[Changes in the serum albumin system during toxic syndrome and their pharmacologic correction]

In connection with the important role of serum albumins in pathogenesis and sanogenesis of numerous toxic states, we examined binding capacity of these proteins and conditions of their binding sites after acute poisoning with tetrachloromethane (TCM) and administration of antihypoxic agents (sodium gamma-hydroxybutirate), antioxidants (Dibunol), and actoprotector (Tomersol) to rats. We demonstrated that tetrachloromethane intoxication (3.2 g/kg over 24 h) was accompanied by a certain decrease (by 13.8%) in the total blood serum level of albumins and a tendency to a decrease in the value of the binding constant of negatively charged fluorescent probe 1-(phenylamino)-8-sulfonaphthalene. Under these conditions, the mean number of probe binding sites per albumin molecule increases, and as a result, the total concentration of albumin binding sites in the serum remains virtually unchanged. We found that accessibility of the probe to a quenching agent (potassium nitrate) increases in the protein--probe complex under intoxication conditions, suggesting that the type of interaction between the protein and the fluorescent probe changes as well. Therapeutic/prophylactic administration of an antioxidant, antihypoxic agent, or actoprotector leads to an increase in the level of albumin in the serum (Tomersol), partial normalization of its binding properties (binding constant in the case of sodium gamma-oxybutirate, mean number of binding sites per molecule for Dibunol and Tomersol), and the state of binding sites (sodium gamma-oxybutirate, Dibunol).