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ALA/R+ with alcohol...
- Thread starter sawastea
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MrMakaveli
New member
juve said:coke is the shit - doesn't kick you out of ketosis, makes you feel like a cyborg and slims you down; no r-ALA needed
Greatest fat burning stack would be X+R-ALA (I'm kidding, NOBODY try this, although R-ALA does prevent X neurotoxicity).
Alcohol+R-ALA? Hm, not sure it would have much of an effect.
MrMakaveli
New member
Back to original topic:
Alpha-lipoic acid prevents ethanol-induced protein oxidation in mouse hippocampal HT22 cells.
Pirlich M, Kiok K, Sandig G, Lochs H, Grune T.
Department of Gastroenterology and Hepatology, University Hospital Charite, Humboldt-University Berlin, Schumannstr. 20/21, 10098, Berlin, Germany.
Oxidative stress is involved in a number of neurological disorders, including the neurotoxic effects of ethanol. Recent studies have described a neuroprotective potential of alpha-lipoic acid (LC) in several models of neuronal cell death related to oxidative stress. We tested the hypothesis that LC could be effective in preventing ethanol-induced neurotoxicity employing the clonal hippocampa cell line HT22. A 24 h incubation with ethanol 100-600 mM caused a dose-dependent loss of cell viability and a significant increase of the overall intracellular protein oxidation. Coincubation with LC 0.1 mM resulted in a significant decrease of ethanol-related neurotoxicity and a complete prevention of the ethanol-induced intracellular protein oxidation. These results indicate that the radical scavenging properties of LC are effective to ameliorate ethanol-induced neurotoxicity.
PMID: 12133563 [PubMed - indexed for MEDLINE]
Alpha-lipoic acid prevents ethanol-induced protein oxidation in mouse hippocampal HT22 cells.
Pirlich M, Kiok K, Sandig G, Lochs H, Grune T.
Department of Gastroenterology and Hepatology, University Hospital Charite, Humboldt-University Berlin, Schumannstr. 20/21, 10098, Berlin, Germany.
Oxidative stress is involved in a number of neurological disorders, including the neurotoxic effects of ethanol. Recent studies have described a neuroprotective potential of alpha-lipoic acid (LC) in several models of neuronal cell death related to oxidative stress. We tested the hypothesis that LC could be effective in preventing ethanol-induced neurotoxicity employing the clonal hippocampa cell line HT22. A 24 h incubation with ethanol 100-600 mM caused a dose-dependent loss of cell viability and a significant increase of the overall intracellular protein oxidation. Coincubation with LC 0.1 mM resulted in a significant decrease of ethanol-related neurotoxicity and a complete prevention of the ethanol-induced intracellular protein oxidation. These results indicate that the radical scavenging properties of LC are effective to ameliorate ethanol-induced neurotoxicity.
PMID: 12133563 [PubMed - indexed for MEDLINE]
juve
New member
Long-term ethanol administration enhances age-dependent modulation of redox state in different brain regions in the rat: protection by acetyl carnitine.
Calabrese V, Scapagnini G, Latteri S, Colombrita C, Ravagna A, Catalano C, Pennisi G, Calvani M, Butterfield DA.
Int J Tissue React. 2002;24(3):97-104.
PMID: 12635862 [PubMed - indexed for MEDLINE]
Effects of L-carnitine on the formation of fatty acid ethyl esters in brain and peripheral organs after short-term ethanol administration in rat.
Calabrese V, Rizza V.
Neurochem Res. 1999 Jan;24(1):79-84.
Institute of Biochemistry, University of Catania, Italy. [email protected]
A study was undertaken in rats to evaluate the effects of short-term oral ethanol administration on the levels of fatty acid ethyl esters (FAEE) in brain and peripheral organs in the presence and absence of pretreatment with L-carnitine. Administration of ethanol to rats for seven days resulted in fatty acid ethyl ester formation, particularly in the heart and brain, but also in the kidney and liver. FAEE generation was associated with a significant increase of GSH transferase activity. Treatment with L-carnitine significantly reduced both FAEE and GSH transferase activity, and these effects were associated with a significant decrease in alcohol blood concentrations. The present evidence supports the hypothesis that fatty acid ethyl esters could be mediators involved in the production of alcohol-dependent syndromes. Administration of L-carnitine through an increment in lipid metabolism and turnover, and by the modulation of cellular antioxidant enzymes, greatly reduces these metabolic abnormalities supporting its potential usefulness as a pharmacological tool in alcoholism management.
Role of acetyl-L-carnitine in the treatment of cognitive deficit in chronic alcoholism.
Tempesta E, Troncon R, Janiri L, Colusso L, Riscica P, Saraceni G, Gesmundo E, Calvani M, Benedetti N, Pola P.
Int J Clin Pharmacol Res. 1990;10(1-2):101-7.
Department of Psychiatry and Pharmacology, Catholic University of Rome, Italy.
Preliminary data are reported from a multicentred double-blind placebo-controlled study concerned with the effects of acetyl-L-carnitine (LAC) on some cognitive deficits of at least one month-abstinent alcoholics. Fifty-five patients, showing impaired performance in at least two out of six mnemonic, praxic and verbal tasks, were randomly assigned to either LAC 2 g/day or a placebo group. They were tested by means of a neuropsychological battery exploring the areas of memory, constructional praxia, deductive-logical functions and language. Testing time was on baseline (T0), after 45 (T45) and 90 (T90) days. On the Rey's 15 word memory test (long-term), the Wechsler memory scale (logical memory), and the Similarities WAIS subtest, the T90 difference between LAC and the placebo was significant in favour of the former treatment. On the copying drawing test (simple copy), the placebo group did not show any T0-T90 variation, while significant improvement in the LAC group was greater than in the placebo group. As LAC has proved to ameliorate the performance or to accelerate the recovery on tests representative of all cognitive areas explored, it is conceivable that the drug acts diffusely, either at the cholinergic transmission or at the neuronal metabolism level. It is concluded that acetyl-L-carnitine can be a useful and safe therapeutic agent in the subtle cognitive disturbances of chronic alcoholics.
Effect of L-propionyl carnitine on some properties of erythrocytes and leukocytes of alcohol abusers.
Conte A, Bianchi I, Guazzelli M, Taponeco G, Bertelli A, Ronca G.
Int J Tissue React. 1995;17(1):21-31.
Department of Animal Biology, University of Modena, Italy.
The effect of L-propionyl carnitine, the carnitine derivative utilized as a more effective drug for membrane protection, on Na-K ATPase activity of erythrocyte ghosts of alcohol-dependent patients and blood donors has been investigated. The effect of L-propionyl carnitine on leukocyte chemotaxis and cytochrome c reduction, a measure of superoxide ion production was also studied. It has been in fact observed that alcohol is immunotoxic on both the non-specific and the specific immune response. In alcohol-dependent erythrocytes, a significant higher value of the 1H-NMR spin lattice relaxation time (T1) was observed as compared to blood-donor erythrocytes. The in-vitro addition of ethanol increases the T1 values of blood donor erythrocytes, whereas it is without effect on the T1 value of alcohol-dependent erythrocytes. The Na-K ATPase activity is higher in alcohol-dependent erythrocyte ghosts as compared to blood-donor ghosts. A non-significant increase of the Na-K ATPase activity of blood-donor ghosts was observed with the increasing of L-propionyl carnitine concentrations (from 0.2 to 5.0 mM), whereas the Na-K ATPase activity of alcohol-dependent ghosts decreases. From these combined effects the differences of Na-K ATPase activity progressively decrease with the increasing of L-propionyl carnitine concentration, and no significant differences are observed between the two groups at L-propionyl carnitine concentrations higher than 0.5 mM. The in-vitro addition of ethanol increases the enzyme activity to a greater extent in blood-donor ghosts as compared to alcohol-dependent ghosts. This in-vitro activation by ethanol is decreased by the addition of L-propionyl carnitine. The chemotaxis induced by N-formyl-methionyl-leucylphenylalanine and the superoxide anion production stimulated by zymosan is significantly lower in alcohol-dependent neutrophils. L-Propionyl carnitine increases, in a dose-dependent way, both chemotaxis and superoxide anion production of alcohol-dependent neutrophils, and no significant difference was observed between the two groups at 5 mM L-propionyl carnitine. These experimental results suggest that L-propionyl carnitine administration may be useful for reducing some acute and chronic damages due to alcohol ingestion. The protective and modulatory actions of L-propionyl carnitine may be even more evident in cells and tissues different from those investigated in this study and in which ethanol determines several biochemical damages
Calabrese V, Scapagnini G, Latteri S, Colombrita C, Ravagna A, Catalano C, Pennisi G, Calvani M, Butterfield DA.
Int J Tissue React. 2002;24(3):97-104.
PMID: 12635862 [PubMed - indexed for MEDLINE]
Effects of L-carnitine on the formation of fatty acid ethyl esters in brain and peripheral organs after short-term ethanol administration in rat.
Calabrese V, Rizza V.
Neurochem Res. 1999 Jan;24(1):79-84.
Institute of Biochemistry, University of Catania, Italy. [email protected]
A study was undertaken in rats to evaluate the effects of short-term oral ethanol administration on the levels of fatty acid ethyl esters (FAEE) in brain and peripheral organs in the presence and absence of pretreatment with L-carnitine. Administration of ethanol to rats for seven days resulted in fatty acid ethyl ester formation, particularly in the heart and brain, but also in the kidney and liver. FAEE generation was associated with a significant increase of GSH transferase activity. Treatment with L-carnitine significantly reduced both FAEE and GSH transferase activity, and these effects were associated with a significant decrease in alcohol blood concentrations. The present evidence supports the hypothesis that fatty acid ethyl esters could be mediators involved in the production of alcohol-dependent syndromes. Administration of L-carnitine through an increment in lipid metabolism and turnover, and by the modulation of cellular antioxidant enzymes, greatly reduces these metabolic abnormalities supporting its potential usefulness as a pharmacological tool in alcoholism management.
Role of acetyl-L-carnitine in the treatment of cognitive deficit in chronic alcoholism.
Tempesta E, Troncon R, Janiri L, Colusso L, Riscica P, Saraceni G, Gesmundo E, Calvani M, Benedetti N, Pola P.
Int J Clin Pharmacol Res. 1990;10(1-2):101-7.
Department of Psychiatry and Pharmacology, Catholic University of Rome, Italy.
Preliminary data are reported from a multicentred double-blind placebo-controlled study concerned with the effects of acetyl-L-carnitine (LAC) on some cognitive deficits of at least one month-abstinent alcoholics. Fifty-five patients, showing impaired performance in at least two out of six mnemonic, praxic and verbal tasks, were randomly assigned to either LAC 2 g/day or a placebo group. They were tested by means of a neuropsychological battery exploring the areas of memory, constructional praxia, deductive-logical functions and language. Testing time was on baseline (T0), after 45 (T45) and 90 (T90) days. On the Rey's 15 word memory test (long-term), the Wechsler memory scale (logical memory), and the Similarities WAIS subtest, the T90 difference between LAC and the placebo was significant in favour of the former treatment. On the copying drawing test (simple copy), the placebo group did not show any T0-T90 variation, while significant improvement in the LAC group was greater than in the placebo group. As LAC has proved to ameliorate the performance or to accelerate the recovery on tests representative of all cognitive areas explored, it is conceivable that the drug acts diffusely, either at the cholinergic transmission or at the neuronal metabolism level. It is concluded that acetyl-L-carnitine can be a useful and safe therapeutic agent in the subtle cognitive disturbances of chronic alcoholics.
Effect of L-propionyl carnitine on some properties of erythrocytes and leukocytes of alcohol abusers.
Conte A, Bianchi I, Guazzelli M, Taponeco G, Bertelli A, Ronca G.
Int J Tissue React. 1995;17(1):21-31.
Department of Animal Biology, University of Modena, Italy.
The effect of L-propionyl carnitine, the carnitine derivative utilized as a more effective drug for membrane protection, on Na-K ATPase activity of erythrocyte ghosts of alcohol-dependent patients and blood donors has been investigated. The effect of L-propionyl carnitine on leukocyte chemotaxis and cytochrome c reduction, a measure of superoxide ion production was also studied. It has been in fact observed that alcohol is immunotoxic on both the non-specific and the specific immune response. In alcohol-dependent erythrocytes, a significant higher value of the 1H-NMR spin lattice relaxation time (T1) was observed as compared to blood-donor erythrocytes. The in-vitro addition of ethanol increases the T1 values of blood donor erythrocytes, whereas it is without effect on the T1 value of alcohol-dependent erythrocytes. The Na-K ATPase activity is higher in alcohol-dependent erythrocyte ghosts as compared to blood-donor ghosts. A non-significant increase of the Na-K ATPase activity of blood-donor ghosts was observed with the increasing of L-propionyl carnitine concentrations (from 0.2 to 5.0 mM), whereas the Na-K ATPase activity of alcohol-dependent ghosts decreases. From these combined effects the differences of Na-K ATPase activity progressively decrease with the increasing of L-propionyl carnitine concentration, and no significant differences are observed between the two groups at L-propionyl carnitine concentrations higher than 0.5 mM. The in-vitro addition of ethanol increases the enzyme activity to a greater extent in blood-donor ghosts as compared to alcohol-dependent ghosts. This in-vitro activation by ethanol is decreased by the addition of L-propionyl carnitine. The chemotaxis induced by N-formyl-methionyl-leucylphenylalanine and the superoxide anion production stimulated by zymosan is significantly lower in alcohol-dependent neutrophils. L-Propionyl carnitine increases, in a dose-dependent way, both chemotaxis and superoxide anion production of alcohol-dependent neutrophils, and no significant difference was observed between the two groups at 5 mM L-propionyl carnitine. These experimental results suggest that L-propionyl carnitine administration may be useful for reducing some acute and chronic damages due to alcohol ingestion. The protective and modulatory actions of L-propionyl carnitine may be even more evident in cells and tissues different from those investigated in this study and in which ethanol determines several biochemical damages
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