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Title
Cytosolic and mitochondrial systems for NADH- and NADPH-dependent reduction of alpha-lipoic acid.
Author
Haramaki N; Han D; Handelman GJ; Tritschler HJ; Packer L
Address
Department of Molecular and Cell Biology, University of California at
Berkeley 94720-3200, USA.
Source
Free Radic Biol Med, 22(3):535-42 1997
Abstract
In cellular, tissue, and organismal systems, exogenously supplied alpha-lipoic acid (thioctic acid) has a variety of significant effects, including direct radical scavenging, redox modulation of cell metabolism, and potential to inhibit oxidatively-induced injury. Because reduction of lipoate to dihydrolipoate is a crucial step in many of these processes, we investigated mechanisms of its reduction. The mitochondrial NADH-dependent dihydrolipoamide dehydrogenase exhibits a marked preference for R(+)-lipoate, whereas NADPH-dependent glutathione reductase shows slightly greater activity toward the S(-)-lipoate stereoisomer. Rat liver mitochondria also reduced exogenous lipoic acid. The rate of reduction was stimulated by substrates which increased the NADH content of the mitochondria, and was inhibited by methoxyindole-2-carboxylic acid, a dihydrolipoamide dehydrogenase inhibitor. In rat liver cytosol, NADPH-dependent reduction was greater than NADH, and lipoate reduction was inhibited by glutathione disulfide. In rat heart, kidney, and brain whole cell-soluble fractions, NADH contributed more to reduction (70-90%) than NADPH, whereas with liver, NADH and NADPH were about equally active. An intact organ, the isolated perfused rat heart, reduced R-lipoate six to eight times more rapidly than S-lipoate, consistent with high mitochondrial dihydrolipoamide dehydrogenase activity and results with isolated cardiac mitochondria. On the other hand, erythrocytes, which lack mitochondria, somewhat more actively reduced S- than R-lipoate. These results demonstrate differing stereospecific reduction by intact cells and tissues. Thus, mechanisms of reduction of alpha-lipoate are highly tissue-specific and effects of exogenously supplied alpha-lipoate are determined by tissue glutathione reductase and dihydrolipoamide dehydrogenase activity.

Title
Effect of DL alpha-lipoic acid on some carbohydrate metabolising enzymes in stone forming rats.
Author
Jayanthi S; Jayanthi G; Varalakshmi P
Address
Department of Medical Biochemistry, University of Madras, India.
Source
Biochem Int, 25(1):123-36 1991 Sep
Abstract
DL alpha-lipoic acid has been shown to prevent the induced precipitation of calcium oxalate crystals in the renal tissues of laboratory animals. The acid seems to have a profound influence on carbohydrate metabolism in diabetic rats. Here the effect of alpha-lipoic acid was studied on certain key carbohydrate metabolising enzymes in the tissues of calcium oxalate stone forming rats administered with glycollate as oxalate precursor. There was augmentation of glycolysis in the renal tissues of stone forming as well as lipoate administered rats. The two major gluconeogenic enzymes, glucose-6-phosphatase (G6P) and fructose-1, 6 diphosphatase (FDP) were significantly inhibited in tissues of calculogenic rats. lipoic acid also reduced the enzyme activities significantly. The citric acid cycle enzymes were not influenced to an appreciable extent. The observed alterations are likely to be due to the regulatory effects of oxalate and lipoate on the enzyme systems.

Title
Relationship between glutathione and DL alpha-lipoic acid againstcadmium-induced hepatotoxicity.
Author
Sumathi R; Baskaran G; Varalakshmi P
Address
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, India.
Source
Jpn J Med Sci Biol, 49(2):39-48 1996 Apr
Abstract
cadmium, a divalent metal toxicant, preferentially localizes in hepatocytes and causes liver injury. DL alpha-lipoic acid is a dithiol which is effective in rendering protection against cadmium-associated liver damage, by virtue of its two sulfhydryl moieties. lipoate was administered to cadmium-exposed rats which were either prior administered with buthionine sulfoximine to deplete liver glutathione or not. During lipoate treatment, significant protection was rendered against cadmium toxicity even under glutathione-depleted experimental condition. This highlights the antioxidant property of lipoic acid and its efficacy in mitigating cadmium-associated liver assault even in the absence of glutathione synthesis.

Title
Relationship between glutathione and DL alpha-lipoic acid against cadmium-induced hepatotoxicity.
Author
Sumathi R; Baskaran G; Varalakshmi P
Address
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, India.
Source
Jpn J Med Sci Biol, 49(2):39-48 1996 Apr
Abstract
cadmium, a divalent metal toxicant, preferentially localizes in hepatocytes and causes liver injury. DL alpha-lipoic acid is a dithiol which is effective in rendering protection against cadmium-associated liver damage, by virtue of its two sulfhydryl moieties. lipoate was administered to cadmium-exposed rats which were either prior administered with buthionine sulfoximine to deplete liver glutathione or not. During lipoate treatment, significant protection was rendered against cadmium toxicity even under glutathione-depleted experimental condition. This highlights the antioxidant property of lipoic acid and its efficacy in mitigating cadmium-associated liver assault even in the absence of glutathione synthesis.

Title
alpha-lipoic acid dependent regeneration of ascorbic acid from dehydroascorbic acid in rat liver mitochondria.
Author
Xu DP; Wells WW
Address
Department of Biochemistry, Michigan State University, East Lansing 48824, USA.
Source
J Bioenerg Biomembr, 28(1):77-85 1996 Feb
Abstract
Rat liver mitochondria were examined for their ability to reduce dehydroascorbic acid to ascorbic acid in an alpha-lipoic acid dependent or independent manner. The alpha-lipoic acid dependent reduction was stimulated by factors that increased the NADH dependent reduction of alpha-lipoic acid to dihydrolipoic acid in coupled reactions. Optimal conditions for dehydroascorbic acid reduction to ascorbic acid were achieved in the presence of pyruvate, alpha-lipoic acid, and ATP. Electron transport inhibitors, rotenone and antimycin A, further enhanced the dehydroascorbic acid reduction. The reactions were strongly inhibited by 1 mM iodoacetamide or sodium arsenite. Mitoplasts were qualitatively similar to intact mitochondria in dehydroascorbate reduction activity. Pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase reduced dehydroascorbic acid to ascorbic acid in an alpha-lipoic acid, coenzyme A, and pyruvate or alpha-ketoglutarate dependent fashion. Dehydroascorbic acid was also catalytically reduced to ascorbic acid by purified lipoamide dehydrogenase in an alpha-lipoic acid (K0.5 = 1.4 +/- 0.8 mM) and lipoamide (K0.5 = 0.9 +/- 0.3 mM) dependent manner.

Title
Preparations of alpha-lipoic acid: the dynamics of their content in the blood and their effect on hemostasis in lesions of the human liver
Author
Loginov AS; Nilova TV; Bendikov EA; Petrakov AV
Source
Farmakol Toksikol, 53(2):47-50 1990 Mar-Apr
Abstract
The changes in blood coagulating activity before and after treatment with alpha-lipoic acid drugs as compared with blood lipoic acid content were studied in 130 patients with chronic diffuse diseases of the liver of the virus and alcohol etiology. A moderate correlation between the increase in blood alpha-lipoic acid concentration in patients with the liver diseases during the replacement therapy with alpha-lipoic acid drugs and a number of parameters of thrombelastogram was established. It was shown that relief of coenzyme deficit against the background of treatment with lipoic acid is associated with relief of hypocoagulative syndrome and an elevation of the blood ATP level. It is suggested that the ability of the coenzyme to stimulate the bioenergetic protection of hemostasis processes plays the important role in the mechanism of action of alpha-lipoic acid drugs.

Title
Alpha-lipoic acid supplementation prevents symptoms of vitamin E deficiency.
Author
Podda M; Tritschler HJ; Ulrich H; Packer L
Address
Department of Molecular and Cell Biology, University of California at Berkeley, 94720-3200.
Source
Biochem Biophys Res Commun, 204(1):98-104 1994 Oct 14
Abstract
alpha-lipoic acid, an essential cofactor in mitochondrial dehydrogenases, has recently been shown to be a potent antioxidant in vitro, as well as being capable of regenerating vitamin E in vitro. In this study, using a new animal model for rapid vitamin E deficiency in adult animals and a new technique for tissue extraction of oxidized and reduced alpha-lipoic acid, we examined the antioxidant action of alpha-lipoic acid in vivo. Vitamin E-deficient adult hairless mice displayed obvious symptoms of deficiency within five weeks, but if the diet was supplemented with alpha-lipoic acid the animals were completely protected. At five weeks on a vitamin E-deficient diet animals exhibited similar decreases in tissue vitamin E levels, whether supplemented or unsupplemented with alpha-lipoic acid: vitamin E levels in liver, kidney, heart, and skin decreased 70 to 85%; levels in brain decreased only 25%. These data show that there was no effect of alpha-lipoic acid supplementation on vitamin E tissue concentrations, arguing against a role for alpha-lipoic acid in regenerating vitamin E in vivo.

Title
Pharmacokinetics of preparations of lipoic acid and their effect on ATP synthesis, processes of microsomal and cytosol oxidation in hepatocytes in liver damage in man
Author
Loginov AS; Nilova TV; Bendikov EA; Petrakov AV
Source
Farmakol Toksikol, 52(4):78-82 1989 Jul-Aug
Abstract
The features of the pharmacokinetics of preparations of alpha-lipoic acid (lipoic acid, thioctacide) as compared with their pharmacodynamic effects were studied in 125 patients with chronic diffuse diseases of the liver of viral and alcohol etiology. After a single administration of the preparations, the authors found an elevation of the maximal blood concentrations and an increase of alpha-lipoic acid elimination half-life in patients with liver cirrhosis as compared with chronic hepatitis patients. During the replacement therapy and elimination of alpha-lipoic acid deficiency by using the preparations containing lipoic acid, there is commonly an increase ATP content, an elevation of functioning mass of hepatocytes and activation of liver detoxifying function according to the data of the tests of galactose cytosol oxidation, microsomal oxidation of antipyrine and conjugation of bilirubin.

Title
Effect of DL alpha-lipoic acid on tissue lipid peroxidation and antioxidant systems in normal and glycollate treated rats.
Author
Sumathi R; Jayanthi S; Kalpanadevi V; Varalakshmi P
Address
Department of Medical Biochemistry, Dr. A. L. Mudaliar Post Graduate Institute of Basic Medical Sciences, Taramani, University of Madras, India.
Source
Pharmacol Res, 27(4):309-18 1993 May-Jun
Abstract
The cytoprotective activity of alpha-lipoic acid against free radical toxicity, manifested during experimental hyperoxaluria, has been investigated. Glycollate was used as the inducer of oxalate hyperoxaluria in rats. The increase in lipid peroxidation and superoxide dismutase (SOD) activity, associated with a decrease in catalase activity and glutathione (GSH) level, are the salient features observed in tissues of hyperoxaluric rats. Free radical toxicity in the glycollate fed rats is effectively counteracted by lipoic acid administration. lipoic acid administration brought about a significant decrease in peroxidative levels with an increase in catalase activity and glutathione level. These observations highlight the antioxidant property of alpha-lipoic acid and its cytoprotective action against experimental hyperoxaluria.

Title
Protective effects of DL-alpha-lipoic acid on cadmium-induced deterioration of rat hepatocytes.
Author
Müller L
Address
Institute of Toxicology, University of Düsseldorf, F.R.G.
Source
Toxicology, 58(2):175-85 1989 Oct 2
Abstract
The suitability of DL-alpha-lipoic acid (LA) to serve as an antidote in cadmium (Cd) toxicity in rat hepatocytes was investigated. Isolated hepatocytes were exposed to 200 and 450 microM Cd in the presence of 0.2, 1.0 and 5.0 mM LA, respectively. After 30 min of incubation various criteria of cell viability were monitored. lipoic acid markedly diminished Cd uptake. Concomitantly, Cd-induced membrane injury, as reflected by the leakage of aspartate aminotransferase and sorbitol dehydrogenase (SDH) was decreased. Moreover, LA protected against intracellular toxic responses to Cd, such as a decrease in cellular SDH activity, a decrease in cellular acid soluble thiols, especially in total glutathione, a decrease in cellular urea and an increase in thiobarbituric acid (TBA) reactants, as a measure of lipid peroxidation. Most protective effects were seen in hepatocytes challenged with the lower Cd concentration and coincubated with 5 mM LA. In contrast, at 450 microM Cd even the highest LA concentration applied either did only reverse Cd-effects incompletely (SDH-response, TBA-reactants) or did not protect at all (Cd uptake, enzyme leakage, loss of glutathione). The data indicate that DL-alpha-lipoic acid serves as a protective tool against Cd-induced membrane damage and cell dysfunction in hepatocytes. This stands as long as Cd exposure is low enough to permit interaction with LA prior to interaction with cell structures.

Title
Influence of alpha-lipoic acid on intracellular glutathione in vitro and in vivo.
Author
Busse E; Zimmer G; Schopohl B; Kornhuber B
Address
Abteilung für Hämatologie und Onkologie, Johann Wolfgang Goethe-Universität, Frankfurt/Main Fed. Rep. of Germany.
Source
Arzneimittelforschung, 42(6):829-31 1992 Jun
Abstract
The influence of alpha-lipoic acid (CAS 62-46-4) on the amount of intracellular glutathione (GSH) was investigated in vitro and in vivo. Using murine neuroblastoma as well as melanoma cell lines in vitro, a dose-dependent increase of GSH content was observed. Dependent on the source of tumor cells the increase was 30-70% compared to untreated controls. Normal lung tissue of mice also revealed about 50% increase in glutathione upon treatment with lipoic acid. This corresponds with protection from irradiation damage in these in vitro studies. Survival rate of irradiated murine neuroblastoma was increased at doses of 100 micrograms lipoic acid/d from 2% to about 10%. In agreement with the in vitro studies, in vivo experiments with whole body irradiation (5 and 8 Gy) in mice revealed that the number of surviving animals was doubled at a dose of 16 mg lipoic acid/kg. Improvement of cell viability and irradiation protection by the physiological compound lipoic acid runs parallel with an increase of intracellular GSH/GSSG ratio.

Title
Hepatic lipoate uptake.
Author
Peinado J; Sies H; Akerboom TP
Address
Institut für Physiologische Chemie I, Universität Düsseldorf, West Germany.
Source
Arch Biochem Biophys, 273(2):389-95 1989 Sep
Abstract
Uptake of [35S]lipoate was studied in perfused rat liver and in isolated rat hepatocytes. During single-pass perfusion of [35S]lipoate about 30% of the radioactivity is retained in the liver. A substantial amount of 5,5'-dithiobis(2-nitrobenzoic acid)-reactive material appears in the effluent perfusate, while hepatic efflux of GSH is unchanged. The hepatic uptake of lipoate, the release of thiols, and also the biliary excretion of 35S-labeled compounds are suppressed by octanoate. In isolated hepatocytes the uptake of lipoate follows saturation kinetics showing a Km value of 38 microM and a Vmax of 180 pmol/mg X 10 s. The uptake is temperature-dependent; from the Arrhenius plot an activation energy of 14.8 kcal/mol at 20 microM lipoate is calculated. At high concentrations of lipoate (above 75 microM) a nonsaturable uptake component becomes predominant. lipoate uptake is selectively inhibited by medium-chain fatty acids. Only slight inhibition is seen in the presence of long-chain fatty acids, and there is no inhibition with acetate or lactate. Substantial inhibition is also observed with acetylsalicylic acid, but not with taurocholate, bromosulfophthalein or biotin. lipoate uptake can be inhibited by high concentrations of phloretin (200 microM) and is rather insensitive to 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (200 microM). The results indicate that hepatic uptake of lipoate at physiological concentrations is largely carrier-mediated.

Title
Studies on the efficacy of lipoate and dihydrolipoate in the alteration of cadmium2+ toxicity in isolated hepatocytes.
Author
Müller L; Menzel H
Address
Institute of Toxicology, University of Düsseldorf, F.R.G.
Source
Biochim Biophys Acta, 1052(3):386-91 1990 May 22
Abstract
lipoate (thioctic acid) is presently used in therapy of a variety of diseases such as liver and neurological disorders. However, nothing is known about the efficacy of lipoate and its reduced form dihydrolipoate in acute cadmium (Cd2+) toxicity which involves severe liver disturbances. Therefore, we investigated the effects of these redox compounds on Cd2(+)-induced injuries in isolated rat hepatocytes. The cells were coincubated with 150 microM Cd2+ and either 1.5-6.0 mM lipoate or 17-89 microM dihydrolipoate for up to 90 min and Cd2+ uptake as well as viability criteria were monitored. Both exposure regimens diminished Cd2+ uptake in correspondence to time and concentration. They also ameliorated Cd2(+)-induced cell deterioration as reflected by the decrease in Cd2(+)-induced membrane damage (leakage of aspartate aminotransferase), by the lessening of the Cd2(+)-stimulated lipid peroxidation (TBA-reactants) and by the increase in Cd2(+)-depleted cellular glutathione (GSH + 2 GSSG). Half-maximal protection was achieved at molar ratios of 9.9 to 19 (lipoate vs. Cd2+) and 0.25 to 0.74 (dihydrolipoate vs. Cd2+), indicating a 19.5 to 50.6 lower protective efficacy of lipoate as compared to dihydrolipoate. lipoate induced an increase in extracellular acid-soluble thiols different from glutathione. It is suggested that dihydrolipoate primarily protects cells by extracellular chelation of Cd2+, whereas intracellular reduction of lipoate to the dihydro-compound followed by complexation of both intra- and extracellular Cd2+ contributes to the amelioration provided by lipoate.

Title
Experimental substantiation of the method of pharmaco-metabolic brain protection against hypoxia in severe craniocerebral injury
Author
Rozanov VA; Tsepkolenko VA; Levitskii MV; Galich IM; Rozanov AIa;
Korol' AP; Nasibullin BA
Source
Fiziol Zh, 37(5):3-11 1991 Sep-Oct
Abstract
The experiment has shown that a complex of functionally related vitamins including thiamine, lipoate, D-pantothenate, nicotinate and riboflavine in "pyruvate-dehydrogenase" ratios decreases inhibition of the activity of alpha-keto acid dehydrogenases in the brain and liver with thiopental anesthesia, intensifies arrival of [35S]-lipoate to the brain and decreases acute toxicity of sodium thiopental (TnNa). The same complex (where thiamine, pantothenate and riboflavine are substituted by the corresponding coenzyme forms) complemented by the components stimulating the function of GABA-bypath of the brain as administered to rats with serious craniocerebral injury on the background of prolonged anaesthesia effect improves recovery of the brain functions, that is followed by normalization of ketoglutarate-dehydrogenase activity, maintenance of GABA-bypath function and by a decrease of GABA and glutamate content in the brain. The results obtained substantiate the advisability to use vitamin-coenzyme-metabolic complex in the acute period of traumatic brain disease aimed to increase efficiency of the antihypoxic TnNa effect and to correct its undesirable effects.

Title
Interaction of functionally coupled vitamins in the distribution and metabolism of [14C]nicotinic acid in tissues and blood cells
Author
Rozanov AIa; Iakubik EIu
Source
Biokhimiia, 50(9):1399-405 1985 Sep
Abstract
Leucocytes adsorb by two orders of magnitude more labeled nicotinic acid ([14C]Na) than erythrocytes (as calculated on a per cell basis). The dynamics of binding of labeled vitamin by leucocytes is biphasic with the formation of predominantly [14C]nicotinic coenzymes already at very short time intervals after their injection to rats. Simultaneous injections of thiamine, riboflavin, lipoate and pantotenate increased the level of total labeled nicotinate metabolites in the blood and leucocytes 2.1- and 4.1-fold, respectively. The metabolism of subcutaneously injected [14C]NA was predominantly localized in the digestive system with a markedly pronounced two-phase dynamics of changes of the level of total labeled metabolites in the liver and small intestine concomitant with their secretion together with digestive juices. The functionally coupled vitamins injected simultaneously sharply increased the incorporation of the total label into liver tissues (up to 45% of the injected dose against 33% in the control) and the increase in the level of [14C]pyridine nucleotides. Similar effects were observed upon accumulation of labeled metabolites of [14C]NA in small intestine membranes. The increase in the maximal accumulation of nicotinate under effects of other group B vitamins in brain, heart and spleen tissues correlated with the dynamics, of their accumulation in the blood. In the postmaximal period in cardiac muscle and brain tissues, the second increase in the [14C]NA binding correlated with the dynamics of its accumulation in the digestive system.(ABSTRACT TRUNCATED AT 250 WORDS)

Title
The association of the autoantigens of primary biliary cirrhosis with the mitochondrial H+-ATPase--a reassessment.
Author
Sudoyo H; Noer AS; Mackay IR; Marzuki S
Address
Department of Biochemistry, Monash University, Clayton, Victoria, Australia.
Source
Biochem Int, 18(5):951-60 1989 May
Abstract
The claimed association between the M2 autoantigens of primary biliary cirrhosis (PBC) and the mitochondrial H+-ATPase has been re-examined in view of the recent reports that PBC autoantibodies react specifically with the lipoate acetyl transferases of 2-oxo acid dehydrogenases. Study of F0F1-ATPase purified from human and yeast mitochondria, and the comparison between immunoprecipitates obtained with antibodies against the H+-ATPase beta subunit and anti-M2 antibodies of PBC, established that the M2 antigens are not associated with the H+-ATPase complex. The M2 antigens did copurify with a crude bovine heart F1-ATPase preparation, but not with F1-ATPase from yeast, human heart or human liver.

Title
Enzymic synthesis of the iron-sulfur cluster of spinach ferredoxin.
Author
Pagani S; Bonomi F; Cerletti P
Source
Eur J Biochem, 142(2):361-6 1984 Jul 16
Abstract
A biologically active spinach ferredoxin was reconstituted from the apoprotein by incubation with catalytic amounts of the sulfurtransferase rhodanese in the presence of thiosulfate, reduced lipoate and ferric ammonium citrate. Analytical and spectroscopical features of the reconstituted ferredoxin were identical to those of the native one; yield of the reconstitution reaction was 80%. Yields and kinetic parameters of the enzymic and chemical reconstitution were also compared. The higher efficiency of the enzymic system is ascribed to a productive interaction between rhodanese and apoferredoxin favouring the process of cluster build-up and insertion. The physiological relevance of this synthetic activity is discussed.

Title
Component X. An immunologically distinct polypeptide associated with mammalian pyruvate dehydrogenase multi-enzyme complex.
Author
De Marcucci O; Lindsay JG
Source
Eur J Biochem, 149(3):641-8 1985 Jun 18
Abstract
The mammalian pyruvate dehydrogenase multi-enzyme complex contains a tightly-associated 50 000-Mr polypeptide of unknown function (component X) in addition to its three constituent enzymes, pyruvate dehydrogenase (E1), lipoate acetyltransferase (E2) and lipoamide dehydrogenase (E3) which are jointly responsible for production of CoASAc and NADH. The presence of component X is apparent on sodium dodecyl sulphate/polyacrylamide gel analysis of the complex, performed in Tris-glycine buffers although it co-migrates with the E3 subunit on standard phosphate gels run under denaturing conditions. Refined immunological techniques, employing subunit-specific antisera to individual components of the pyruvate dehydrogenase complex, have demonstrated that protein X is not a proteolytic fragment of E2 (or E3) as suggested previously. In addition, anti-X serum elicits no cross-reaction with either subunit of the intrinsic kinase of the pyruvate dehydrogenase complex. Immune-blotting analysis of SDS extracts of bovine, rat and pig cell lines and derived subcellular fractions have indicated that protein X is a normal cellular component with a specific mitochondrial location. It remains tightly-associated with the 'core' enzyme, E2, on dissociation of the complex at pH 9.5 or by treatment with 0.25 M MgCl2. This polypeptide is not released to any significant extent from E2 by p-hydroxymercuriphenyl sulphonate, a reagent which promotes dissociation of the specific kinase of the complex from the 'core' enzyme. Incubation of the complex with [2-14C]pyruvate in the absence of CoASH promotes the incorporation of radio-label, probably in the form of acetyl groups, into both E2 and component X.

 

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