ABSTRACT
The effects of sodium chlorate and of sodium nitrite on human erythrocytes were studied in vitro. Nitrite rapidly oxidised haemoglobin and glutathione; reduction of methaemoglobin (Hbi) by methylene blue was complete during 3 h of incubation with nitrite. With chlorate, a concentration-dependent lag phase was seen before Hbi was formed. After prolonged incubation, Hbi could no longer be reduced with methylene blue. Several other effects were observed that explain the clinical picture of chlorate poisoning which involves haemolysis followed by disseminated intravascular coagulation and renal failure: increased permeability to cations, increased resistance to hypotonic haemolysis and prolonged filtration time through polycarbonate membranes with cylindrical pores of 5 micron diameter. This suggests an increased membrane rigidity due to membrane protein polymerisation, as demonstrated by SDS polyacrylamide gel electrophoresis. Simultaneously, erythrocyte enzymes were inactivated, primarily glucose-6-phosphate dehydrogenase which is necessary for the therapeutic effect of methylene blue. This explains the inefficacy of methylene blue in the treatment of a case of chlorate poisoning that we observed (Arch. Toxicol., 48 (1981) 281).
Subject(s)
Chlorates/toxicity , Erythrocyte Membrane/drug effects , Electrophoresis, Polyacrylamide Gel , Glutathione/blood , Hemolysis/drug effects , Humans , In Vitro Techniques , Membrane Fluidity/drug effects , Methemoglobinemia/chemically induced , Nitrites/pharmacology , Oxidation-Reduction/drug effects , Potassium/blood , Sodium/bloodABSTRACT
A method is presented that allows the measurement of erythrocyte filtration times that are extremely prolonged. Filtration times through polycarbonate sieves are increased by a factor of 40 after 2 h incubation with 30 mM sodium chlorate. This increase in red cell rigidity offers an explanation for the haemolysis observed in chlorate poisoning in vivo.
