The Experts below are selected from a list of 99 Experts worldwide ranked by ideXlab platform
Pitchai Balakumar - One of the best experts on this subject based on the ideXlab platform.
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the defensive effect of benfotiamine in sodium arsenite induced experimental vascular endothelial dysfunction
Biological Trace Element Research, 2010Co-Authors: Sanjali Verma, Krishna Reddy, Pitchai BalakumarAbstract:The present study has been designed to investigate the effect of benfotiamine, a Thiamine Derivative, in sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. Sodium arsenite (1.5 mg−1 kg−1 day−1 i.p., 2 weeks) was administered in rats to produce VED. The development of VED was assessed by employing isolated aortic ring preparation and estimating the serum and aortic concentrations of nitrite/nitrate. Further, the integrity of vascular endothelium in thoracic aorta was assessed by scanning electron microscopy. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of sodium arsenite markedly produced VED by attenuating acetylcholine-induced endothelium-dependent relaxation, decreasing serum and aortic concentrations of nitrite/nitrate, and impairing the integrity of vascular endothelium. Further, sodium arsenite produced oxidative stress by increasing serum TBARS and aortic superoxide generation. The treatment with benfotiamine (25, 50, and 100 mg−1 kg−1 day−1 p.o.) or atorvastatin (30 mg−1 kg−1 day−1 p.o., a standard agent) prevented sodium arsenite-induced VED and oxidative stress. However, the beneficial effects of benfotiamine in preventing the sodium arsenite-induced VED were attenuated by co-administration with N-omega-nitro-l-arginine methyl ester (L-NAME) (25 mg−1 kg−1 day−1, i.p.), an inhibitor of NOS. Thus, it may be concluded that benfotiamine reduces oxidative stress and activates endothelial nitric oxide synthase to enhance the generation and bioavailability of NO and subsequently improves the integrity of vascular endothelium to prevent sodium arsenite-induced experimental VED.
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the defensive effect of benfotiamine in sodium arsenite induced experimental vascular endothelial dysfunction
Biological Trace Element Research, 2010Co-Authors: Sanjali Verma, Krishna Reddy, Pitchai BalakumarAbstract:The present study has been designed to investigate the effect of benfotiamine, a Thiamine Derivative, in sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. Sodium arsenite (1.5 mg−1 kg−1 day−1 i.p., 2 weeks) was administered in rats to produce VED. The development of VED was assessed by employing isolated aortic ring preparation and estimating the serum and aortic concentrations of nitrite/nitrate. Further, the integrity of vascular endothelium in thoracic aorta was assessed by scanning electron microscopy. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of sodium arsenite markedly produced VED by attenuating acetylcholine-induced endothelium-dependent relaxation, decreasing serum and aortic concentrations of nitrite/nitrate, and impairing the integrity of vascular endothelium. Further, sodium arsenite produced oxidative stress by increasing serum TBARS and aortic superoxide generation. The treatment with benfotiamine (25, 50, and 100 mg−1 kg−1 day−1 p.o.) or atorvastatin (30 mg−1 kg−1 day−1 p.o., a standard agent) prevented sodium arsenite-induced VED and oxidative stress. However, the beneficial effects of benfotiamine in preventing the sodium arsenite-induced VED were attenuated by co-administration with N-omega-nitro-l-arginine methyl ester (L-NAME) (25 mg−1 kg−1 day−1, i.p.), an inhibitor of NOS. Thus, it may be concluded that benfotiamine reduces oxidative stress and activates endothelial nitric oxide synthase to enhance the generation and bioavailability of NO and subsequently improves the integrity of vascular endothelium to prevent sodium arsenite-induced experimental VED.
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benfotiamine attenuates nicotine and uric acid induced vascular endothelial dysfunction in the rat
Pharmacological Research, 2008Co-Authors: Pitchai Balakumar, Ramica Sharma, Manjeet SinghAbstract:Abstract The study has been designed to investigate the effect of benfotiamine, a Thiamine Derivative, in nicotine and uric acid-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg kg −1 day −1 , i.p., 4 weeks) and uric acid (150 mg kg −1 day −1 , i.p., 3 weeks) were administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy (SEM) of thoracic aorta. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of nicotine and uric acid produced VED by impairing the integrity of vascular endothelium and subsequently decreasing serum and aortic concentration of nitrite/nitrate and attenuating acetylcholine-induced endothelium dependent relaxation. Further, nicotine and uric acid produced oxidative stress, which was assessed in terms of increase in serum TBARS and aortic superoxide generation. However, treatment with benfotiamine (70 mg kg −1 day −1 , p.o.) or atorvastatin (30 mg kg −1 day −1 p.o., a standard agent) markedly prevented nicotine and uric acid-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentration of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Thus, it may be concluded that benfotiamine reduces the oxidative stress and consequently improves the integrity of vascular endothelium and enhances the generation of nitric oxide to prevent nicotine and uric acid-induced experimental VED.
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benfotiamine attenuates nicotine and uric acid induced vascular endothelial dysfunction in the rat
Pharmacological Research, 2008Co-Authors: Pitchai Balakumar, Ramica Sharma, Manjeet SinghAbstract:Abstract The study has been designed to investigate the effect of benfotiamine, a Thiamine Derivative, in nicotine and uric acid-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg kg −1 day −1 , i.p., 4 weeks) and uric acid (150 mg kg −1 day −1 , i.p., 3 weeks) were administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy (SEM) of thoracic aorta. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of nicotine and uric acid produced VED by impairing the integrity of vascular endothelium and subsequently decreasing serum and aortic concentration of nitrite/nitrate and attenuating acetylcholine-induced endothelium dependent relaxation. Further, nicotine and uric acid produced oxidative stress, which was assessed in terms of increase in serum TBARS and aortic superoxide generation. However, treatment with benfotiamine (70 mg kg −1 day −1 , p.o.) or atorvastatin (30 mg kg −1 day −1 p.o., a standard agent) markedly prevented nicotine and uric acid-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentration of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Thus, it may be concluded that benfotiamine reduces the oxidative stress and consequently improves the integrity of vascular endothelium and enhances the generation of nitric oxide to prevent nicotine and uric acid-induced experimental VED.
Manjeet Singh - One of the best experts on this subject based on the ideXlab platform.
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benfotiamine attenuates nicotine and uric acid induced vascular endothelial dysfunction in the rat
Pharmacological Research, 2008Co-Authors: Pitchai Balakumar, Ramica Sharma, Manjeet SinghAbstract:Abstract The study has been designed to investigate the effect of benfotiamine, a Thiamine Derivative, in nicotine and uric acid-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg kg −1 day −1 , i.p., 4 weeks) and uric acid (150 mg kg −1 day −1 , i.p., 3 weeks) were administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy (SEM) of thoracic aorta. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of nicotine and uric acid produced VED by impairing the integrity of vascular endothelium and subsequently decreasing serum and aortic concentration of nitrite/nitrate and attenuating acetylcholine-induced endothelium dependent relaxation. Further, nicotine and uric acid produced oxidative stress, which was assessed in terms of increase in serum TBARS and aortic superoxide generation. However, treatment with benfotiamine (70 mg kg −1 day −1 , p.o.) or atorvastatin (30 mg kg −1 day −1 p.o., a standard agent) markedly prevented nicotine and uric acid-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentration of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Thus, it may be concluded that benfotiamine reduces the oxidative stress and consequently improves the integrity of vascular endothelium and enhances the generation of nitric oxide to prevent nicotine and uric acid-induced experimental VED.
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benfotiamine attenuates nicotine and uric acid induced vascular endothelial dysfunction in the rat
Pharmacological Research, 2008Co-Authors: Pitchai Balakumar, Ramica Sharma, Manjeet SinghAbstract:Abstract The study has been designed to investigate the effect of benfotiamine, a Thiamine Derivative, in nicotine and uric acid-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg kg −1 day −1 , i.p., 4 weeks) and uric acid (150 mg kg −1 day −1 , i.p., 3 weeks) were administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy (SEM) of thoracic aorta. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of nicotine and uric acid produced VED by impairing the integrity of vascular endothelium and subsequently decreasing serum and aortic concentration of nitrite/nitrate and attenuating acetylcholine-induced endothelium dependent relaxation. Further, nicotine and uric acid produced oxidative stress, which was assessed in terms of increase in serum TBARS and aortic superoxide generation. However, treatment with benfotiamine (70 mg kg −1 day −1 , p.o.) or atorvastatin (30 mg kg −1 day −1 p.o., a standard agent) markedly prevented nicotine and uric acid-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentration of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Thus, it may be concluded that benfotiamine reduces the oxidative stress and consequently improves the integrity of vascular endothelium and enhances the generation of nitric oxide to prevent nicotine and uric acid-induced experimental VED.
Lucien Bettendorff - One of the best experts on this subject based on the ideXlab platform.
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Biochemistry of Thiamine and Thiamine Phosphate Compounds
Encyclopedia of Biological Chemistry, 2013Co-Authors: Lucien Bettendorff, Pierre WinsAbstract:Thiamine (vitamin B1) is an essential molecule for all living organisms. It is the precursor for several phosphorylated Derivatives, the most important being the coenzyme Thiamine diphosphate (ThDP). Plants and microorganisms synthesize Thiamine, but humans and other animals must rely on exogenous dietary sources. Thiamine is transported into cells by specific transporters and pyrophosphorylated to ThDP in the cytosol. ThDP is a cofactor for important catabolic reactions, that is, pyruvate dehydrogenase, 2-oxoglutarate dehydrogenase (a limiting step in the Krebs cycle), branched-chain 2-oxo acid dehydrogenase, and transketolase (a key enzyme in the pentose phosphate pathway). Therefore, ThDP is indispensable for oxidative energy metabolism. Humans are particularly sensitive to Thiamine deficiency, which mainly affects the nervous system and causes two classical diseases, beriberi (a polyneuritic syndrome) and Wernicke–Korsakoff syndrome (encephalopathy and dementia linked to alcoholism). The selective vulnerability of some brain regions is difficult to explain by general metabolic impairment; hence, a non-cofactor role of some Thiamine Derivative(s) has been suggested. ThDP is the precursor for two triphosphorylated Derivatives, Thiamine triphosphate and adenosine Thiamine triphosphate. In bacteria, those compounds are produced in response to specific conditions of nutritional downshift. Their possible role(s) in eukaryotic organisms are unknown.
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Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives-1
2011Co-Authors: Marielaure Volvert, Sandrine Seyen, Marie Piette, Brigitte Evrard, Marjorie Gangolf, Jean Christophe Plumier, Lucien BettendorffAbstract:Copyright information:Taken from "Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives"http://www.biomedcentral.com/1471-2210/8/10BMC Pharmacology 2008;8():10-10.Published online 12 Jun 2008PMCID:PMC2435522.
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Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives-0
2011Co-Authors: Marielaure Volvert, Sandrine Seyen, Marie Piette, Brigitte Evrard, Marjorie Gangolf, Jean Christophe Plumier, Lucien BettendorffAbstract:, p < 0.01). The results are expressed as mean ± SEM for 4 animals in each group.Copyright information:Taken from "Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives"http://www.biomedcentral.com/1471-2210/8/10BMC Pharmacology 2008;8():10-10.Published online 12 Jun 2008PMCID:PMC2435522.
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Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives-4
2011Co-Authors: Marielaure Volvert, Sandrine Seyen, Marie Piette, Brigitte Evrard, Marjorie Gangolf, Jean Christophe Plumier, Lucien BettendorffAbstract:Llular Thiamine Derivatives were determined at the times indicated. The data (mean ± SEM, n = 3) were analyzed by two-way ANOVA followed by the Bonferroni post-test for comparison of the benfotiamine and the Thiamine groups at different times (*, p < 0.05).Copyright information:Taken from "Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives"http://www.biomedcentral.com/1471-2210/8/10BMC Pharmacology 2008;8():10-10.Published online 12 Jun 2008PMCID:PMC2435522.
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benfotiamine a synthetic s acyl Thiamine Derivative has different mechanisms of action and a different pharmacological profile than lipid soluble Thiamine disulfide Derivatives
BMC Pharmacology, 2008Co-Authors: Marielaure Volvert, Sandrine Seyen, Marie Piette, Brigitte Evrard, Marjorie Gangolf, Jean Christophe Plumier, Lucien BettendorffAbstract:Background Lipid-soluble Thiamine precursors have a much higher bioavailability than genuine Thiamine and therefore are more suitable for therapeutic purposes. Benfotiamine (S-benzoylThiamine O-monophosphate), an amphiphilic S-acyl Thiamine Derivative, prevents the progression of diabetic complications, probably by increasing tissue levels of Thiamine diphosphate and so enhancing transketolase activity. As the brain is particularly sensitive to Thiamine deficiency, we wanted to test whether intracellular Thiamine and Thiamine phosphate levels are increased in the brain after oral benfotiamine administration.
Ramica Sharma - One of the best experts on this subject based on the ideXlab platform.
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benfotiamine attenuates nicotine and uric acid induced vascular endothelial dysfunction in the rat
Pharmacological Research, 2008Co-Authors: Pitchai Balakumar, Ramica Sharma, Manjeet SinghAbstract:Abstract The study has been designed to investigate the effect of benfotiamine, a Thiamine Derivative, in nicotine and uric acid-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg kg −1 day −1 , i.p., 4 weeks) and uric acid (150 mg kg −1 day −1 , i.p., 3 weeks) were administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy (SEM) of thoracic aorta. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of nicotine and uric acid produced VED by impairing the integrity of vascular endothelium and subsequently decreasing serum and aortic concentration of nitrite/nitrate and attenuating acetylcholine-induced endothelium dependent relaxation. Further, nicotine and uric acid produced oxidative stress, which was assessed in terms of increase in serum TBARS and aortic superoxide generation. However, treatment with benfotiamine (70 mg kg −1 day −1 , p.o.) or atorvastatin (30 mg kg −1 day −1 p.o., a standard agent) markedly prevented nicotine and uric acid-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentration of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Thus, it may be concluded that benfotiamine reduces the oxidative stress and consequently improves the integrity of vascular endothelium and enhances the generation of nitric oxide to prevent nicotine and uric acid-induced experimental VED.
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benfotiamine attenuates nicotine and uric acid induced vascular endothelial dysfunction in the rat
Pharmacological Research, 2008Co-Authors: Pitchai Balakumar, Ramica Sharma, Manjeet SinghAbstract:Abstract The study has been designed to investigate the effect of benfotiamine, a Thiamine Derivative, in nicotine and uric acid-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg kg −1 day −1 , i.p., 4 weeks) and uric acid (150 mg kg −1 day −1 , i.p., 3 weeks) were administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy (SEM) of thoracic aorta. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of nicotine and uric acid produced VED by impairing the integrity of vascular endothelium and subsequently decreasing serum and aortic concentration of nitrite/nitrate and attenuating acetylcholine-induced endothelium dependent relaxation. Further, nicotine and uric acid produced oxidative stress, which was assessed in terms of increase in serum TBARS and aortic superoxide generation. However, treatment with benfotiamine (70 mg kg −1 day −1 , p.o.) or atorvastatin (30 mg kg −1 day −1 p.o., a standard agent) markedly prevented nicotine and uric acid-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentration of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Thus, it may be concluded that benfotiamine reduces the oxidative stress and consequently improves the integrity of vascular endothelium and enhances the generation of nitric oxide to prevent nicotine and uric acid-induced experimental VED.
Marjorie Gangolf - One of the best experts on this subject based on the ideXlab platform.
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Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives-1
2011Co-Authors: Marielaure Volvert, Sandrine Seyen, Marie Piette, Brigitte Evrard, Marjorie Gangolf, Jean Christophe Plumier, Lucien BettendorffAbstract:Copyright information:Taken from "Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives"http://www.biomedcentral.com/1471-2210/8/10BMC Pharmacology 2008;8():10-10.Published online 12 Jun 2008PMCID:PMC2435522.
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Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives-0
2011Co-Authors: Marielaure Volvert, Sandrine Seyen, Marie Piette, Brigitte Evrard, Marjorie Gangolf, Jean Christophe Plumier, Lucien BettendorffAbstract:, p < 0.01). The results are expressed as mean ± SEM for 4 animals in each group.Copyright information:Taken from "Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives"http://www.biomedcentral.com/1471-2210/8/10BMC Pharmacology 2008;8():10-10.Published online 12 Jun 2008PMCID:PMC2435522.
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Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives-4
2011Co-Authors: Marielaure Volvert, Sandrine Seyen, Marie Piette, Brigitte Evrard, Marjorie Gangolf, Jean Christophe Plumier, Lucien BettendorffAbstract:Llular Thiamine Derivatives were determined at the times indicated. The data (mean ± SEM, n = 3) were analyzed by two-way ANOVA followed by the Bonferroni post-test for comparison of the benfotiamine and the Thiamine groups at different times (*, p < 0.05).Copyright information:Taken from "Benfotiamine, a synthetic S-acyl Thiamine Derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble Thiamine disulfide Derivatives"http://www.biomedcentral.com/1471-2210/8/10BMC Pharmacology 2008;8():10-10.Published online 12 Jun 2008PMCID:PMC2435522.
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thiaminylated adenine nucleotides chemical synthesis structural characterization and natural occurrence
FEBS Journal, 2009Co-Authors: Michel Frederich, Tiziana Gigliobianco, Gabriel Mazzucchelli, Luc Angenot, Marjorie Gangolf, Edwin De Pauw, David Delvaux, Georges Dive, Benjamin Elias, Pierre WinsAbstract:Thiamine and its three phosphorylated Derivatives (mono-, di- and triphosphate) occur naturally in most cells. Recently, we reported the presence of a fourth Thiamine Derivative, adenosine Thiamine triphosphate, produced in Escherichia coli in response to carbon starvation. Here, we show that the chemical synthesis of adenosine Thiamine triphosphate leads to another new compound, adenosine Thiamine diphosphate, as a side product. The structure of both compounds was confirmed by MS analysis and H-1-, C-13- and P-31-NMR, and some of their chemical properties were determined. Our results show an upfield shifting of the C-2 proton of the thiazolium ring in adenosine Thiamine Derivatives compared with conventional Thiamine phosphate Derivatives. This modification of the electronic environment of the C-2 proton might be explained by a through-space interaction with the adenosine moiety, suggesting U-shaped folding of adenosine Thiamine Derivatives. Such a structure in which the C-2 proton is embedded in a closed conformation can be located using molecular modeling as an energy minimum. In E. coli, adenosine Thiamine triphosphate may account for 15% of the total Thiamine under energy stress. It is less abundant in eukaryotic organisms, but is consistently found in mammalian tissues and some cell lines. Using HPLC, we show for the first time that adenosine Thiamine diphosphate may also occur in small amounts in E. coli and in vertebrate liver. The discovery of two natural Thiamine adenine compounds further highlights the complexity and diversity of Thiamine biochemistry, which is not restricted to the cofactor role of Thiamine diphosphate.
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benfotiamine a synthetic s acyl Thiamine Derivative has different mechanisms of action and a different pharmacological profile than lipid soluble Thiamine disulfide Derivatives
BMC Pharmacology, 2008Co-Authors: Marielaure Volvert, Sandrine Seyen, Marie Piette, Brigitte Evrard, Marjorie Gangolf, Jean Christophe Plumier, Lucien BettendorffAbstract:Background Lipid-soluble Thiamine precursors have a much higher bioavailability than genuine Thiamine and therefore are more suitable for therapeutic purposes. Benfotiamine (S-benzoylThiamine O-monophosphate), an amphiphilic S-acyl Thiamine Derivative, prevents the progression of diabetic complications, probably by increasing tissue levels of Thiamine diphosphate and so enhancing transketolase activity. As the brain is particularly sensitive to Thiamine deficiency, we wanted to test whether intracellular Thiamine and Thiamine phosphate levels are increased in the brain after oral benfotiamine administration.