EFFECTS OF INHALED ACRYLIC-ACID DERIVATIVES IN RATS

Chemical reactivity with glutathione, urinary thioether excretion, total (T-SH) and non-protein-SH (NP-SH) groups in tissues and blood glucose were studied in male Wistar rats exposed to acrylic acid derivatives. The 6-h inhalation of acrylonitrile (AN), methyl acrylate (MA), ethyl acrylate (EA), n-butyl acrylate (BA) and 2-ethylhexyl acrylate (2-EHA) in several concentrations increased the urinary thioether excretion; the portion metabolized to thioethers was 35-18% of the acrylonitrile dose, but only 1.5-8% for the acrylates. Total-SH levels in the liver significantly decreased after the inhalation of AN, EA, BA and 2-EHA. In blood there was a decrease only after EA. Most pronounced NP-SH depletion was in the liver, less in blood and moderate in brain and lungs. There was an exponential relationship between the tissue NP-SH and the inhaled concentrations. Calculated concentrations inducing 50% NP-SH depletion indicated that reaction of acrylic acid derivatives with SH groups was decreasing in the order AN >> 2-EHA > EA = BA for the chemicals and liver > blood > lungs > brain for the tissues. All inhaled acrylates induced hyperglycemia, but acrylic acid was without effect. The chemical reactivity of acrylates with glutathione (GSH) decreased in the order EA > BA > MA > AN > 2-EHA. The results suggest that GSH depletion may participate in acute lethal and biochemical toxic effects of acrylic acid esters.