I. Linhart et al., BIOTRANSFORMATION OF ACROLEIN IN RAT - EXCRETION OF MERCAPTURIC ACIDSAFTER INHALATION AND INTRAPERITONEAL INJECTION, Toxicology and applied pharmacology, 136(1), 1996, pp. 155-160
Biotransformation of acrolein (ACR) was studied in vivo in the rat fol
lowing inhalation and ip administration. The major and minor urinary m
etabolites were 3-hydroxypropylmercapturic acid (HPMA) and 2-carboxyet
hylmercapturic acid (CEMA), respectively. Male Wistar rats were expose
d to ACR, 23, 42, 77 and 126 mg/m(3), for 1 hr. The sum of mercapturic
acids HPMA and CEMA excreted within 24 hr after the exposure amounted
to 0.87 +/- 0.12, 1.34 +/- 0.5, 2.81 +/- 1.15, and 7.13 +/- 1.56 mu m
ol/kg, i.e., 10.9 +/- 1.5, 13.3 +/- 5.0, 16.7 +/- 6.9, and 21.5 +/- 4.
8% of the estimated absorbed dose, respectively. The dose estimate was
based on reported values of minute respiratory volume and respiratory
tract retention and was corrected for the ACR-induced changes in minu
te respiratory volume. In the relevant dose range (8.9 to 35.7 mu mol/
kg) the portion of mercapturic acids excreted was nearly constant for
ip exposed rats. The sum of HPMA and CEMA amounted to 29.1 +/- 6.5% of
the dose. These results indicate that the deficiency in rat lung meta
bolism of ACR to acrylic acid previously observed is not compensated b
y the other detoxication pathway in vivo, mercapturic acid formation.
The health hazard arising from inhalation of ACR is likely to be highe
r than that from other routes of exposure. (C) 1996 Academic Press, In
c.