16 melanoma cells in culture.

Treatment of B-16 melanoma cells in culture with d-alpha-tocopheryl succinate (vitamin E succinate) at concentrations of 11.3 and 15.1 microM inhibited growth and induced cell differentiation in culture. Vitamin E succinate treatment decreased the levels of c-myc and H-ras specific mRNAs in melanoma cells. Similar results were obtained by the vitamin retinoic acid and the nonvitamin agents R020-1724 (4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone), an inhibitor of cyclic nucleotide phosphodiesterase (0.72 mM), and sodium butyrate (1 mM), which induced differentiation and (or) inhibited growth of melanoma cells in culture. The extent of inhibition of c-myc mRNA was greater than that of H-ras mRNA. These results indicate that vitamin E succinate induced reduction of the levels of c-myc and H-ras mRNAs is related to growth inhibition of melanoma cells in culture.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed2004

Differential response of human ovarian cancer cells to induction of apoptosis by vitamin E Succinate and vitamin E analogue, alpha-TEA.

A vitamin E derivative, vitamin E succinate (VES; RRR-alpha-tocopheryl succinate), and a vitamin E analogue, 2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid (alpha-TEA), induce human breast, prostate, colon, lung, cervical, and endometrial tumor cells in culture to undergo apoptosis but not normal human mammary epithelial cells, immortalized, nontumorigenic breast cells, or normal human prostate epithelial cells. Human ovarian and cervical cancer cell lines are exceptions, with alpha-TEA exhibiting greater proapoptotic effects. Although both VES and alpha-TEA can induce A2780 and subline A2780/cp70 ovarian cancer cells to undergo DNA synthesis arrest within 24 h of treatment, only alpha-TEA is an effective inducer of apoptosis. VES or alpha-TEA treatment of cp70 cells with 5, 10, or 20 microg/ml for 3 days induced 5, 6, and 19% versus 9, 36, and 71% apoptosis, respectively. Colony formation data provide additional evidence that cp70 cells are more sensitive to growth inhibition by alpha-TEA than VES. Differences in stability of the ester-linked succinate moiety of VES versus the ether-linked acetic acid moiety of alpha-TEA were demonstrated by high-performance liquid chromatography analyses that showed alpha-TEA to remain intact, whereas VES was hydrolyzed to the free phenol, RRR-alpha-tocopherol. Pretreatment of cp70 cells with bis-(p-nitrophenyl) phosphate, an esterase inhibitor, before VES treatment, resulted in increased levels of intact VES and apoptosis. Taken together, these data show alpha-TEA to be a potent and stable proapoptotic agent for human ovarian tumor cells and suggest that endogenous ovarian esterases can hydrolyze the succinate moiety of VES, yielding RRR-alpha-tocopherol, an ineffective apoptotic-inducing agent.

Apoptosis↗
PubMed2004

c-Jun N-terminal kinase is required for vitamin E succinate-induced apoptosis in human gastric cancer cells.

AIM: To investigate the roles of c-Jun N-terminal kinase (JNK) signaling pathway in vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells. METHODS: Human gastric cancer cell lines (SGC-7901) were treated with vitamin E succinate (VES) at 5, 10, 20 mg/L. Succinic acid and vitamin E were used as vehicle controls and condition medium only as an untreated (UT) control. Apoptosis was observed by 4', 6-diamidine-2'-phenylindole dihydrochloride (DAPI) staining for morphological changes and by DNA fragmentation for biochemical alterations. Western blot analysis was applied to measure the expression of JNK and phosphorylated JNK. After the cells were transiently transfected with dominant negative mutant of JNK (DN-JNK) followed by treatment of VES, the expression of JNK and c-Jun protein was determined. RESULTS: The apoptotic changes were observed after VES treatment by DNA fragmentation. DNA ladder in the 20 mg/L VES group was more clearly seen than that in 10 mg/L VES group and was not detected following treatment of UT control, succinate and vitamin E. VES at 5, 10 and 20 mg/L increased the expression of p-JNK by 2.5-, 2.8- and 4.2-fold, respectively. VES induced the phosphorylation of JNK beginning at 1.5 h and produced a sustained increase for 24 h with the peak level at 12 h. Transient transfection of DN-JNK blocked VES-triggered apoptosis by 52%. DN-JNK significantly increased the level of JNK, while decreasing the expression of VES-induced c-Jun protein. CONCLUSION: VES-induced apoptosis in human gastric cancer SGC-7901 cells involves JNK signaling pathway via c-Jun and its downstream transcription factor.

Apoptosis↗
PubMed1999

[Tocopherol Succinate Reference Standard (Control 981) of National Institute of Health Sciences].

The raw material of tocopherol succinate was tested for preparation of the "Tocopherol Succinate Reference Standard (Control 981)". The analytical data obtained were: infrared spectrum same as that of the Tocopherol Succinate Reference Standard (Control 8510); specific absorbance, E(1%)1 cm (286 nm) = 40.7; thin-layer chromatography, no impurities detected until 50.0 microgram; high-performance liquid chromatography (HPLC),three impurities detected and amount of tocopherol succinate estimated to be 98.2%, loss on drying, 0.19%, assay by HPLC, 101.7%. Based on the above results, the raw material was authorized as the Japanese Pharmacopoeia Reference Standard (Control 981).

Government Agencies↗
PubMed2002

[Tocopherol Succinate Reference Standard (Control 021) of National Institute of Health Sciences].

The raw material of tocopherol succinate was tested for the preparation of the "Tocopherol Succinate Reference Standard (Control 021)". Analytical data obtained were as follows: infrared spectrum, same as that of the Tocopherol Succinate Reference Standard (Control 981); specific absorbance, E1% 1 cm (286 nm) = 40.7; thin-layer chromatography, no impurities were detected until 50.0 micrograms; high-performance liquid chromatography (HPLC), four impurities were detected and the amount of tocopherol succinate was estimated to be 99.0%; loss on drying, 0.11%. Based on the above results, the raw material was authorized as the Japanese Pharmacopoeia Reference Standard (Control 021).

Chromatography, High Pressure Liquid↗
PubMed2004

[Effects of hydrocortisone sodium succinate on sodium current in human and guinea pig cardiac myocytes].

AIM: To study the effects of hydrocortisone sodium succinate on sodium current in human atrial myocytes and in guinea pig ventricular myocytes. METHODS: Single cardiac myocytes were isolated by enzyme. The effects of hydrocortisone sodium succinate on sodium current (INa) were assessed by applying whole-cell patch clamp techniques. RESULTS: Hydrocortisone sodium succinate (1, 3, 10 micromol x L(-1)) was shown to inhibit INa of both human atrial myocytes and guinea pig ventricular myocytes in concentration dependent manner and the IC50 were 6.97 and 8.74 micromol x L(-1), respectively. The inhibition effects acted quickly (1-3 min) and the maximal activating voltage of INa was not changed in both human and guinea pig cardiac myocytes. CONCLUSION: Hydrocortisone sodium succinate can exhibit inhibitory effects on INa in both human and guinea pig cardiac myocytes, and its inhibitory effects act rapidly, which are not consistent with genomic effects, so there may be nongenomic effects.

Adolescent↗
PubMed1989

Interaction of succinate Ubiquinone reductase with sulphate ion.

A new type of slow change of succinate Ubiquinone reductase (EC 1.3.99), activity which is induced by sulphate ion is described. After preincubation of submitochondrial particles or succinate ubiquinone reductase with sulphate both preparations catalyze succinate: phenazine methosulphate reductase reaction with a significant lag. When added to the assay medium sulphate ion induces biphasic time-dependent competitive inhibition of the enzyme. The sulphate-induced inhibition is apparently due to a rapid interaction of the anion with an active site of the enzyme which is followed by a slow pH-dependent (pK = 7.2) transformation of the enzyme inhibitor complex. pH profiles of the overall succinate ubiquinone reductase reaction and of equilibrium between fast and slow enzyme-sulphate complexes suggest that the same protolytic equilibrium step is involved in the formation of an active intermediate and an inactive enzyme-sulphate complex.

Journal Article↗
PubMed1991

Cardiovascular effects of nonivamide succinate.

Intravenous injection of nonivamide or nonivamide succinate (25, 250 nmol/kg) into Wistar rats induced bradycardia, hypotension, apnea and a triphasic blood pressure response: an initial short fall (effect A), an intermediate rise (effect B), and a subsequent delayed fall (effect C) of blood pressure. This blood pressure response remained unchanged after treatment with propranolol or phentolamine. In atropine-pretreatment rats the initial effect A was markedly decreased and effect C was slight increased. Effect A was absent after bilateral vagotomy. Unilateral microinjection of nonivamide succinate (3, 30 fmol) into the nucleus tractus solitarii produced a marked reduction in blood pressure and heart rate. In the isolated aorta of the guinea pig, application of either nonivamide or its succinate (10(-8) to 10(-5) M) eliminated the smooth muscle tone produced by phenylephrine (10(-6) M). Re-exposure to these agents, however, produced an immediate tachyphylactic relaxing response and prolonged rebound contractile response. Both compounds induced a vascular contraction rather than relaxation during tachyphylaxis. The potency of nonivamide succinate was found to be slightly greater than that of nonivamide.

Animals↗
PubMed1990

[Severe bronchial reaction induced by hydrocortisone sodium succinate in an aspirin-sensitive asthmatic patient].

This is a report of a female patient who had an anaphylaxis-like reactions to hydrocortisone sodium succinate (Saxizon). A 31-year-old female with intrinsic bronchial asthma and aspirin sensitivity was admitted to our hospital because of an episode of asthmatic attack. The patient had had episodes of dyspnea since 1976, and had been treated with oral bronchodilators and intermittent corticosteroids. After admission, she was given 100 mg of hydrocortisone sodium succinate intravenously. A few minutes later she developed severe bronchospasm and lost consciousness. An endotracheal tube was inserted and she was mechanically ventilated for 2 hours. The patient recovered after 1 hour. An inhalation challenge test with Sulpyrin was positive. When the provocation challenge test with 100 mg of hydrocortisone sodium succinate (Saxizon) injection was performed, she developed subjective and objective evidence of bronchospasm. Intradermal skin test revealed positive immediate reactions to Saxizon, Solu-cortef, Predonine. It is suggested that she had immediate hypersensitivity to hydrocortisone sodium succinate, but the mechanism of this anaphylaxis-like reaction to steroids is not certain.

Adult↗
PubMed1987

Hydrocortisone succinate and hydrocortisone simultaneously determined in plasma by reversed-phase liquid chromatography, and their pharmacokinetics in asthmatic children.

Hydrocortisone succinate and hydrocortisone are chromatographed with a mobile phase consisting of sodium acetate/acetonitrile (77/23, by vol), the effluent being monitored at 254 nm. p-Hydroxybenzoate-N-propyl is used as the internal standard. Detection limits are 0.5 mg/L for hydrocortisone succinate, 0.2 mg/L for hydrocortisone. For five different concentrations the respective mean analytical recoveries were 88.2% and 100.5%, the mean intra-assay CVs for slope 3.9% and 2.1%, and the inter-assay CVs 3.3% and 1.6%. Simultaneous measurement of hydrocortisone and its succinate ester may be useful for pharmacokinetic study. Concentration-time profiles for plasma after administration of hydrocortisone sodium succinate are presented.

Adolescent↗
PubMed1985

Prednisolone succinate and prednisolone acetate in cattle: pharmacokinetics and action on the adrenal gland.

The pharmacokinetics of prednisolone were studied in a group of 6 cows given prednisolone 21-sodium succinate IV and IM (600 micrograms/kg of body weight expressed as prednisolone alcohol) and prednisolone acetate IM (600 micrograms/kg of body weight expressed as prednisolone alcohol). After IV administration of prednisolone 21-sodium succinate, the half-life of elimination was 3.6 +/- 1.177 hours. After IM administration of prednisolone 21-sodium succinate, absorption was rapid and complete. After IM administration of prednisolone acetate, absorption was very slow with an absorption half-life of 48 hours, but was still complete. Basal plasma hydrocortisone was about 7.5 ng/ml. After IV and IM administration of prednisolone 21-sodium succinate, plasma hydrocortisone returned to normal values within 48 hours. In contrast, after IM administration of prednisolone acetate, a long adrenal suppression lasting from 4 to 6 weeks was observed.

Adrenal Glands↗