Toxicity and biochemical changes in rats after inhalation exposure to 1,1-dichloroethylene, bromobenzene, styrene, acrylonitrile or 2-chlorobutadiene
Jaeger, RJ; Conolly, RB; Murphy, SD
HERO ID
1162910
Reference Type
Journal Article
Subtype
Abstract
Year
1974
Language
English
| HERO ID | 1162910 |
|---|---|
| Material Type | Abstract |
| In Press | No |
| Year | 1974 |
| Title | Toxicity and biochemical changes in rats after inhalation exposure to 1,1-dichloroethylene, bromobenzene, styrene, acrylonitrile or 2-chlorobutadiene |
| Authors | Jaeger, RJ; Conolly, RB; Murphy, SD |
| Journal | Toxicology and Applied Pharmacology |
| Volume | 29 |
| Issue | 1 |
| Page Numbers | 81 |
| Abstract | Previously, we showed that the inhalation toxicity of 1,1-dichloroethylene (DCB), a plastics monomer, was increased when male rats were fasted overnight prior to exposure. Toxicity was measured by serum transaminase (ST) elevation, by estimated 4 hr LC50, or by minimum lethal concentration (MLC). Enhancement of toxicity with fasting was correlated with a lower hepatic glutathione (GSH) concentration prior to exposure. After exposure to DCB both fed and fasted rats had a further decreased liver GSH concentration. It has been demonstrated by others (Reid and Krishna, Exp. Molec. Pathol. 18, 80, 1973) that depletion of glutathione enhances hepatic injury produced by ip administration of bromobenzene (B). This suggested the possibility that DCB is similar in mechanism of toxic action to B. When B was administered by inhalation to fed and fasted phenobarbital-pretreated rats, fed rats were somewhat more sensitive to the toxic effects of B than were fasted rats. Without phenobarbital induction, both fed and fasted rats were resistant to the lethal effect of B, and hepatic injury was quite variable. Additional inhalation experiments with other plastics monomers known to react with GSH were undertaken. Acrylonitrile (ACN), styrene (S) and 2-chlorobutadiene (CBD), all depleted liver GSH. As anticipated, S and ACN caused no apparent liver injury. S caused death by pulmonary irritation and edema. The estimated LC50 for fed and fasted animals was 2700 ppm. ACN was lethal to all fasted rats at 275 ppm with no apparent effect on fed rats. The approximate LC50 values were 150 and 425 ppm for fasted and fed rats respectively. CBD caused liver injury and fasting enhanced its toxicity as measured by ST and MLC. Significant 24-hr elevation of ST occurred in fasted rats at 560 ppm while comparable values for fed rats were not measured until 4200 ppm. The MLC for fasted rats was below 560 ppm, the lowest concentration tested, while this value for fed rats was between 4200 and 8100 ppm. These data suggest that fed-fasted differences in rats are significant in inhalation toxicity testing. (Supported by Research Grants OH-00315 and ES-00002.) |
| Wosid | WOS:A1974T653800022 |
| Url | https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016161684&partnerID=40&md5=aa01081ac60beabfd82af35326d9f74c |
| Is Certified Translation | No |
| Dupe Override | No |
| Conference Location | Washington, D.C. |
| Conference Name | Thirteenth Annual Meeting of the Society of Toxicology |
| Conference Date | March 10–14, 1974 |
| Is Public | Yes |
| Language Text | English |
| Relationship(s) |
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