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1,2‐Dichloropropane hepatotoxicity in rats after inhalation exposure
Author(s) -
di Nucci A.,
Gregotti C.,
Manzo L.,
Imbriani M.,
Ghittori S.,
Bianco L.,
Maestri L.,
Capodaglio E.
Publication year - 1990
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550100602
Subject(s) - chemistry , inhalation , lipid peroxidation , inhalation exposure , thiol , metabolism , medicine , endocrinology , toxicity , glutathione , biochemistry , oxidative stress , enzyme , anesthesia , organic chemistry
The hepatic effects of 1,2‐dichloropropane (DCP) were investigated in male Wistar rats exposed to 15, 50, 100, 250, 450, 1000, 1300, 1800 or 4900 mg DCP m −3 . At the end of a 4‐h period of exposure, average blood DCP levels were 0.025 and 5.38 μg ml −1 in animals treated with 15 and 1300 mg m −3 , respectively. Blood DCP concentrations were correlated with the air DCP concentrations in the inhalation chamber. At DCP concentrations of 100 mg m −3 or higher, the liver non‐protein thiol (NPT) content was significantly reduced. Assays performed 20 h after 4‐h DCP exposure showed that exposure to 100–1000 mg DCP m −3 had no effect on hepatic NPT levels. The NPT content increased only in the liver of rats exposed to higher (1300–4900 mg m −3 ) DCP concentrations. Treatment with DCP did not cause hepatic lipid peroxidation and did not modify total protein content. The observed changes in liver cell thiol homeostasis are likely to reflect the action of reactive intermediates formed during DCP metabolism. These changes can occur in rats following exposure to considerably low levels of DCP vapour.