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PubMed2000

The LipB protein is a negative regulator of dam gene expression in Escherichia coli.

Transcription initiation of the major promoter (P2) of the Escherichia coli dam gene increases with growth rate. The presence of three partially palindromic motifs, (TTCAGT(N(20))TGAG), designated G (growth)-boxes, within the -52 to +31 region of the promoter, may be related to growth rate control. Deletion of two of these repeats, downstream of the transcription initiation point, result in constitutive high activity of the promoter. The unlinked cde-4::miniTn10 insertion also results in severalfold higher activity of the dam P2 promoter, suggesting that this mutation resulted in the loss of a putative dam P2 repressor. The cde-4 mutation was mapped to the lipB (lipoic acid) gene, which we show encodes a 24 kDa protein initiating at a TTG codon. LipB is a highly conserved protein in animal and plant species, other bacteria, Archaea, and yeast. Plasmids expressing the native or hexahistidine-tagged LipB complement the phenotype of the cde-4 mutant strain. The level of LipB in vivo was higher in exponentially growing cells than those in the stationary phase. Three G-box motifs were also found in the lipB region. Models for the regulation of expression of the two genes are discussed.

Amino Acid Sequence↗
PubMed1998

Lipoamide dehydrogenase from streptomyces seoulensis: biochemical and genetic properties.

Lipoamide dehydrogenase was purified around 22-fold relative to the crude extracts of Streptomyces seoulensis with an overall yield of 9. 5%. The enzyme was composed of two identical subunits with a molecular mass of 54 kDa and contained 1 mol of FAD per mol of subunit. The absorption spectra of the enzyme revealed the absorption maxima of flavoprotein at 272, 349, and 457 nm. Catalytically active two-electron reduced lipoamide dehydrogenase was produced by anaerobic reduction with one equivalent of NADH. Addition of excess amount of NADH led to the four-electron reduced lipoamide dehydrogenase. The reaction of the enzyme in the reduction reaction of lipoamide or lipoic acid could be explained by a ping-pong mechanism like many other lipoamide dehydrogenases reported earlier. The enzyme also catalysed the reduction of various quinone compounds with NADH as electron donor via a ping-pong mechanism. The enzyme can catalyse a single electron transfer in case of quinone-reducing process, evidenced by the production of 1, 4-naphthosemiquinone radical anion. The quinone-reducing activity of the enzyme was dramatically inhibited by NAD+, indicating the involvement of four-electron reduced form. The structural gene for the enzyme was cloned using a DNA fragment PCR-amplified with the primers designed from N-terminal and internal amino acid sequences. The deduced amino acid sequence shared striking similarity with those of lipoamide dehydrogenases from prokaryotes and eukaryotes. The gene was named lpd. All tested Streptomyces contained one homologue of the lpd gene, which is consistent with the fact that most organisms contain only one lipoamide dehydrogenase.

Amino Acid Sequence↗
PubMed2001

Protein thiol oxidation by haloperidol results in inhibition of mitochondrial complex I in brain regions: comparison with atypical antipsychotics.

Usage of 'typical' but not 'atypical' antipsychotic drugs is associated with severe side effects involving extrapyramidal tract (EPT). Single dose of haloperidol caused selective inhibition of complex I in frontal cortex, striatum and midbrain (41 and 26%, respectively) which was abolished by pretreatment of mice with thiol antioxidants, alpha-lipoic acid and glutathione isopropyl ester, and reversed, in vitro, by disulfide reductant, dithiothreitol. Prolonged administration of haloperidol to mice resulted in complex I loss in frontal cortex, hippocampus, striatum and midbrain, while chronic dosing with clozapine affected only hippocampus and frontal cortex. Risperidone caused complex I loss in frontal cortex, hippocampus and striatum but not in midbrain from which extrapyramidal tract emanates. Inhibition of the electron transport chain component, complex I by haloperidol is mediated through oxidation of essential thiol groups to disulfides, in vivo. Further, loss of complex I in extrapyramidal brain regions by anti-psychotics correlated with their known propensity to generate side-effects involving extra-pyramidal tract.

Animals↗
PubMed2000

Antioxidant loading reduces oxidative stress induced by high-energy impulse noise (blast) exposure.

Detonation of explosives, firing of large caliber weapons and occupational explosions, professional or accidental, produce high-energy impulse noise (blast) waves characterized by a rapid rise in atmospheric pressure (overpressure) followed by gradual decay to ambient level. Exposure to blast waves causes injury, predominantly to the hollow organs such as ears and lungs. We have previously reported that blast exposure can induce free radical-mediated oxidative stress in the lung characterized by antioxidant depletion, lipid peroxidation, and hemoglobin (Hb) oxidation. In this study, we examined whether pre-loading, adequately fed rats, with pharmacological doses of antioxidants would reduce the response to blast. Sprague-Dawley rats weighing 300-350 g were loaded with either 800 IU vitamin E (VE), 1000 mg vitamin C (VC) or 25 mg lipoic acid (LA) for 3 consecutive days by gavage before exposure to blast. Both VE, and LA were dissolved in 2 ml corn oil, but VC in 2 ml water. After the 3-day antioxidant loading, the rats were divided into six groups (five rats per group), deeply anesthetized with sodium pentobarbital (60 mg/kg body weight), then exposed to a low-level blast (62+/-2 kPa peak pressure and 5 ms duration). A matched number of groups were sham exposed and served as controls. One hour after exposure, all rats were euthanized then blood, and lung tissue was analyzed. We found that antioxidant loading resulted in restored Hb oxygenation, and reduced lipid peroxidation. Lung tissue VE content was elevated after loading but VC did not change possibly due to their different bioavailability and saturation kinetics. These observations, suggest that brief antioxidant loading with pharmacological doses can reduce blast-induced oxidative stress, and may have occupational and clinical implications.

Animals↗
PubMed1997

Utilization of renal slices to evaluate the efficacy of chelating agents for removing mercury from the kidney.

Mercury is an environmental contaminant that preferentially accumulates in the kidney. It has been previously shown using proton-induced X-ray emission analysis that mercury (HgCl2) accumulated in precision-cut rabbit renal cortical slices. In this study, the efficacy of seven chelating agents for the removal of Hg from renal slices has been examined. Rabbits were injected with HgCl2 (10 mg/kg) and 3 h later kidneys were sliced, or renal slices were exposed in vitro to a mildly toxic concentration of HgCl2 (5 x 10(-5)M, 4 h). The slices were then treated in vitro with 10 mM concentrations of EDTA, lipoic acid (LA), penicillamine (PA), glutathione (GSH), 1,4-dithiothreitol (DTT), DMSA, or DMPS. DMPS proved to be the most effective in mobilizing Hg from in vivo or in vitro HgCl2-exposed renal tissue ( > 85% of control after 3 h incubation). Relative efficacies for the seven agents were DMPS > DMSA, PA > DTT, GSH > LA, EDTA. The use of renal slices appears to be a useful in vitro tool for assessing the efficacy of chelating agents on mobilizing accumulated Hg from renal tissue.

Animals↗
PubMed1997

Structural studies of the glycine decarboxylase complex from pea leaf mitochondria.

The glycine decarboxylase complex consists of four different component enzymes (P-, H-, T- and L-proteins). The 14-kDa lipoamide-containing H-protein plays a pivotal role in the complete sequence of reactions since its prosthetic group (lipoic acid) interacts successively with the three other components of the complex and undergoes a cycle of reductive methylamination, methylamine transfer and electron transfer. The X-ray crystal structure of different forms of the H-protein has shown a unique conformation of the protein. This leads to the hypothesis of a three-dimensional recognition of the H-protein by the other components of the system and also by the ligase which lipoylates the H-protein. Striking structural similarities are observed between the H-protein and other lipoate domains of 2-oxo acid dehydrogenases and with the biotin carrier protein of acetyl-CoA carboxylase. In the H-protein, the lipoamide arm is free to move in the solvent when oxidized but is pivoted and tightly bound into a cleft at the protein surface when methylamine-loaded. This implies that the H-protein and the T-component form a stable complex during the catalytic transfer of the methylene unit to the tetrahydrofolate cofactor of the T-protein. This complex has been detected by small angle scattering experiments. In conclusion, in the glycine decarboxylase system, the lipoamide arm does not swing freely from one catalytic site to another as was proposed in other systems.

Amino Acid Oxidoreductases↗
PubMed1999

Polarographic properties and potential carcinogenicity of some natural nucleosides and their synthetic analogues.

The polarographic reduction and the index of potential carcinogenicity tg alpha determined polarographically in aprotic conditions and in the presence of alpha-lipoic acid of nine naturally occurring and synthetic pyrimidine and six synthetic 1,3,5-triazine (5-aza) nucleosides was compared to the reduction of eight synthetic 1,3,6-triazine (6-aza) nucleosides. Nucleosides are of interest because of their key role in the nucleic acid structure and because of the antimetabolite and cytotoxic/antileukemia properties of their synthetic analogues. It was shown that polarographic reduction of the studied compounds is achieved at gradually increased potentials in the order of 6-aza < 5-aza < pyrimidine nucleosides. On other hand, the potential carcinogenicity of studied compounds increases usually in the order of pyrimidine < 6-aza << 5-aza nucleoside. The only compounds with remarkable potential carcinogenicity identified at this study were those ones from the 5-aza (1,3,5-triazine) antimetabolite series-arabinosyl-5-azacytosine (0.275), 5-aza-cytidine (0.295) and 5-aza-uracil (0.400)-and 2,2'-anhydrouridine (0.260). The relation of the data obtained to biological activity of nucleosides included in the study is discussed.

Carcinogens↗
PubMed2001

Advanced glycation endproducts change glutathione redox status in SH-SY5Y human neuroblastoma cells by a hydrogen peroxide dependent mechanism.

The reaction of proteins with reducing sugars leads to the formation of 'advanced glycation endproducts' (AGEs). They accumulate in Alzheimer's disease brain in the vicinity of beta-amyloid plaques. AGEs are cytotoxic by a mechanism involving reactive oxygen species, which implies that they could compromise glutathione redox status. In this study, we show that AGEs (BSA-AGE and beta-amyloid-AGE) persistently increase the ratio of oxidized to reduced glutathione in a dose- and time-dependent manner in SH-SY5Y neuroblastoma cells. The level of oxidized glutathione accounted to 10-14% and persisted for up to 24 h in the presence of added AGEs. In contrast, the unmodified beta-amyloid peptides A beta (1-40) and A beta (25-35) had no significant effect on glutathione redox status. The AGE-induced increase in oxidized glutathione could be prevented by the radical scavengers N-acetylcysteine, alpha-lipoic acid and 17beta-estradiol or by application of catalase, indicating that superoxide and hydrogen peroxide production precedes the AGE-mediated depletion of reduced glutathione.

Alzheimer Disease↗
PubMedDate not supplied

Neurobehavioral aspects of antioxidants in aging.

Both aging and age-associated neurodegenerative diseases are associated with various degrees of behavioral impairments, and among the prime candidates responsible for producing the neuronal changes mediating these behavioral deficits appear to be free radicals and the oxidative stress they generate. Therefore, there have been a number of studies which have examined the putative positive benefits of antioxidants in altering, reversing, or forestalling these neuronal/behavioral decrements, with varying degrees of success. Additional experiments have examined the effects of diets rich in fruits and vegetables or herbal extracts in reducing certain types of cancer and cardiovascular diseases, and evidence emerging from such experiments suggests that these kinds of dietary modifications may be beneficial in altering neuronal/behavioral deficits in aging, as well. These kinds of diets are particularly rich in antioxidants such as vitamins A, C, E, and bioflavonoids (such as flavones, tannins, and anthocyanins), and thus, there may be synergistic effects among them. The present paper will review studies concerning the influence of dietary and synthetic antioxidants on normal, pathological age-related, and reactive oxygen species-induced behavioral changes in human and animal subjects. The antioxidants reviewed are vitamin E, alpha-lipoic acid, and the phytochemicals contained in herbals, fruits and vegetables.

Aged↗
PubMedDate not supplied

Could antioxidant supplementation reduce antiretroviral therapy-induced chronic stable hyperlactatemia?

OBJECTIVE: To determine if asymptomatic stable chronic hyperlactatemia in human immunodeficiency virus (HIV)-infected patients under highly active antiretroviral therapy (HAART, including nucleoside analog reverse transcriptase inhibitors (NRTI)) could be improved by antioxidant supplementation. DESIGN: To match two groups of patients taking NRTI for at least 24 months: 15 without and 15 with antioxidant supplementation (vitamin E, beta-carotene, N-acetylcysteine, selenium, Gingko biloba extracts and nutritional supplements). For both the groups, the supplementation by antioxidants or its lack was carefully assessed. Venous lactatemia, blood oxidative stress markers (plasma lipid peroxidation, enzymatic and non-enzymatic antioxidants), CDC revisited classification, CD4 count and viral load, NRTI (with or without stavudine) and other antiretroviral drugs used, lipoatrophy, central fat accumulation were assessed. RESULTS: Patients were not statistically different with respect to the CDC classification, CD4 count, viral load and characteristics of antiretroviral therapy. Blood oxidative stress markers, i.e. vitamin E, vitamin A and beta-carotene tended to be higher in the supplemented group. The difference observed in venous lactate concentration between the two groups was significant (1.37 +/- 0.10 vs. 1.82 +/- 0.19 mmol/l in the supplemented and non-supplemented groups, respectively P = 0.04). CONCLUSION: Antioxidant supplementation improves the asymptomatic stable chronic hyperlactatemia observed in HIV-infected patients taking HAART including NRTI for a long time. Controlled studies are needed to demonstrate the efficacy of this supplementation on mitochondrial toxicity observed during HAART and the possible usefulness of its combination with mitochondrial cofactors like carnitine, riboflavine, coenzyme Q, alpha-lipoic acid.

Adipose Tissue↗
PubMed2001

Restoration of glutathione levels in vascular smooth muscle cells exposed to high glucose conditions.

Hyperglycemia-induced oxidative stress may play a key role in the pathogenesis of diabetic vascular disease. The purpose of this study was to determine the effects of glucose on levels of glutathione (a major intracellular antioxidant), the expression of gamma-glutamylcysteine synthetase (the rate-limiting enzyme in glutathione de novo synthesis), and DNA damage in human vascular smooth muscle cells in vitro. High glucose conditions and buthionine sulphoximine, an inhibitor of gamma-glutamylcysteine synthetase, reduced intracellular glutathione levels in vascular smooth muscle cells. This reduction was accompanied by a decrease in the mRNA expression of both subunits of gamma-glutamylcysteine synthetase as well as an increase in DNA damage. In high glucose conditions, incubation of the vascular smooth muscle cells with alpha-lipoic acid and L-cystine restored glutathione levels. We suggest that the decrease in GSH levels seen in high glucose conditions is mediated by the availability of cysteine (rate-limiting substrate in de novo glutathione synthesis) and the gene expression of the gamma-glutamylcysteine synthetase enzyme. Glutathione depletion is associated with an increase in DNA damage, which can be reduced when glutathione levels are restored.

Aorta↗
PubMed2003

Reduction of inclusion body pathology in ApoE-deficient mice fed a combination of antioxidants.

Clinical studies have shown that the antioxidant vitamin E can slow the progression of Alzheimer's disease (AD). Other antioxidants reported to affect cognitive function include ginkgo biloba, vitamin C, and lipoic acid. To examine the effects of combination antioxidant therapy (CAT) on longevity and neuropathology in mice, we supplemented the diet of ApoE-deficient mice with vitamin E, ginkgo biloba, pycnogenol, and ascorbyl palmitate. ApoE-deficient mice normally exhibit increased numbers of PAS-positive inclusion bodies with aging. However, supplementation with CAT resulted in a significant increase in life span and a marked reduction of inclusion body histopathology in the hippocampus. In addition, while untreated apoE-deficient mice exhibited increased levels of TUNEL staining, a marker of DNA fragmentation, supplementation with CAT resulted in a significant reduction in the levels of TUNEL staining. These findings suggest that oxidative mechanisms, perhaps related to neuronal apoptosis, are integral to inclusion body formation in aging mice. The association between the reduced number of apoptotic cells and the reduction in inclusion bodies may explain in part the increased longevity of mice fed CAT, and supports the contention that the combined actions of selected antioxidants may be therapeutically effective against neurodegenerative diseases.

Animal Feed↗
PubMed2000

Sickle cell anemia: a potential nutritional approach for a molecular disease.

A certain population of red blood cells in patients with sickle cell anemia has an elevated density and possesses an abnormal membrane. These "dense cells" have a tendency to adhere to neutrophils, platelets, and vascular endothelial cells, and, thus, they could trigger vasoocclusion and the subsequent painful crisis from which these patients suffer. We developed a laboratory method of preparing such dense cells and found that nutritional antioxidant supplements, hydroxyl radical scavengers, and iron-binding agents could inhibit the formation of dense cells in vitro. The concentrations at which effective nutritional supplements could inhibit dense cell formation by 50% were 4.0 mg/mL for aged garlic extract, 0.38 mg/mL for black tea extract, 0.13 mg/mL for green tea extract, 0.07 mg/mL for Pycnogenol, 930 microM for alpha-lipoic acid, 270 microM for vitamin E, 45 microM for coenzyme Q(10), and 32 microM for beta-carotene. Both an ex vivo study and a pilot clinical trial demonstrated that a cocktail consisting of daily doses of 6 g of aged garlic extract, 4-6 g of vitamin C, and 800 to 1200 IU of vitamin E may indeed be beneficial to the patients.

Adolescent↗
PubMed2000

Influence of diabetes on cardiac nitric oxide synthase expression and activity.

UNLABELLED: There is some evidence that the endothelium dependent vasodilatation of coronary arteries is impaired in both types of diabetes. The underlying mechanisms are not yet clear, in particular whether this defect is caused by a direct effect of diabetes on the activity and the expression of nitric oxide synthases (NOS) or indirectly by an enhanced inactivation of nitric oxide. METHODS: To study this question we determined the activity (conversion of L-arginine to citrulline) and the mRNAs encoding the isoforms of NOS (using polymerase chain reaction after reverse transcription of the mRNAs into cDNAs by reverse transcriptase) in hearts of streptozotocin diabetic rats and in rat heart endothelial cells (RHEC). The formation of reactive oxygen intermediates (ROI) was measured by the dichloro-dihydro-fluorescein method. RESULTS: The activity of total NOS and the amounts of mRNAs encoding ecNOS and iNOS were dependent on the duration of diabetes. After a diabetes duration of 4 to 6 weeks both the total activity as well as the mRNAs encoding ecNOS and iNOS were elevated. A reduction of NOS activity and the amounts of mRNAs of ecNOS and iNOS was only seen after a diabetes duration longer than 20 weeks, a time at which a loss of endothelium has been described. In RHEC, high glucose (22 mM) and H(2)O(2) (100 microM) were able to increase the mRNA encoding ecNOS, but not iNOS. This increase in ecNOS mRNA was inhibited by lipoic acid (1 microM). In addition, high glucose (22 and 30 mM) led to an enhanced formation of ROI and to activation of the transcription NF kappa B. CONCLUSION: These observations suggest that diabetes causes a temporary increase in NOS activity and ecNOS mRNA in the rat heart which is presumably the consequence of an enhanced oxidative stress exerted by hyperglycaemia. Together with previously published observations, our data suggest that the impairment of endothelium dependent vasodilatation in rat heart is not the consequence of a reduced activity and expression of NOS, but is caused by an enhanced inactivation of nitric oxide by ROI.

Animals↗
PubMed1997

Photocleavage of plasmid DNA by the prophyrin meso-tetrakis[4-(carboxymethyleneoxy)phenyl]porphyrin.

meso-Tetrakis[4-(carboxymethyleneoxy)phenyl]porphyrin (H2T4CPP) cleaves pBR322 plasmid DNA to single strand breaks in the presence of molecular oxygen and visible light. The above photocleavage was much more efficient in D2O buffer of sodium phosphate (pD = 7.4) than H2O buffer of sodium phosphate (pH = 7.4). In addition this photocleavage of plasmid DNA was inhibited in the presence of sodium azide, lipoic acid, tert-butanol or mannitol suggesting the involvement of 1O2 and.OH in the photocleavage of plasmid DNA. The photocleavage was observed to be more efficient in the presence of H2T4CPP than in the presence of H2CPP [meso-tetrakis (4-carboxy-phenyl)porphyrin]. Our spectral studies using UV-visible, fluorescence and circular dichroism techniques suggest that H2T4CPP binds to DNA while H2CPP does not. Thus, the difference in photocleavage may be caused by the nonbinding of H2CPP and by the binding of H2T4CPP to calf thymus (CT) DNA.

Circular Dichroism↗
PubMed2001

The glycine decarboxylase system: a fascinating complex.

The mitochondrial glycine decarboxylase multienzyme system, connected to serine hydroxymethyltransferase through a soluble pool of tetrahydrofolate, consists of four different component enzymes, the P-, H-, T- and L-proteins. In a multi-step reaction, it catalyses the rapid destruction of glycine molecules flooding out of the peroxisomes during the course of photorespiration. In green leaves, this multienzyme system is present at tremendously high concentrations within the mitochondrial matrix. The structure, mechanism and biogenesis of glycine decarboxylase are discussed. In the catalytic cycle of glycine decarboxylase, emphasis is given to the lipoate-dependent H-protein that plays a pivotal role, acting as a mobile substrate that commutes successively between the other three proteins. Plant mitochondria possess all the necessary enzymatic equipment for de novo synthesis of tetrahydrofolate and lipoic acid, serving as cofactors for glycine decarboxylase and serine hydroxymethyltransferase functioning.

Amino Acid Oxidoreductases↗
PubMed2007

Oriented immobilization of antibodies with GST-fused multiple Fc-specific B-domains on a gold surface.

We have constructed a novel platform for the oriented buildup of immunoglobulins on a gold surface for a surface plasmon resonance imaging microarray. To this end, genetically engineered glutathione S-transferase proteins bearing one, two, and three Fc-specific B-domains in protein G from Streptococci (GST-GB1, -GB2, and -GB3, respectively) were produced. In order to tether these GST-GBx proteins specifically, a novel glutathione-derivatized ligand (LA-GSH) was also synthesized from a biaminated tri(ethylene glycol) backbone. Each end of the backbone was further functionalized with a maleimide group for a glutathione modification and a lipoic acid for surface immobilization. The glutathione ligand demonstrated a negligible nonspecific protein adsorption toward other spectator proteins while showing a strong specific association toward GST-GBx proteins. This Fc-specific surface exhibited at least a 2-fold enhancement in the immunoglobulin density (from human and mouse) with its antigen capture capability totally conserved compared to a covalently tethered GBx proteins. A single antibody tethered on the GST-GB3 is estimated to capture two antigens (enhanced green fluorescent protein), and this antigen capture ratio seems to be the most efficient value ever observed.

Animals↗
PubMed2000

Escherichia coli LipA is a lipoyl synthase: in vitro biosynthesis of lipoylated pyruvate dehydrogenase complex from octanoyl-acyl carrier protein.

The Escherichia coli lipA gene product has been genetically linked to carbon-sulfur bond formation in lipoic acid biosynthesis [Vanden Boom, T. J., Reed, K. E., and Cronan, J. E., Jr. (1991) J. Bacteriol. 173, 6411-6420], although in vitro lipoate biosynthesis with LipA has never been observed. In this study, the lipA gene and a hexahistidine tagged lipA construct (LipA-His) were overexpressed in E. coli as soluble proteins. The proteins were purified as a mixture of monomeric and dimeric species that contain approximately four iron atoms per LipA polypeptide and a similar amount of acid-labile sulfide. Electron paramagnetic resonance and electronic absorbance spectroscopy indicate that the proteins contain a mixture of [3Fe-4S] and [4Fe-4S] cluster states. Reduction with sodium dithionite results in small quantities of an S = 1/2 [4Fe-4S](1+) cluster with the majority of the protein containing a species consistent with an S = 0 [4Fe-4S](2+) cluster. LipA was assayed for lipoate or lipoyl-ACP formation using E. coli lipoate-protein ligase A (LplA) or lipoyl-[acyl-carrier-protein]-protein-N-lipoyltransferase (LipB), respectively, to lipoylate apo-pyruvate dehydrogenase complex (apo-PDC) [Jordan, S. W., and Cronan, J. E. (1997) Methods Enzymol. 279, 176-183]. When sodium dithionite-reduced LipA was incubated with octanoyl-ACP, LipB, apo-PDC, and S-adenosyl methionine (AdoMet), lipoylated PDC was formed. As shown by this assay, octanoic acid is not a substrate for LipA. Confirmation that LipA catalyzes formation of lipoyl groups from octanoyl-ACP was obtained by MALDI mass spectrometry of a recombinant PDC lipoyl-binding domain that had been lipoylated in a LipA reaction. These results provide information about the mechanism of LipA catalysis and place LipA within the family of iron-sulfur proteins that utilize AdoMet for radical-based chemistry.

Acyl Carrier Protein↗