Alcohol depletion, mechanism

Ethanol also inhibits ADH-catalyzed retinol oxidation in vitro, and ethanol treatment of mouse embtyos has been demonstrated to reduce endogenous RA levels. The inhibition of cytosolic RolDH activity and stimulation of microsomal RolDH activity could explain ethanol-mediated vitamin A depletion, separate from ADH isoenzymes. Although the exact mechanism of inhibition of retinoid metabolism by ethanol is unclear, these observations are consistent with the finding that patients with alcoholic liver disease have depletedhepatic vitamin A reserves [review see [2]. 

The preparation of di-w-butyl ether is illustrative (Scheme 2.6). No reaction occurred with n-butanol alone for 2 h at 200 °C. However, in the presence of 10 mol % n-butyl bromide, 26% conversion of the alcohol to the ether was obtained after 1 h, without apparent depletion of the catalyst. It is known that addition of alkaline metal salts can accelerate solvolytic processes, including the rate of ionization of RX [41]. This was confirmed when the introduction of LiBr (10 mol %) along with n-butyl bromide, afforded a conversion of 54% after 1 h at 200 °C. Ethers incorporating a secondary butyl moiety were not detected, precluding mechanisms involving elimination followed by Markovnikov addition. 

Allyl formate is cleaved by nonspecific esterases to allyl alcohol, which is then oxidized by alcohol dehydrogenases to the reactive acrolein, which is responsible for the hepatotoxic action. The toxicity of allyl alcohol via its metabolite acrolein is dependent on the concentration of glutathione (GSH). After depletion of GSH, the reactive metabolite of allyl alcohol can bind to essential sulfhydryl groups in the cellular macromolecules, leading to structural and functional modifications that can be responsible for hepatic injury. Appearance of lipid peroxidation signals events that follow toxication mechanisms initiated by acrolein, and subsequent and continued lipid peroxidation could be merely the consequence of cell death. 

B vitamins are not the only ones affected. Ethanol has been shown to deplete the liver of its entire vitamin A (carotene) stores. Somehow the alcohol triggers a mechanism by which all the vitamin A is released from its stores at one time. High vitamin A concentrations are found in the blood for a short time, then none. All is metabolised out. Cirrhotic livers are poor In vitamin A. The lack of vitamin A is resonsible for "night blindness" in some cases. 

Contact of one cm of a 0.025 molar solution of dialkyl phosphite in tetradecane at 403 K (130 C) with one gram of iron powder which had been ball milled under pentane resulted in depletion of the phosphorus in solution, as shown in Fig. 11-9. Reaction as well as adsorption took place, for soluble iron was found in the solutions of di(2-ethyIhexy1), dilauryl and distearyl phosphites. Chromatography of the solutions after contact revealed large quantities of alcohol dibutyl phosphite and di(2-ethylhexyl) phosphite yielded 92-97% of the theoretical amount of alcohol after 24 hours. Hydrolysis of the phosphite esters was ascribed to water adsorbed on the walls of the reaction tube and on the iron powder. Forbes and Battersby [46] postulated that hydrolysis is an important aspect of the mechanism of the additive action of phosphite esters. Oxidation to phosphate by the oxygen of the ambient air is deemed minor maximum augmentation of the oxygen uptake by a 6.5% solution of dibutyl phosphite over that of the tetradecane carrier fluid in the presence of iron was 20%. The easy hydrolysis of phosphites is well known. Partial... 

Oxidation of aliphatic aldehydes by benzyltrimethylammonium chlorobromate to the corresponding carboxylic acid proceeds via the transfer of a hydride ion from the aldehyde hydrate to the oxidant. The oxidation of aUyl alcohol with potassium bromate in the presence of osmium(Vin) catalyst in aqueous acidic medium is first order in bromate, Os(Vni) and substrate, but inverse fractional order in H+ the stoichiometry of the reaction is 2 3 (oxidantsubstrate). The active species of oxidant and catalyst in the reaction were understood to be BrOs and H2OSO5, respectively, which form a complex. Autocatalysis by Br, one of the products, was observed, and attributed to complex formation between Br and osmium(VIII). First-order kinetics each in BrOs, Ru(VI), and substrate were observed for the ruthenium(VI)-catalyzed oxidation of cyclopentanol by alkaline KBrOs containing Hg(OAc)2. A zero-order dependence on HO concentration was observed and a suitable mechanism was postulated. The oxidation reaction of aniUne blue (AB+) with bromate at low pH exhibits interesting non-linear phenomena. The depletion of AB+ in the presence of excess of bromate and acid occurs at a distinctly slow rate, followed by a very rapid reaction. A 12-step reaction mechanism, consistent with the reaction dynamics, has been proposed. The novel cyclohexane-l,4-dione-bromate-acid system has been shown to exhibit a rapid oscillatory redox reaction superimposed on a slower... 

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