共查询到20条相似文献,搜索用时 15 毫秒
1.
Intraperitoneal administration of lipoic acid (10 mg/100 g) does not effect changes in serum insulin levels in normal and
alloxan diabetic rats, while normalising increased serum pyruvate, and impaired liver pyruvic dehydrogenase characteristic
of the diabetic state. Dihydrolipoic acid has been shown to participate in activation of fatty acids with equal facility as
coenzyme A. Fatty acyl dihydrolipoic acid however is sparsely thiolyzed to yield acetyl dihydrolipoic acid. Also acetyl dihydrolipoic
acid does not activate pyruvate carboxylase unlike acetyl coenzyme A. The reduced thiolysis of Β-keto fatty acyl dihydrolipoic
acid esters and the lack of activation of pyruvic carboxylase by acetyl dihydrolipoic acid could account for the antiketotic
and antigluconeogenic effects of lipoic acid 相似文献
2.
Effect of Fidarestat and α-Lipoic Acid on Diabetes-Induced Epineurial Arteriole Vascular Dysfunction
M. A. Yorek L. J. Coppey J. S. Gellett E. P. Davidson D. D. Lund 《Experimental diabetes research》2004,5(2):123-135
In the present study, the authors examined whether treating
streptozotocin-induced diabetic rats with the combination
of α-lipoic acid and fidarestat, an aldose reductase inhibitor,
can promote the formation of dihydrolipoic acid
in diabetic animals and thereby enhance the efficacy of
α-lipoic acid as monotherapy toward preventing diabetic
vascular and neural dysfunction.Treating diabetic rats with
the combination of 0.25% α-lipoic acid (in the diet) and
fidarestat (3 mg/kg body weight) prevented the diabetesinduced
slowing of motor nerve conduction velocity and
endoneurial blood flow. This therapy also significantly improved
acetylcholine-mediated vasodilation in epineurial
arterioles of the sciatic nerve compared to nontreated diabetic
rats. Treating diabetic rats with 0.25% α-lipoic acid
and fidarestat (3 mg/kg body weight) was equally or more
effective in preventing vascular and neural dysfunction than
was monotherapy of diabetic rats with higher doses of
α-lipoic acid or fidarestat. Treating diabetic rats with the
combination of 0.25% α-lipoic acid and fidarestat (3 mg/kg
body weight) significantly improved several markers of oxidative
stress and increased the serum levels of both α-lipoic
acid and dihydrolipoic acid. These studies suggest that combination
therapy consisting of α-lipoic acid and fidarestat
may be more efficacious in preventing diabetes-induced vascular
and neural dysfunction in peripheral tissue compared
to monotherapy, which requires higher doses to be equally effective. The effect of this combination therapy may in part
be due to the increased production and/or level of dihydrolipoic
acid. 相似文献
3.
Simbula G Columbano A Ledda-Columbano GM Sanna L Deidda M Diana A Pibiri M 《Apoptosis : an international journal on programmed cell death》2007,12(1):113-123
α-lipoic acid (α-LA) is an antioxidant used for the treatment of a variety of diseases, including liver cirrhosis, heavy metal
poisoining, and diabetic polyneuropathy. In addition to its protective effect against oxidative stress, α-LA induces apoptosis
in different cancer cells types. However, whether α-LA acid induces apoptosis of hepatoma cells is unknown. Herein, we investigated
whether α-LA induces apoptosis in two different hepatoma cell lines FaO and HepG2. The results showed that α-LA inhibits the
growth of both cell lines as indicated by the reduction in cell number, the reduced expression of cyclin A and the increased
levels of the cyclin/CDKs inhibitors, p27Kip1 and p21Cip1. Cell cycle arrest was associated with cell loss, and DNA laddering indicative of apoptosis. Apoptosis was preceded by increased
generation of reactive oxygen species, and associated with p53 activation, increased expression of Bax, release of cytochrome
c from mitochondria, caspases activation, decreased levels of survivin, induction of pro-apoptotic signaling (i.e JNK) and
inhibition of anti-apoptotic signaling (i.e. PKB/Akt) pathways. In conclusion, this study provides evidence that α-LA induces
apoptosis in hepatoma cells, describes a possible sequence of molecular events underlying its lethal effect, and suggests
that it may prove useful in liver cancer therapy. 相似文献
4.
Diabetic patients reveal significant disorders, such as nephropathy, cardiomyopathy, and neuropathy. As oxidative stress and
inflammation seem to be implicated in the pathogenesis of diabetic brain, we aimed to investigate the effects of caffeic acid
phenethyl ester (CAPE) on oxidative stress and inflammation in diabetic rat brain. Diabetes was induced by a single dose of
streptozotocin (45 mg kg−1, i.p.) injection into rats. Two days after streptozotocin treatment 10 μM kg−1 day−1 CAPE was administrated and continued for 60 days. Here, we demonstrate that CAPE significantly decreased the levels of nitric
oxide and malondialdehyde induced by diabetes, and the activities of catalase, glutathione peroxidase, and xanthine oxidase
in the brain. However, glutathione levels were increased by CAPE. The mRNA expressions of tumor necrosis factor (TNF)-α and
interferon (IFN)-γ, and inducible nitric oxide synthase (iNOS) were remarkably enhanced in brain by diabetes. CAPE treatments significantly suppressed these inflammatory cytokines
(about 70% for TNF-α, 26% for IFN-γ) and NOS (completely). Anti-inflammatory cytokine IL-10 mRNA expression was not affected
by either diabetes or CAPE treatments. In conclusion, diabetes induces oxidative stress and inflammation in the brain, and
these may be contributory mechanisms involved in this disorder. CAPE treatment may reverse the diabetic-induced oxidative
stress in rat brains. Moreover, CAPE reduces the mRNA expressions of TNF-α and IFN-γ in diabetic brain; suggesting CAPE suppresses
inflammation as well as oxidative stress occurred in the brain of diabetic patients. 相似文献
5.
The development of nontoxic but effective radioprotectors is needed because of the increasing risk of human exposure to ionizing
radiation. We have reported that α-lipoic acid confers considerable radio-protective effect in mouse tissues when given prior
to x-irradiation. In the present study, α-lipoic acid supplementation prior to x-irradiation with 4 and 6 Gy significantly
inhibited the radiation-induced decline in total antioxidant capacity (TAC) of plasma. Radiation-induced decline in non-protein
sulfhydryl content (NPSH) of different tissues, namely, brain, liver, spleen, kidney, and testis, was also ameliorated significantly
at both 4 and 6 Gy doses. Maximal augmentation of radiation-induced protein carbonyl content was observed in spleen followed
by brain, kidney, testis, and liver. Maximal protection in terms of carbonyl content was observed in spleen (116%) at 6 Gy
dose, and minimal protection was found in liver (22.94%) at 4 Gy dose. Maximal increase in MDA (malondialdehyde) content was
observed in brain, followed by testis, spleen, kidney, and liver. Protection by α-lipoic acid pretreatment in terms of MDA
content was maximal in brain (51.67%) and minimal in spleen. The findings support the idea that α-lipoic acid is a free-radical
scavenger and a potent antioxidant. 相似文献
6.
Hong-de Yan Zhao Wang Ling-jie Chen 《Journal of industrial microbiology & biotechnology》2009,36(5):643-648
Kinetic resolution of α-lipoic acid, a case of remote stereocenter discrimination, was accomplished using lipase from Aspergillus oryzae WZ007. Performance of this lipase was investigated for enantioselective esterification of (S)-α-lipoic acid, leaving the target product (R)-α-lipoic acid in unreacted form. The effects of chain length of alcohol, type of solvent, molar ratio of alcohol:acid, and
reaction temperature were studied. The optimum reaction conditions were found to be esterification with n-octanol at 50°C in heptane with an alcohol:acid molar ratio of 5:1. The conversion rate of α-lipoic acid was 75.2%, with
an enantiomeric excess of 92.5% towards unreacted substrate in a reaction time of 48 h. 相似文献
7.
Rat liver mitochondria were examined for their ability to reduce dehydroascorbic acid to ascorbic acid in an -lipoic acid dependent or independent manner. The a-lipoic acid dependent reduction was stimulated by factors that increased the NADH dependent reduction of -lipoic acid to dihydrolipoic acid in coupled reactions. Optimal conditions for dehydroascorbic acid reduction to ascorbic acid were achieved in the presence of pyruvate, -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 -ketoglutarate dehydrogenase reduced dehydroascorbic acid to ascorbic acid in an -lipoic acid, coenzyme A, and pyruvate or -ketoglutarate dependent fashion. Dehydroascorbic acid was also catalytically reduced to ascorbic acid by purified lipoamide dehydrogenase in an -lipoic acid (K
0.5=1.4±0.8 mM) and lipoamide (K
0.5=0.9±0.3 mM) dependent manner. 相似文献
8.
Zalejska-Fiolka J Wielkoszyński T Kasperczyk S Kasperczyk A Birkner E 《Biological trace element research》2012,145(2):217-221
The effects of administration of oxidized rapeseed oil and α-lipoic acid on activities of blood antioxidant enzymes and malondialdehyde
(MDA) concentration were studied in laboratory rats fed a high-fat diet. Addition of oxidized oil resulted in increased production
of oxygen radicals, evidenced by elevated plasma MDA production. Such effect was counteracted by administration of α-lipoic
acid. There was an increase of the activities of superoxide dismutase (total and Cu/Zn-SOD) and catalase in rats fed a high-fat
diet to which 10% oxidized oil was added. Administration of α-lipoic acid resulted in a decrease of the activities of these
enzymes. 相似文献
9.
Both α-lipoic acid (LA) and ascorbic acid (vitamin C) have been shown to improve endothelial dysfunction, a precursor of atherosclerosis.
Since oxidant stress can cause endothelial dysfunction, we tested the interaction and efficacy of these antioxidants in preventing
oxidant damage to lipids due to both intra- and extracellular oxidant stresses in EA.hy926 endothelial cells. LA spared intracellular
ascorbate in culture and in response to an intracellular oxidant stress induced by the redox cycling agent menadione. Extracellular
oxidant stress generated by incubating cells for 2 h in with 0.2 mg/ml LDL and 5 μM Cu2+ caused a time-dependent increase of the lipid peroxidation product malondialdehyde in both cells and LDL, preceded by rapid
disappearance of` α-tocopherol in LDL. α-Lipoic acid at concentrations of 40–80 μM blunted these effects. Similarly, intracellular
ascorbate concentrations of 1–2 mM also prevented Cu2+-induced lipid peroxidation in LDL and cells. Cu2+-dependent oxidation of LDL in the presence of ascorbate-loaded cells decreased intracellular ascorbate by 20%, but this decrease
was not reversed by LA. Both LA and ascorbate protect endothelial cells and LDL from either intra- or extracellular oxidant
stress, but that LA does not spare ascorbate in oxidatively stressed cells. 相似文献
10.
Rat liver lipoyl transacetylase catalyzes the formation of acetyl dihydrolipoic acid from acetyl coenzyme A and dihydrolipoic
acid. In an earlier paper the formation of acetyl dihydrolipoic from pyruvate and dihydrolipoic acid catalyzed by pyruvate
dehydrogenase has been reported. Acetyl dihydrolipoic acid is a substrate for citrate synthase, acetyl coenzyme A carboxylase
and fatty acid synthetase. The Vmax. for citrate synthase with acetyl dihydrolipoic acid was identical to acetyl coenzyme A (approximately 1 μmol citrate formed/min/mg
protein) while the apparent Km was approximately 4 times higher with acetyl dihydrolipoic acid as the substrate. This may be due to the fact that synthetic
acetyl dihydrolipoic acid is a mixture of 4 possible isomers and only one of them may be the substrate for the enzymatic reaction.
While dihydrolipoic acid can replace coenzyme A in the activation of succinate catalyzed by succinyl coenzyme A synthetase,
the transfer of coenzyme A between succinate and acetoacetyl dihydrolipoic acid catalyzed by succinyl coenzyme A: 3 oxo-acid
coenzyme A transferase does not occur. 相似文献
11.
Potential carcinogenicity of some transition metal ions was tested using a direct-current polarography method. The measurements
were based on the reduction of tested compounds in an anhydrous solution using α-lipoic acid as the detection compound. The
potential carcinogenicity was expressed in terms of the parameter tg α, which is known to directly correlate with the carcinogenicity
of tested compounds. For the metal ions tested, tg α was found to decrease in the following sequence: Fe(III) > Pb(II) > V(IV)
> Fe(II) > Mn(II) > Cu(II). Zero values of tg α were found for Cd(II) and Mn(III). 相似文献
12.
Morsy MA Abdalla AM Mahmoud AM Abdelwahab SA Mahmoud ME 《Journal of physiology and biochemistry》2012,68(1):29-35
Liver fibrosis is a major health problem that can lead to the development of liver cirrhosis and hepatocellular carcinoma.
On the other hand, several antioxidants have been shown to possess protective effect against liver fibrosis. Therefore, in
the present work, the effectiveness of curcumin, α-lipoic acid, and N-acetylcysteine in protecting against carbon tetrachloride (CCl4)-induced liver fibrosis as well as the mechanism(s) implicated in this protective effect was studied. The antioxidants used
in this study resulted in hepatoprotective effect as evident by substantial decreases in collagen deposition in histopathological
examinations in addition to significant decrease in serum levels of alanine aminotransferase, aspartate aminotransferase,
gamma glutamyl transpeptidase, bilirubin, and transforming growth factor-alpha (TGF-α) as well as hepatic malondialdehyde
concentration, with a concurrent increase in serum matrix metalloproteinase-13 (MMP-13) and hepatic reduced glutathione (GSH)
levels as compared to CCl4 fibrotic group. In conclusion, curcumin, α-lipoic acid, and N-acetylcysteine protect rats against CCl4-induced liver fibrosis most possibly through their antioxidant activities and their capacities to induce MMP-13 and to inhibit
TGF-α levels. 相似文献
13.
Masao Yamasaki Shozen Soda Yoichi Sakakibara Masahito Suiko 《Bioscience, biotechnology, and biochemistry》2013,77(11):1939-1942
Here, we show that cell surface β1-integrin expression, cell adhesion to fibronectin, migration, and invasion were all significantly inhibited by α-lipoic acid. These effects were not observed when cells were treated with dihydrolipoic acid or caprylic acid. These data reveal that the 1,2-dithiolane structure plays an important role in the action of α-lipoic acid. 相似文献
14.
Davis GD Masilamoni JG Arul V Kumar MS Baraneedharan U Paul SF Sakthivelu IV Jesudason EP Jayakumar R 《Cell biology and toxicology》2009,25(4):331-340
During the course of cancer radiation treatment, normal skin invariably suffers from the cytotoxic effects of γ-radiation
and reactive oxygen species (ROS), which are generated from the interaction between radiation and the water molecules in cells.
The present study was designed to investigate the radioprotective role of α-lipoic acid (LA), an antioxidant on murine skin
fibroblasts exposed to a single dose of 2, 4, 6, or 8Gy γ-radiation. Irradiation of fibroblasts significantly increased ROS,
nitric oxide, and lipid peroxidation (P < 0.001); all of these factors substantially decreased with 100 μM LA treatment. Hydroxyl radical (OH⋅) production from 8Gy irradiated fibroblasts was measured directly by electron spin resonance using spin-trapping techniques.
LA was found to inhibit OH⋅ production at 100-μM concentrations. Dose-dependent depletion of antioxidants, such as catalase and glutathione reductase,
was observed in irradiated fibroblasts (P < 0.001), along with increased superoxide dismutase (P < 0.001). LA treatment restored antioxidant levels. Concentration of the pro-inflammatory cytokine IL-1β was significantly
reduced in irradiated fibroblasts when treated with LA. MTT and lactate dehydrogenase assays demonstrated that LA treatment
reduced cell injury and protected cells against irradiation-induced cytotoxicity. Thus, we conclude that results are encouraging
and need further experiments to demonstrate a possible benefit in cancer patients and the reduction of harmful effects of
radiation therapy. 相似文献
15.
KDN is an abbreviation for 2-keto-3-deoxy-D-glycero-D-galacto-nononic acid, and its natural occurrence was revealed in 1986 by a research group including the present authors. Since sialic
acid was used as a synonym for N-acylneuraminic acid at that time, there was an argument if this deaminated neuraminic acid belongs to the family of sialic
acids. In this review, we describe the 20 years history of studies on KDN (KDNology), through which KDN has established its
position as a distinct member of the sialic acid family. These studies have clarified that: (1) KDN occurs widely among vertebrates
and bacteria similar to the occurrence of the more common sialic acid, N-acetylneuraminic acid (Neu5Ac), but its abundant occurrence in animals is limited to lower vertebrates. (2) KDN is found
in almost all types of glycoconjugates, including glycolipids, glycoproteins and capsular polysaccharides. (3) KDN residues
are linked to almost all glycan structures in place of Neu5Ac. All linkage types known for Neu5Ac; α2,3-, α2,4-, α2,6-, and
α2,8- are also found for KDN. (4) KDN is biosynthesized de novo using mannose as a precursor sugar, which is activated to CMP-KDN and transferred to acceptor sugar residues. These reactions
are catalyzed by enzymes, some of which preferably recognize KDN, but many others prefer Neu5Ac to KDN. In addition to these
basic findings, elevated expression of KDN was found in fetal human red blood cells compared with adult red blood cells, and
ovarian tumor tissues compared with normal controls. KDNase, an enzyme which specifically cleaves KDN-linkages, was discovered
in a bacterium and monoclonal antibodies that specifically recognize KDN residues in KDNα2,3-Gal- and KDNα2,8-KDN-linkages
have been developed. These have been used for identification of KDN-containing molecules. Based on past basic studies and
variety of findings, future perspective of KDNology is presented. 相似文献
16.
Riedel W Lang U Oetjen U Schlapp U Shibata M 《Molecular and cellular biochemistry》2003,247(1-2):83-94
Phagocytic cells contain NADPH oxidase that they use for host defense by catalyzing the production of superoxide. Bacterial lipopolysaccharide (LPS) has been found to stimulate NADPH oxidase in mobile and sessile macrophages and microglia. It also evokes fever in homeothermic animals and men, a reaction mediated by central nervous system (CNS) activities. The purpose of the present study was to determine whether reactive oxygen species are involved in LPS-induced fever. In rabbits we found that plasma hydroperoxide levels increased and catalase activity decreased 15 min after LPS injection and that fever started with a similar latency, while plasma levels of tumor necrosis factor- (TNF) increased 30 min after the injection. Treating rabbits with methylene blue or aspirin did not affect TNF secretion but prevented the LPS-induced rise of hydroperoxides and the inactivation of catalase, abolishing fever. Incubation of human blood with nitroblue tetrazolium and LPS increased the number of formazan-positive neutrophils from 10 ± 5 to 52 ± 9%. Adding LPS to blood preincubated with either methylene blue, -lipoic acid, or aspirin respectively decreased the number of formazan-positive neutrophils to 0.9 ± 0.8, 0.8 ± 0.9, or 2.0 ± 0.9%, disclosing the antioxidant capacity of these drugs. Systemic application of 80 mg/kg -lipoic acid elicited heat-loss reactions within 15 min and decreased core temperature by 2.2 ± 0.3°C within 2 h. -Lipoic acid applied 45 min after LPS induced antipyresis within 15 min, and this antipyresis was associated with a decrease of elevated hydroperoxide levels and restoration of catalase activity. Our results show that fever is prevented when the production of reactive oxygen species is blocked and that an elevated body temperature returns to normal when oxygen radical production decreases. Estimation of plasma dihydrolipoic acid (DHLA) levels following injection of 80 mg/kg -lipoic acid in afebrile and febrile rabbits revealed that this acid is converted into DHLA, which in afebrile rabbits increased the plasma DHLA concentration from 2.22 ± 0.26 g/ml to peak values of 8.60 ± 2.28 g/ml DHLA within 30 min and which in febrile rabbits increased it from 0.84 ± 0.22 g/ml to peak values of 3.90 ± 0.94 g/ml within 15 min. Methylene blue, aspirin, and -lipoic acid, which all cross the blood–brain barrier, seem to act not only on peripheral tissues but also on the CNS. Brain structures that have been shown to sense oxidative stress are vicinal thiol groups attached to the NMDA subtype of glutamate receptor. Their reduction by thiol-reducing drugs like dithiothreitol or DHLA has been found to increase glutamate-mediated neuronal excitability, while the opposite effect has been observed after their oxidation. Because we found that systemic application of -lipoic acid in the afebrile state elicits hypothermia and in the febrile state is antipyretic, we think this type of NMDA receptor is involved in thermoregulation and that oxidation of its thiol groups induces fever. It appears that temperature homeostasis can be maintained only if the redox homeostasis of the brain is guaranteed. 相似文献
17.
Kumaran S Panneerselvam KS Shila S Sivarajan K Panneerselvam C 《Molecular and cellular biochemistry》2005,280(1-2):83-89
Mitochondrial damage has implicated a major contributor for ageing process. In the present study, we measured mitochondrial
membrane swelling, mitochondrial respiration (state 3 and 4) by using oxygen electrode in skeletal muscle of young (3–4 months
old) and aged rats (above 24 months old) with supplementation of l-carnitine and dl-α-lipoic acid. Our results shows that the mitochondrial membrane swelling and state 4 respiration were increased more in
skeletal muscle mitochondria of aged rats than in young control rats, whereas the state 3 respiration, respiratory control
ratio (RCR) and ADP:O ratio decreased more in aged rats than in young rats. After supplementation of carnitine and lipoic
acid to aged rats for 30 days, the state 3 respiration and RCR were increased, whereas the state 4 and mitochondrial membrane
swelling were decreased to near normal rats. From our results, we conclude that combined supplementation of carnitine and
lipoic acids to aged rats increases the skeletal muscle mitochondrial respiration, thereby increasing the level of ATP. (Mol
Cell Biochem xxx: 83–89, 2005) 相似文献
18.
A mutant strain of Escherichia coli K12 requiring lipoic acid, W1485 lip 2 (ATCC 25645), was used to develop a turbidimetric assay for lipoic acid and a polarographic assay based on the oxidation of pyruvate by suspensions of lipoic acid-deficient organisms. The turbidimetric assay was more sensitive with a working range equivalent to 0.2–2.0 ng of dl-α-lipoic acid compared with 5–50 ng for the polarographic method. The mutant responded equally to racemic mixtures of α-lipoic acid, β-lipoic acid and dihydrolipoic acid but gave little response to lipoamide, and other derivatives without prior hydrolysis; 8-methyllipoic acid was a competitive inhibitor of the response to lipoic acid. A high specificity of the mutant for the natural stereoisomer was indicated by the fact that (+)-α-lipoic acid had twice the activity of the racemic mixture. Escherichia coli K12 contained less than 0.05 ng of free (+)-α-lipoic acid per mg dry weight but, depending on the growth substrate, the equivalent of between 13 and 47 ng of (+)-α-lipoic acid per mg dry weight after acid extraction. There was a strong correlation between the lipoic acid content and the sum of the specific activities for the pyruvate and α-ketoglutarate dehydrogenase complexes. Experiments with washed suspensions of Escherichia coli showed only small increases in lipoic acid content (18%) when incubated with pyruvate, cysteine and methionine. When supplied with exogenous lipoic acid the mutant, W1485 lip 2, accumulated very little more than was demanded by its metabolism. The lipoic acid contents of several organisms were measured and correlated with their metabolism. 相似文献
19.
Bera T Nandi N Sudhahar D Akbar MA Sen A Das P 《Journal of bioenergetics and biomembranes》2006,38(5-6):299-308
Entamoeba histolytica, an amitochondriate parasitic protist, was demonstrated to be capable of reducing the oxidized form of α-lipoic acid, a non permeable electron acceptor outside the plasma membrane. This transmembrane reduction of non permeable electron acceptors with redox potentials ranging from −290 mV to +360 mV takes place at neutral pH. The transmembrane reduction of non permeable electron acceptors was not inhibited by mitochondrial electron transport inhibitors such as antimycin A, rotenone, cyanide and azide. However, a clear inhibition with complex III inhibitor, 2-(n-heptyl)-4-hydroxyquinoline-N-oxide; modifiers of sulphydryl groups and inhibitors of glycolysis was revealed. The iron-sulphur centre inhibitor thenoyltrifluoroacetone failed to inhibit the reduction of non permeable electron acceptors whereas capsaicin, an inhibitor of energy coupling NADH oxidase, showed substantial inhibition. p-trifluromethoxychlorophenylhydrazone, a protonophore uncoupler, resulted in the stimulation of α-lipoic acid reduction but inhibition in oxygen uptake. Mitochondrial electron transport inhibitors substantially inhibited the oxygen uptake in E. histolytica. Transmembrane reduction of α-lipoic acid was strongly stimulated by anaerobiosis and anaerobic stimulation was inhibited by 2-(n-heptyl)-4-hydroxyquinoline-N-oxide. Transmembrane redox system of E. histolytica was also found to be sensitive to UV irradiation. All these findings clearly demonstrate the existence of transplasma membrane electron transport system in E. histolytica and possible involvment of a naphthoquinone coenzyme in transmembrane redox of E. histolytica which is different from that of mammalian host and therefore can provide a novel target for future rational chemotherapeutic drug designing. 相似文献
20.
Kazuhisa Sugimoto Koji Nomura Hiromi Nishiura Kohji Ohdan Takahisa Nishimura Hideo Hayashi Takashi Kuriki 《Biologia》2008,63(6):1015-1019
Two sucrose phosphorylases were employed for glycosylation of carboxylic acid compounds. Streptococcus mutans sucrose phosphorylase showed remarkable transglycosylating activity, especially under acidic conditions. Leuconostoc mesenteroides sucrose phosphorylase exhibited very weak transglycosylating activity. Three main products were detected from the reaction
mixture using benzoic acid and sucrose as an acceptor and a donor molecule, respectively. These compounds were identified
as 1-O-benzoyl α-d-glucopyranoside, 2-O-benzoyl α-d-glucopyranose, and 2-O-benzoyl β-d-glucopyranose by 1D-and 2D-NMR analyses of the isolated products and their acetylated products. Time-course analyses proved
that 1-O-benzoyl α-d-glucopyranoside was initially produced by the transglycosylation reaction of the enzyme. 2-O-Benzoyl α-d-glucopyranose and 2-O-benzoyl β-d-glucopyranose were produced from 1-O-benzoyl α-d-glucopyranoside by intramolecular acyl migration reaction. S. mutans sucrose phosphorylase showed broad acceptor-specificity. This sucrose phosphorylase catalyzed transglycosylation to various
carboxylic compounds such as short-chain fatty acids, hydroxy acids, dicarboxylic acids, and phenolic carboxylic acids. 1-O-Acetyl α-d-glucopyranoside was also enzymatically synthesized by transglucosylation reaction of the enzyme. The sensory test of acetic
acid and the glucosides revealed that the sour taste of acetic acid glucosides was significantly lower than that of acetic
acid. 相似文献