![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
PG Forkert and M Moussa
Department of Anatomy, Queen's University, Kingston, Ontario, Canada.
Administration of 1,1-dichloroethylene (DCE) to mice evokes cytotoxicity involving Clara cells in lung, and at higher doses, centrilobular hepatocytes in liver. Our objective is to investigate temporal alterations in nonprotein sulfhydryl [glutathione (GSH)] content in lung and liver after administration of a dose of DCE (125 mg/kg). Contribution of GSH from whole blood comprised 54% and 14% of the amounts found in lung and liver, respectively, of DCE-treated mice, and were taken into account to determine tissue content of GSH. In lung, a significant decrease in GSH (60% of control) was first detected at 6 hr, and levels remained low from 8 to 12 hr. In liver, a 50% decrease was initially detected at 1 hr after DCE treatment. Progressive increases were found thereafter, with a return to the control level at 24 hr. Histochemical staining for GSH in liver revealed homogeneous labeling in hepatocytes across the lobule; DCE treatment diminished staining uniformly in all hepatocytes. In control lung, histochemical reactivity was exhibited in bronchiolar epithelium and alveolar septa. Clara cells were stained to the greatest extent and with considerable variability, whereas staining was more uniform in alveolar septa. Staining was markedly diminished by DCE treatment, and was initially abolished in the alveolar septa, but retained to a limited extent within a small number of Clara cells. These findings suggest that susceptibility of a subpopulation of Clara cells to cytotoxicity may be associated, in part, with low expression of nonprotein sulfhydryl content at the time of DCE treatment.
This article has been cited by other articles:
|
|
 |
|
  R. C. Lantz, R. Lemus, R. W. Lange, and M. H. Karol Rapid Reduction of Intracellular Glutathione in Human Bronchial Epithelial Cells Exposed to Occupational Levels of Toluene Diisocyanate Toxicol. Sci., April 1, 2001; 60(2): 348 - 355. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P.-G. Forkert In Vivo Formation and Localization of 1,1-Dichloroethylene Epoxide in Murine Liver: Identification of Its Glutathione Conjugate 2-S-Glutathionyl Acetate J. Pharmacol. Exp. Ther., September 1, 1999; 290(3): 1299 - 1306. [Abstract] [Full Text]
|
|
|
|
 |
|
 P.-G. Forkert 1,1-Dichloroethylene-Induced Clara Cell Damage Is Associated with In Situ Formation of the Reactive Epoxide . Immunohistochemical Detection of Its Glutathione Conjugate Am. J. Respir. Cell Mol. Biol., June 1, 1999; 20(6): 1310 - 1318. [Abstract] [Full Text]
|
|
|
|
 |
|
 P.-G. Forkert, A. M. Malkinson, P. Rice, and M. Moussa Diminished CYP2E1 Expression and Formation of 2-S-Glutathionyl Acetate, a Glutathione Conjugate Derived from 1,1-Dichloroethylene Epoxide, in Murine Lung Tumors Drug Metab. Dispos., January 1, 1999; 27(1): 68 - 73. [Abstract] [Full Text]
|
|
|
|
|
|
P.-G. Forkert, D. D'Costa, and M. El-Mestrah Expression and Inducibility of Alpha, Pi, and Mu Glutathione S-Transferase Protein and mRNA in Murine Lung Am. J. Respir. Cell Mol. Biol., January 1, 1999; 20(1): 143 - 152. [Abstract] [Full Text]
|
|
|
|
 |
|
 T. E. Gram Chemically Reactive Intermediates and Pulmonary Xenobiotic Toxicity Pharmacol. Rev., December 1, 1997; 49(4): 297 - 342. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P.-G. Forkert, K. S. Collins, T. F. Dowsley, and G. M. Ross J. Pharmacol. Exp. Ther., June 1, 1997; 281(3): 1422 - 1430. [Abstract]
|
|
 |
 |
 |
|
 |
 |
 |
