rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    title: Cytotoxicity and modulation of gene expression in adult rat hepatocytes by benzo(a)pyrene and related aromatic hydrocarbons
  name:
    name part: Zhao, Wei
    name part: 1960-
    role:
      role term: creator
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: xx
    date issued: 1996
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: print
    extent: xi, 130 leaves : illustrations ; 28 cm.
  abstract: The goal of the present study was to define the cellular and
  abstract: molecular targets of BaP and related AHs in liver
  abstract: parenchymal cells, and to define the relative contribution of
  abstract: AhR-dependent events and/or free radical mechanisms in the
  abstract: responses elicited by these chemicals. The cytotoxic
  abstract: responses of rat hepatocytes to selected AHs were assessed
  abstract: to determine if class-specific differences in toxicity
  abstract: potential exist among these chemicals. Hepatocytes were
  abstract: exposed to various concentrations of BaP, TCDD, TCDF, NAPH,
  abstract: 2-MNAPH, or PCP for designated times. 3H-Thymidine
  abstract: incorporation into DNA, cellular levels of GSH, mitochondrial
  abstract: membrane fragility, and LDH leakage were monitored as indices
  abstract: of cytotoxicity. The data indicated that BaP, TCDD and TCDF
  abstract: induced a concentration-dependent inhibition of DNA
  abstract: synthesis, while NAPH, 2-MNAPH, and PCP were without effect.
  abstract: Significant increases in GSH levels were induced by BaP at
  abstract: all concentrations, while only modest increases occurred in
  abstract: cultures treated with TCDD or TCDF. Upregulation of cellular
  abstract: GSH levels in treated cultures was preceded by depletion at 6
  abstract: to 18 hr. All other hydrocarbons failed to modulate cellular
  abstract: GSH levels significantly, Only BaP and PCP induced
  abstract: significant increases of mitochondrial membrane fragility
  abstract: after exposure for 4 hr, while LDH leakage was only observed
  abstract: in hepatocytes treated with PCP at 1000 []m. To study
  abstract: molecular targets of AHs in hepatocytes, we investigated the
  abstract: modulation of protooncogene expression induced by BaP or
  abstract: TCDD. Hepatocytes were exposed to 3 []M BaP or 1 nM TCDD for
  abstract: 4 hr and patterns of c-fos, c-jun, c-myc, and c-Ha-ras
  abstract: expression monitored by Northern analysis. BaP and TCDD
  abstract: increased c-ras and c-myc gene expression, but decreased c-
  abstract: fos and c-jun mRNA levels. Inhibition of AP1-TRE binding was
  abstract: observed using a gel shift assay when hepatocytes were
  abstract: exposed to 3 []M BaP, but not 1 nM TCDD for 2 hr. To
  abstract: investigate the contribution of AhR-dependent events to the
  abstract: responses elicited by BaP and related AHs, the effects of AhR
  abstract: antagonists ([]-naphthoflavone) or of inhibitors of CYPlAl-
  abstract: catalyzed metabolism of AHs (ellipticine), as well as AH
  abstract: analogs of low affinity for the Ah receptor (e.g. BeP and
  abstract: perylene) on selected endpoints were examined. The results
  abstract: of these studies implicated the AhR in the inhibition of DNA
  abstract: synthesis and cellular GSH levels, as well as in the
  abstract: modulation of protooncogene expression. In studies to assess
  abstract: the role of free radical mechanisms in the hepatotoxic
  abstract: effects of BaP and related AHs, we found that treatment of
  abstract: cells with diamide to induce oxidative stress and
  abstract: downregulate antioxidant capacity increased mitochondrial
  abstract: membrane fragility and protooncogene expression in a manner
  abstract: consistent with the pattern induced by BaP. Collectively,
  abstract: these data suggest that the hepatotoxic effects of BaP and
  abstract: related AHs involve AhR-, as well as oxidative stress-
  abstract: mediated effects.
  note: by Wei Zhao.
  note: Vita.
  note: "Major Subject: Toxicology".
  note: Issued also on microfiche from University Microfilms Inc.
  note: Includes bibliographical references: pages 95-128.
  note: Ph. D. Texas A&M University 1996.
  subject:
    topic: Major toxicology
  identifier: 97-18489 UMI
  identifier: http://proxy.library.tamu.edu/login
  related item:
    location:
      url: http://proxy.library.tamu.edu/login
  record info:
    record content source: TXA
    record creation date: 970813
    record change date: 20190325093327.0
    record identifier: in00001379141