Early events in naphthalene-induced acute Clara cell toxicity. II. Comparison of glutathione depletion and histopathology by airway location.

@article{Plopper2001EarlyEI,
  title={Early events in naphthalene-induced acute Clara cell toxicity. II. Comparison of glutathione depletion and histopathology by airway location.},
  author={Charles G. Plopper and Laura S. Van Winkle and Michelle V. Fanucchi and S R Malburg and Susan J. Nishio and A M Chang and Alan Buckpitt},
  journal={American journal of respiratory cell and molecular biology},
  year={2001},
  volume={24 3},
  pages={
          272-81
        }
}
One of the presumed roles of intracellular glutathione (GSH) is the protection of cells from injury by reactive intermediates produced by the metabolism of xenobiotics. To establish whether GSH depletion is a critical step in the initiation of events that lead to cytotoxicity by P450-activated cytotoxicants, naphthalene, a well-defined Clara cell cytotoxicant, was administered to mice (200 mg/kg) by intraperitoneal injection. Shortly after injection (1, 2, and 3 h), intracellular GSH content… 
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Prevention of naphthalene‐induced pulmonary toxicity by glutathione prodrugs: Roles for glutathione depletion in adduct formation and cell injury
TLDR
It is concluded that glutathione prodrugs can prevent naphthalene toxicity in Clara cells, theProdrugs effectively prevent glutATHione loss in vivo, and cysteine–glutathione mixed disulfide prevents naphthaene injury in vitro without raising glutathion levels.
Glutathione depletion is a major determinant of inhaled naphthalene respiratory toxicity and naphthalene metabolism in mice.
TLDR
GSH depletion occurs in airways independent of hepatic function, sufficient GSH is not supplied by the liver to maintain respiratory GSH pools, or to prevent injury from inhaled naphthalene, and GSH loss precedes injury and increases protein adduct formation.
Consequences of Abrupt Glutathione Depletion in Murine Clara Cells: Ultrastructural and Biochemical Investigations into the Role of Glutathione Loss in Naphthalene Cytotoxicity
TLDR
Compared with the lethal injury caused by naphthalene, the disruptive cellular changes associated with glutathione loss from diethylmaleate seemed to be reversible after recovery of glutATHione levels, suggesting that glutathion depletion may be responsible for some aspects of naphhalene cytotoxicity, but it is not sufficient to cause cell death without further stresses.
Naphthalene cytotoxicity in microsomal epoxide hydrolase deficient mice.
Gender differences in naphthalene metabolism and naphthalene-induced acute lung injury.
TLDR
It is concluded that there are clear gender differences in susceptibility to naphthalene-induced injury and that differences in metabolism of naphhalene may play a role in elevated susceptibility in female mice.
Molecular model of naphthalene-induced DNA damage in the murine lung
TLDR
Findings indicate a time-dependent accumulation of γH2AX foci in mouse airway epithelial cells following administration of naphthalene, which can be adapted as a suitable model for further investigation of genotoxic damage for evaluating the efficacy of potential therapeutics.
Keratinocyte growth factor protects against Clara cell injury induced by naphthalene
TLDR
The present results demonstrate that pre-treatment with N-terminally truncated recombinant human keratinocyte growth factor protects against naphthalene-induced injury, and suggests that N- terminally truncate recombinantHuman keratinocytes growth factor exerts its beneficial effect through a decrease in the expression of cytochrome P450 isoform 2F2.
Naphthalene toxicity and antioxidant nutrients.
Regulation of uteroglobin/Clara cell protein expression after acute lung exposure to an organophosphoreted insecticide
TLDR
The stimulation of UG/CC16 synthesis occurring during inflammatory processes of the respiratory tract caused by acute inhalation of a toxicant appears to be functional without the intervention of glucocorticoids and mediated by IFN-γ as a mechanism for local control of the inflammatory response.
Pulmonary heat shock protein expression after exposure to a metabolically activated Clara cell toxicant: relationship to protein adduct formation.
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