Energy metabolism alcohol

Dan MX, Wang CC (2000) Role of alcohol dehydrogenase E (ADHE) in the energy metabolism of Giardia lamblia. Mol Biochem Parasitol 109 25-36... 

Release of the chloride substituent in 2 produces ethyl acetoacetate (1) which is an inhibitor of alcohol dehydrogenase (ADH, EC 1.1.1.1) and thereby affects energy metabolism. Above all, NAD+ regeneration is impaired. As a consequence acetaldehyde becomes an overflow metabolite which is excreted into the medium or reacts with activated positions in the molecule (Fig. 3.5). 

Alcoholic fermentation is less efficient in producing ATP than aerobic root respiration thus, net energy production by the anaerobic pathway is only a fraction of that produced by the aerobic respiration. Root energy metabolism under aerobic and anaerobic conditions is as follows ... 

Type 1. Type-1 situations include processes in which product accumulation is directly associated with growth this is the case for primary metabolites, in which the formation of the product is linked to the energy metabolism. Examples include fermentation to produce alcohol and gluconic acid (Koga et al., 1967), and situations in biological waste water treatment. 

The energy provision by carbohydrate metabolism has been extensively studied Ihm the beginning of this century, chiefly in an attempt to understand the basic biochemistry of alcohol production from carbohydrafe. However, many laboratory culture media contain only nitrogenous compounds and their metabolism is of importance as it clearly provides energy for growth and maintenance. 

Pool concentration of a substance that exceeds the threshold - for example megadose vitamin C - or substances that are excreted unchanged because they cannot be metabolised, such as sugar alcohols, or compounds that are not biologically essential, such as carcinogens, bacterial toxins and some minor plant constituents, are also bioavailable (and thus bioactive) in that they have a metabolic impact, even if this is only the stimulation of detoxification processes, or the use of energy for their excretion. 

For some toxins it is possible to demonstrate an apparent improvement in functional response at levels of exposure which are below a threshold. This effect, which has been termed hormesis , is most effectively demonstrated in the consistently improved longevity of animals whose caloric intake is restricted rather than allowing them to feed ad lib (Tannenbaum, 1942). Clearly in this instance, the observed effects are the result of exposure to a complex mixture of chemicals whose metabolism determines the total amount of energy available to the organism. But it is also possible to show similar effects when single chemicals such as alcohol (Maclure, 1993), or caffeic acid (Lutz et al., 1997) are administered, as well as for more toxic chemicals such as arsenic (Pisciotto and Graziano, 1980) or even tetrachloro-p-dibenzodioxin (TCDD) ( Huff et al., 1994) when administered at very low doses. It is possible that there are toxins that effect a modest, reversible disruption in homeostasis which results in an over-compensation, and that this is the mechanism of the beneficial effect observed. These effects would not be observed in the animal bioassays since to show them it would be necessary to have at least three dose groups below the NOAEL. In addition, the strain of animal used would have to have a very low incidence of disease to show any effect. 

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