| Gym Addict
Join Date: Jun 2008
Posts: 136
| Re: how to beat a hangover
Quote:
Originally Posted by pauly7582  It's not possible to protect yourself against them by eating certain foods or doing this and that. It's not possible to improve your ability to metabolise aldehydes. | yes there is.
pparalpha agonists upregulate aldehyde dehydrogenase production. Alcohol Clin Exp Res. 2005 Nov;29(11 Suppl):116S-120S.  Links
Sesamin ingestion regulates the transcription levels of hepatic metabolizing enzymes for alcohol and lipids in rats.
Kiso Y, Tsuruoka N, Kidokoro A, Matsumoto I, Abe K.
Suntory Institute for Health Care Science, Osaka, Japan. Yoshinobu_Kiso@suntory.co.jp
BACKGROUND: Sesamin, a major lignan in sesame seeds, has multiple functions such as stimulation effect of ethanol metabolism in mice and human, and prevention of ethanol-induced fatty liver in rats. However, the mechanism has not been clarified yet. METHODS: The changes of gene expression were investigated in rats given 250 mg/kg of sesamin (sesamin rats) or vehicle (control rats) for three days by using a DNA microarray analysis. At 4 hr after the final ingestion, the profiles of gene expression in rat livers were compared. RESULTS: The analysis showed that 38 transcripts were up-regulated with a significant change of more than two-fold and eight transcripts were down-regulated with a significant change to less than half in the livers of sesamin rats versus control rats. The gene expression levels of the early stage enzymes of beta-oxidation including long-chain acyl-CoA synthetase, very long-chain acyl-CoA synthetase and carnitine palmitoyltransferase were not changed, however, those of the late stage enzymes of beta-oxidation including trifunctional enzyme in mitochondria, and acyl-CoA oxidase, bifunctional enzyme and 3-ketoacyl-CoA thiolase in peroxisomes, were significantly increased by sesamin ingestion. Also, in sesamin rats, the gene expression of aldehyde dehydrogenase was increased about three-fold, whereas alcohol dehydrogenase, liver catalase and CYP2E1 were not changed. Changes in the gene expression of alcohol- and aldehyde-metabolizing enzymes observed in a DNA microarray were also confirmed by a real-time PCR method. CONCLUSIONS: These results suggested that sesamin ingestion regulated the transcription levels of hepatic metabolizing enzymes for alcohol and lipids.
: Toxicol Sci. 2008 Jan;101(1):51-64. Epub 2007 Nov 12.  Links
Tissue distribution, ontogeny, and regulation of aldehyde dehydrogenase (Aldh) enzymes mRNA by prototypical microsomal enzyme inducers in mice.
Alnouti Y, Klaassen CD.
Kansas Life Sciences Innovation Center, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.
Aldehyde dehydrogenases (Aldhs) are a group of nicotinamide adenine dinucleotide phosphate-dependent enzymes that catalyze the oxidation of a wide spectrum of aldehydes to carboxylic acids. Tissue distribution and developmental changes in the expression of the messenger RNA (mRNA) of 15 Aldh enzymes were quantified in male and female mice tissues using the branched DNA signal amplification assay. Furthermore, the regulation of the mRNA expression of Aldhs by 15 typical microsomal enzyme inducers (MEIs) was studied. Aldh1a1 mRNA expression was highest in ovary; 1a2 in testis; 1a3 in placenta; 1a7 in lung; 1b1 in small intestine; 2 in liver; 3a1 in stomach; 3a2 and 3b1 expression was ubiquitous; 4a1, 6a1, 7a1, and 8a1 in liver and kidney; 9a1 in liver, kidney, and small intestine; and 18a1 in ovary and small intestine. mRNAs of different Aldh enzymes were detected at lower levels in fetuses than adult mice and gradually increased after birth to reach adult levels between 15 and 45 days of age, when the gender difference began to appear. Aromatic hydrocarbon receptor (AhR) ligands induced the liver mRNA expression of Aldh1a7, 1b1, and 3a1, constitutive androstane receptor (CAR) activators induced Aldh1a1 and 1a7, whereas pregnane X receptor (PXR) ligands and NF-E2 related factor 2 (Nrf2) activators induced Aldh1a1, 1a7, and 1b1. Peroxisome proliferator activator receptor alpha (PPAR alpha) ligands induced the mRNA expression in liver of almost all Aldhs. The Aldh organ-specific distribution may be important in elucidating their role in metabolism, elimination, and organ-specific toxicity of xenobiotics. Finally, in contrast to other phase-I metabolic enzymes such as CYP450 enzymes, Aldh mRNA expression seems to be generally insensitive to typical microsomal inducers except PPAR alpha ligands.
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