Formation Op Pyruvate-lactate Index and Op Glucose Level in Controlled Alcoholemia

Assuming that the oxidation of alcohol runs parallelly with the other metabolic process in hepatic cells, further investigations of alcoholemia aimed at finding distemper exponents in NADH and NADPH coenzyme reoxidation, and secondarily in behaviour of hydrogen accepting substrates (1,2,3) should be undertaken. These products take part in coenzyme reoxidation as carriers retransporting H ions from cytosol to mitochondria, where again they are incorporated into the enzyme flavine respiratory chain. Pyruvates/lactates oxalates/ /svecinates and others belong to carries of so correlated pairs 0.2,3). It seems necassary to take into account additional ethyl alcohol oxidation in microsomal enzyme system (MEOS arrangement) or with the employment of kathalase shifting redox potential to NADH abundance and reducing oxidase cell potential with all the consequences like, among others, dimunition of hydrogen accepting substrates (pyruvates). Carbohydrate transformation (fructose), and in particular,glycolysis processes, which might be a source of hydrogen accepting substrates, are connected with an adequate pyroracemic and lactic acid supply (4,5,7). Data from some reports may indicate (1,4,6,8) that vacillation of cell redox potential in longer lasting alcoholemia manifests in level variation of pyroracemic and lactic acids and in blood glucose. Since the nature of this phenomenon in many-hour lasting alcoho­ lemia has not been fully understood, we have decided on undertaking our own investigations, comprising several control variants.