Ethanol oxidation to acetaldehyde

Method 6(when acardite III alone is present as stabilizer and gelatinizer) Procs a) to e)— same as in Method 4 f)In order to establish that the sample contains acardite III and not acardite 11, treat the solnfafter removal of N gas) with chromic mixt(KaCr207 + Ha S04) in order to oxidize ethanol to acetaldehyde. Treat the oxidized soln with fuchsin, previously... 

The liver enzymes that oxidize ethanol to acetaldehyde are the same as those that oxidize methanol to formaldehyde. Physicians take advantage of this in the treatment of wood alcohol poisoning by trying to keep those enzymes busy with a reaction that produces a less toxic (not nontoxic) by-product. In cases of methanol poisoning, the patient receives ethanol intravenously. The ethanol should then be in greater concentration than methanol and should compete successfully for the liver enzymes and be converted to acetaldehyde. This gives the body time to excrete the methanol before it is oxidized to the potentially deadly formaldehyde. 

Al Martini was not able to clear his blood ethanol rapidly enough to stay within the legal limit for driving. Ethanol is cleared from the blood at about Vz ounce/hr (15 mg/dL per hour). Liver metabolism accounts for more than 90% of ethanol clearance from the blood. The major route of ethanol metabolism in the liver is the enzyme liver alcohol dehydrogenase (ADH), which oxidizes ethanol to acetaldehyde with generation of NADH. 

The maximal capacity of MEOS (cytochrome P450-2E1) is increased in the liver with continued ingestion of ethanol through a mechanism involving induction of gene transcription. Thus, Al Martini has a higher capacity to oxidize ethanol to acetaldehyde than a naive drinker (a person not previously subjected to alcohol). Nevertheless, the persistance of his elevated blood alcohol level shows he has saturated his capacity for ethanol oxidation (V-maxed out). Once his enzymes are operating near Vmax. any additional ethanol he drinks will not appreciably increase the rate of ethanol clearance from his blood. 

Ethanol is a dietary fuel that is metabolized to acetate principally in the liver, with the generation ofNADH. The principal route for metabolism of ethanol is through hepatic alcohol dehydrogenases, which oxidize ethanol to acetaldehyde in the cytosol (Fig. 25.1). Acetaldehyde is further oxidized by acetaldehyde dehydrogenases to acetate, principally in mitochondria. Acetaldehyde, which is toxic, also may enter the blood. NADH produced by these reactions is used for adenosine triphosphate (ATP) generation through oxidative phosphorylation. Most of the acetate enters the blood and is taken up by skeletal muscles and other tissues, where it is activated to acetyl CoA and is oxidized in the TCA cycle. 

The major route of ethanol metabolism in the hver is through hver alcohol dehydrogenase, a cytosohc enzyme that oxidizes ethanol to acetaldehyde with reduction of NAD to NADH (Fig.25.2). If it is not removed by metabolism, acetaldehyde exerts toxic actions in the liver and can enter the blood and exert toxic effects in other tissues. 

The other principal route of ethanol oxidation in the liver is the microsomal ethanol oxidizing system (MEOS), which also oxidizes ethanol to acetaldehyde (Fig. 25.3). The principal microsomal enzyme involved is a cytochrome P450 mixed-function oxidase isozyme (CYP2E1), which uses NADPH as an additional electron donor and O2 as an electron acceptor. This route accounts for only 10 to 20% of ethanol oxidation in a moderate drinker. 

Alcohol dehydrogenase and aldehyde dehydrogenase were used as the enzymes for anodic ethanol oxidation. Together with the coenzyme NAD" " (nicotinamide adenine dinucleotide), they formed the NAD+/NADH redox system. Aided by these enzymes, this reaction occurs in two steps. First, the former enzyme oxidizes ethanol to acetaldehyde, and then the latter enzyme oxidizes the aldehyde to acetic acid. 

ADH is used to measure ethanol in body fluids. ADH oxidizes ethanol to acetaldehyde in the presence of a coenzyme NAD, which is reduced to NADH that is measured spectrophotometrically at 340 nm ... 

First-generation calix ligands are unusually highly air stable. Peroxidic shunt from Cu(II) was thus used to study their reactivity. With H2O2 as an oxidant, calix-tris(pyridine) Cu(II) oxidized ethanol to acetaldehyde and acetic acid, and benzene to phenol and benzoquinone (Figure 32a). Similar reactivity (without formation of acetic acid) was observed with calix-tris(imidazole)Cu(II). UV-vis spectroscopy exhibited an LMCT HOO Cu(II) at 375 nm, ascribed to a Cu(II)-OOH species. 

Reduction of Nitro Compounds p-Nitroacetophenone A hydroxylamine intermediate is detected by the photo-induced reduction ofp-nitroacetophenone with high yields by the irradiation of suspensions of P25 Ti02 in ethanol. The photogenerated electrons reduce the nitro compound, whereas the holes oxidize ethanol to acetaldehyde with the formation of hydrogen. 

Whereas Acetobacter produces limited amounts of acetic acid through carbohydrate metabolism, much more of the acid is synthesized through the oxidation of ethanol (Eschenbruch and Dittrich, 1986). Two membrane-bound enzymes, an alcohol dehydrogenase and an aldehyde dehydrogenase, are involved in this conversion (Saeki et al., 1997). Alcohol dehydrogenase oxidizes ethanol to acetaldehyde, which is further oxidized to acetic acid hy the aldehyde dehydrogenase as follows ... 

In addition to oxidizing ethanol to acetaldehyde, alcohol dehydrogenase can oxidize methanol to formaldehyde. Formaldehyde is damaging to many tissues and since eye tissue is particularly sensitive, methanol ingestion can cause blindness. 

Asai (21) proposed that the primary Kombucha bacterium, Acetobacter, initially oxidizes ethanol to acetaldehyde and then to acetic acid. Ethanol is oxidized to acetaldehyde by alcohol-cytochrome-553 reductase and the resulting electrons are successively delivered to the heme iron of cytochrome-553. The acetaldehyde thus formed is oxidized further by coenzyme-independent aldehyde dehydrogenase or by NADP-dependent aldehyde dehydrogenase. Observations on alcohol dehydrogenase have been made by Ameyama and Adachi (22) who... 

Ethanol is the most commonly abused drug in the United States. When ingested in small amounts, ethanol may produce a feeling of euphoria in the body despite the fact that it is a depressant. In the liver, enzymes such as alcohol dehydrogenase oxidize ethanol to acetaldehyde, a substance that impairs mental and physical coordination. If the blood alcohol concentration exceeds 0.4%, coma or death may occur. Table 12.3 gives some of the typical behaviors exhibited at various blood alcohol levels. 

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