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Ala And Alcohol
- Thread starter PANTS
- Start date
Here are a few of abstracts I found on pubmed. Thioctic acid is another name for lipoic acid. I'd say that ALA would help protect your entire body from alcohol. Especially if you take it at the same time.
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In vitro effects of vitamin C, thioctic acid and dihydrolipoic acid on the cytotoxicity of post-ethanol serum.
Wickramasinghe SN, Hasan R.
Department of Haematology, St Mary's Hospital Medical School, Imperial College of Science, London, U.K.
The serum of subjects consuming ethanol contains a non-dialysable cytotoxic activity, which is thought to reside in unstable acetaldehyde-protein adducts: the cytotoxic effects have been attributed to the transfer of acetaldehyde molecules from such adducts to target cells. When post-alcohol sera are incubated for 3 hr with ascorbic acid, thioctic acid or dihydrolipoic acid at a concentration of 10-500 micrograms/mL, their cytotoxicity against A9 cells is reduced. Post-alcohol sera incubated with these concentrations of thioctic acid or dihydrolipoic acid also had reduced cytotoxic activity against phytohaemagglutinin-transformed normal human lymphocytes. Studies with artificially produced [14C]acetaldehyde-125I-albumin complexes showed that treatment with thioctic acid or dihydrolipoic acid resulted in a reduced transfer of [14C]acetaldehyde to K562 cells. If these in vitro data also apply in vivo and if circulating acetaldehyde-protein adducts play a role in alcohol-mediated tissue damage, vitamin C and, to a greater extent, thioctic acid may have a beneficial effect in patients with acute and chronic alcohol toxicity.
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Thioctic acid protection against ethanol-induced gastric mucosal lesions involves sulfhydryl and prostaglandin participation.
Gutierrez-Cabano CA.
Department of Surgical Pathology II, Faculty of Medical Sciences, National University of Rosario.
Thioctic acid, a sulfhydryl agent, given orally macroscopically protected the gastric mucosa from 96% ethanol-induced lesions in a dose-and time dependent fashion. The inhibition of the lesions was 56.0 and 90.3% at doses of 25 and 50 mg/kg, respectively. The duration of its protective effect was approximately 120 minutes. Histopathologically, the oral administration of thioctic acid prevented necrotic mucosal lesions in the deeper part of the mucosa but did not protect the surface epithelial cells against ethanol challenge. Gastric motility measured by a balloon method, was dose-dependently inhibited by the oral administration of thioctic acid. Thioctic acid protection was suppressed by pretreatment with indomethacin (30 mg/kg), a cyclooxygenase inhibitor, and iodoacetamide (100 mg/kg), a sulfhydryl blocker. The gastric motility inhibited by oral thioctic acid was not reversed by indomethacin or iodoacetamide. These doses of indomethacin or iodomethamide were administered because previously they had been used to suppress endogenous prostaglandins, and nonprotein sulfhydryls of the gastric mucosa, respectively. There was an increase in the fluid volume retained in the gastric lumen for thioctic acid (50 mg/kg) at 30, 60, 90, and 120 minutes after administration. There was an increase in the mucus volume retained in the gastric lumen for thioctic acid (50, 25 mg/kg) at 120 minutes after administration. The lesion area in the rats treated with 70 microliters of vehicle and in the rats treated with 250 microliters of vehicle were significantly higher than in the rats treated with 450 microliters of vehicle. The present study suggests that thioctic acid administered orally, offered protection to the rat gastric mucosa against 96% ethanol-induced lesions. This protective effect appears to be dependent on prostaglandin-and sulfhydryl-sensitive mechanisms, together with an increase in both the fluid volume and the mucus volume retained in the gastric lumen, and is not associated with the inhibition of gastric motor activity.
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Alpha-lipoic acid in liver metabolism and disease.
Bustamante J, Lodge JK, Marcocci L, Tritschler HJ, Packer L, Rihn BH.
Department of Molecular and Cell Biology, University of California, Berkeley 94720-3200, USA.
R-alpha-Lipoic acid is found naturally occurring as a prosthetic group in alpha-keto acid dehydrogenase complexes of the mitochondria, and as such plays a fundamental role in metabolism. Although this has been known for decades, only recently has free supplemented alpha-lipoic acid been found to affect cellular metabolic processes in vitro, as it has the ability to alter the redox status of cells and interact with thiols and other antioxidants. Therefore, it appears that this compound has important therapeutic potential in conditions where oxidative stress is involved. Early case studies with alpha-lipoic acid were performed with little knowledge of the action of alpha-lipoic acid at a cellular level, but with the rationale that because the naturally occurring protein bound form of alpha-lipoic acid has a pivotal role in metabolism, that supplementation may have some beneficial effect. Such studies sought to evaluate the effect of supplemented alpha-lipoic acid, using low doses, on lipid or carbohydrate metabolism, but little or no effect was observed. A common response in these trials was an increase in glucose uptake, but increased plasma levels of pyruvate and lactate were also observed, suggesting that an inhibitory effect on the pyruvate dehydrogenase complex was occurring. During the same period, alpha-lipoic acid was also used as a therapeutic agent in a number of conditions relating to liver disease, including alcohol-induced damage, mushroom poisoning, metal intoxification, and CCl4 poisoning. Alpha-Lipoic acid supplementation was successful in the treatment for these conditions in many cases. Experimental studies and clinical trials in the last 5 years using high doses of alpha-lipoic acid (600 mg in humans) have provided new and consistent evidence for the therapeutic role of antioxidant alpha-lipoic acid in the treatment of insulin resistance and diabetic polyneuropathy. This new insight should encourage clinicians to use alpha-lipoic acid in diseases affecting liver in which oxidative stress is involved.
--
In vitro effects of vitamin C, thioctic acid and dihydrolipoic acid on the cytotoxicity of post-ethanol serum.
Wickramasinghe SN, Hasan R.
Department of Haematology, St Mary's Hospital Medical School, Imperial College of Science, London, U.K.
The serum of subjects consuming ethanol contains a non-dialysable cytotoxic activity, which is thought to reside in unstable acetaldehyde-protein adducts: the cytotoxic effects have been attributed to the transfer of acetaldehyde molecules from such adducts to target cells. When post-alcohol sera are incubated for 3 hr with ascorbic acid, thioctic acid or dihydrolipoic acid at a concentration of 10-500 micrograms/mL, their cytotoxicity against A9 cells is reduced. Post-alcohol sera incubated with these concentrations of thioctic acid or dihydrolipoic acid also had reduced cytotoxic activity against phytohaemagglutinin-transformed normal human lymphocytes. Studies with artificially produced [14C]acetaldehyde-125I-albumin complexes showed that treatment with thioctic acid or dihydrolipoic acid resulted in a reduced transfer of [14C]acetaldehyde to K562 cells. If these in vitro data also apply in vivo and if circulating acetaldehyde-protein adducts play a role in alcohol-mediated tissue damage, vitamin C and, to a greater extent, thioctic acid may have a beneficial effect in patients with acute and chronic alcohol toxicity.
--
Thioctic acid protection against ethanol-induced gastric mucosal lesions involves sulfhydryl and prostaglandin participation.
Gutierrez-Cabano CA.
Department of Surgical Pathology II, Faculty of Medical Sciences, National University of Rosario.
Thioctic acid, a sulfhydryl agent, given orally macroscopically protected the gastric mucosa from 96% ethanol-induced lesions in a dose-and time dependent fashion. The inhibition of the lesions was 56.0 and 90.3% at doses of 25 and 50 mg/kg, respectively. The duration of its protective effect was approximately 120 minutes. Histopathologically, the oral administration of thioctic acid prevented necrotic mucosal lesions in the deeper part of the mucosa but did not protect the surface epithelial cells against ethanol challenge. Gastric motility measured by a balloon method, was dose-dependently inhibited by the oral administration of thioctic acid. Thioctic acid protection was suppressed by pretreatment with indomethacin (30 mg/kg), a cyclooxygenase inhibitor, and iodoacetamide (100 mg/kg), a sulfhydryl blocker. The gastric motility inhibited by oral thioctic acid was not reversed by indomethacin or iodoacetamide. These doses of indomethacin or iodomethamide were administered because previously they had been used to suppress endogenous prostaglandins, and nonprotein sulfhydryls of the gastric mucosa, respectively. There was an increase in the fluid volume retained in the gastric lumen for thioctic acid (50 mg/kg) at 30, 60, 90, and 120 minutes after administration. There was an increase in the mucus volume retained in the gastric lumen for thioctic acid (50, 25 mg/kg) at 120 minutes after administration. The lesion area in the rats treated with 70 microliters of vehicle and in the rats treated with 250 microliters of vehicle were significantly higher than in the rats treated with 450 microliters of vehicle. The present study suggests that thioctic acid administered orally, offered protection to the rat gastric mucosa against 96% ethanol-induced lesions. This protective effect appears to be dependent on prostaglandin-and sulfhydryl-sensitive mechanisms, together with an increase in both the fluid volume and the mucus volume retained in the gastric lumen, and is not associated with the inhibition of gastric motor activity.
--
Alpha-lipoic acid in liver metabolism and disease.
Bustamante J, Lodge JK, Marcocci L, Tritschler HJ, Packer L, Rihn BH.
Department of Molecular and Cell Biology, University of California, Berkeley 94720-3200, USA.
R-alpha-Lipoic acid is found naturally occurring as a prosthetic group in alpha-keto acid dehydrogenase complexes of the mitochondria, and as such plays a fundamental role in metabolism. Although this has been known for decades, only recently has free supplemented alpha-lipoic acid been found to affect cellular metabolic processes in vitro, as it has the ability to alter the redox status of cells and interact with thiols and other antioxidants. Therefore, it appears that this compound has important therapeutic potential in conditions where oxidative stress is involved. Early case studies with alpha-lipoic acid were performed with little knowledge of the action of alpha-lipoic acid at a cellular level, but with the rationale that because the naturally occurring protein bound form of alpha-lipoic acid has a pivotal role in metabolism, that supplementation may have some beneficial effect. Such studies sought to evaluate the effect of supplemented alpha-lipoic acid, using low doses, on lipid or carbohydrate metabolism, but little or no effect was observed. A common response in these trials was an increase in glucose uptake, but increased plasma levels of pyruvate and lactate were also observed, suggesting that an inhibitory effect on the pyruvate dehydrogenase complex was occurring. During the same period, alpha-lipoic acid was also used as a therapeutic agent in a number of conditions relating to liver disease, including alcohol-induced damage, mushroom poisoning, metal intoxification, and CCl4 poisoning. Alpha-Lipoic acid supplementation was successful in the treatment for these conditions in many cases. Experimental studies and clinical trials in the last 5 years using high doses of alpha-lipoic acid (600 mg in humans) have provided new and consistent evidence for the therapeutic role of antioxidant alpha-lipoic acid in the treatment of insulin resistance and diabetic polyneuropathy. This new insight should encourage clinicians to use alpha-lipoic acid in diseases affecting liver in which oxidative stress is involved.
