Protection against Acetaldehyde Toxicity in the rat byl-cysteine, thiamin andl-2-Methylthiazolidine-4-carboxylic acid

  title={Protection against Acetaldehyde Toxicity in the rat byl-cysteine, thiamin andl-2-Methylthiazolidine-4-carboxylic acid},
  author={Herbert Sprince and Clarence M. Parker and George G. Smith and Leon J. Gonzales},
  journal={Agents and Actions},
Acetaldehyde is 10–30 times more toxic than ethanol and has been implicated in alcoholic cardiomyopathy. Its oral LD50 and LD90 Litchfield-Wilcoxon values were found to be 15.0 (14.4–15.6) mM/kg and 18.0 (15.5–20.5) mM/kg, respectively. Protection against acetaldehyde lethality was obtained by oral intubation of test compounds 30–45 minutes prior to oral intubation of 18 mM/kg of acetaldehyde. At 2.0 mM/kg, survival after 24–72 hours withl-cysteine free base(FB)was80%;withl-2-methylthiazolidine… 
Protective action of ascorbic acid and sulfur compounds against acetaldehyde toxicity: Implications in alcoholism and smoking
These findings could point the way to a possible build-up of natural protection against the chronic body insult of acetaldehyde arising from heavy drinking of alcohol and heavy smoking of cigarettes.
Permeability and toxicity characteristics of L-cysteine and 2-methyl-thiazolidine-4-carboxylic acid in Caco-2 cells
Results showed that when l-cysteine is administered in formulations releasing it locally in the lower parts of GI tract, it is not absorbed but can react with acetaldehyde, and that neither l- Cysteine nor MTCA is harmful to the cells when present locally inThe upper parts ofGI tract.
Comparison of Protection byl-ascorbic acid,l-cysteine, and adrenergic-blocking agents against acetaldehyde, acrolein, and formaldehyde toxicity: Implications in smoking
Acrolein and formaldehyde, as well as acetaldehyde, are currently regarded as important toxicants in cigarette smoke. In this study with rats, previously-reported protectants against acetaldehyde
Occurrence of 2-methylthiazolidine-4-carboxylic acid, a condensation product of cysteine and acetaldehyde, in human blood as a consequence of ethanol consumption
Lack of hydrolytic stability under physiological conditions may hamper the use of MTCA as a quantitative marker of acetaldehyde exposure, such as resulting from alcohol consumption.
Effects of pantothenic acid derivatives on the acute toxicity of ethanol and acetaldehyde
The action of ethanol (E) and A on the organism is accompanied by changes in the protein, fat, and carbohydrate metabolism [2-4]. Let us note that in alcoholism patients the metabolism of various
Reduction of ethanol-derived acetaldehyde induced motivational properties by L-cysteine.
BACKGROUND Experimental evidences suggest that acetaldehyde (ACD) contributes to the positive motivational properties of ethanol (EtOH) as assessed by the place conditioning paradigm; indeed, we
Conjugation of acetaldehyde with cysteinylglycine, the first metabolite in glutathione breakdown byγ-glutamyltranspeptidase
Cysteinylglycine, the first metabolite in the glutathione breakdown by γ-glutamyltranspeptidase showed a rapid and equimolar reactivity to acetaldehyde and such was comparable to the reaction seen withl-cysteine ord-penicillamine, which probably conjugates with acetaldehyde to form thiazolidinecarboxylic acid derivatives.
Effect of (L)-cysteine on acetaldehyde self-administration.
Acetaldehyde (ACD), the first metabolite of ethanol, has been implicated in several behavioural actions of alcohol, including its reinforcing effects. Recently, we reported that l-cysteine, a
Cellular and Molecular Evidence of Acetaldehyde Elimination and Intracellular Environment Antioxidation by L-Cysteine
Acetaldehyde is a harmful metabolite of smoking and drinking. This study was initially intended to facilitate the understanding of the possible injury mechanism of A549 cells damaged by acetaldehyde
Behavioral and Biochemical Effects of N-Acetylcysteine in Zebrafish Acutely Exposed to Ethanol
Zebrafish exposed to EtOH displayed a decrease in the distance traveled, crossings, entries and time spent in the top area in the novel tank test, and NAC prevented both the behavioral alterations and the oxidative stress observed in EtOH+ animals.


Biochemical Changes Following Poisoning of Rats by Alphanaphthylthiourea
  • K. P. Dubois, L. W. Holm, W. Doyle
  • Chemistry, Medicine
    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine
  • 1946
While these experiments demonstrate a disturbance in carbohydrate metabolism, they do not prove that death from ANTU is due to these changes and the relation between lung damage and impairment of glycolysis and/or respiration is under investigation.
Cardiac effects of some simple aliphatic aldehydes.
  • T. N. James, E. Bear
  • Chemistry, Medicine
    The Journal of pharmacology and experimental therapeutics
  • 1968
It was determined that the sympathomimetic activity of aliphatic aldehydes depends on the presene of a terminal aldehyde and a free contralateral, nearby terminal methyl group, and that this action was stromigest in the compound containing only these two essential groups (acetaldehyde).
Inactivation of coenzyme a by ethanol. I. Acetaldehyde as mediator of the inactivation of coenzyme A following the administration of ethanol in vivo.
It is concluded that the action of ethanol on coenzyme A is mediated by acetaldehyde, and brain tissue is not able to oxidize ethanol in measurable quantities and, therefore, acetaldehyde is formed only in liver homogenates.
Effects of inhaled acetaldehyde and propionaldehyde on blood pressure and heart rate.
  • J. Egle
  • Chemistry, Medicine
    Toxicology and applied pharmacology
  • 1972
It appears that concentrations of acetaldehyde and propionaldehyde producing significant changes in blood pressure and heart rate are somewhat higher than those that would be encountered in cigarette smoking.
Production of Pulmonary Edema by Thiourea in the Rat, and Its Relation to Age.∗
Thiourea, in addition to effecting thyroid enlargement and a decline in the B.M.R.R., produces in appropriate doses, rapid and fatal pulmonary edema in adult rats and the immature rat is much less susceptible to themonary edema and more susceptibility to the thyroid enlargements produced by this compound.
The Metabolism of Alcohol in Normals and Alcoholics: Enzymes
The knowledge about the metabolism of ethanol and the participating enzymes offers, in several ways, a basis for a better understanding of biochemical processes involved in acute and chronic alcohol
Effects of ethanol and acetaldehyde on the heart.
Both the acute and chronic cardiac effects of alcoholism may be due in part to the release of myocardial norepinephrine by acetaldehyde, the principal metabolite of ethanol.
Myocardial depression accompanying chronic consumption of alcohol.
A consistent decrease in potential ventricular contractile force, blood pressure, and heart rate occurred after 4 months of alcohol administration, and the decrease appears to be the result of alcohol itself, rather than nutritional or vitamin deficiencies.
The anatomical basis of the straub phenomenon.
It was concluded that the phenomenon described by Straub (1911) was produced mainly by the action of the sacro-coccygeus dorsalis muscle, and that it was also necessary that the lumbo-sacral cord with its peripheral nervous outflow should be intact and that these functioning units should have an adequate circulation.
A simplified method of evaluating dose-effect experiments.
The method provides means for the rapid test of parallelism of two curves and easy computation of relative potency with its confidence limits and its accuracy is commensurate with the nature of dose-per cent effect data.