Modulation of parathion toxicity by glucose feeding: Is nitric oxide involved?

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  • Author(s): Liu J;Liu J; Gupta RC; Goad JT; Karanth S; Pope C
  • Source:
    Toxicology and applied pharmacology [Toxicol Appl Pharmacol] 2007 Mar; Vol. 219 (2-3), pp. 106-13. Date of Electronic Publication: 2006 Nov 11.
  • Publication Type:
    Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Academic Press Country of Publication: United States NLM ID: 0416575 Publication Model: Print-Electronic Cited Medium: Print ISSN: 0041-008X (Print) Linking ISSN: 0041008X NLM ISO Abbreviation: Toxicol Appl Pharmacol Subsets: MEDLINE
    • Publication Information:
      Publication: New York, NY : Academic Press
      Original Publication: New York.
    • Subject Terms:
      Brain/*drug effects ; Cholinesterase Inhibitors/*toxicity ; Glucose/*adverse effects ; Nitric Oxide/*physiology ; Oxidative Stress/*drug effects ; Parathion/*toxicity; Adenine Nucleotides/metabolism ; Administration, Oral ; Animals ; Brain/enzymology ; Brain/metabolism ; Cholinesterases/metabolism ; Citrulline/metabolism ; Creatine/metabolism ; Glucose/administration & dosage ; Male ; NADPH Oxidases/metabolism ; Rats ; Rats, Sprague-Dawley
    • Abstract:
      Glucose feeding can markedly exacerbate the toxicity of the anticholinesterase insecticide, parathion. We determined the effects of parathion on brain nitric oxide and its possible role in potentiation of toxicity by glucose feeding. Adult rats were given water or 15% glucose in water for 3 days and challenged with vehicle or parathion (18 mg/kg, s.c.) on day 4. Functional signs, plasma glucose and brain cholinesterase, citrulline (an indicator of nitric oxide production) and high-energy phosphates (HEPs) were measured 1-3 days after parathion. Glucose feeding exacerbated cholinergic toxicity. Parathion increased plasma glucose (15-33%) and decreased cortical cholinesterase activity (81-90%), with no significant differences between water and glucose treatment groups. In contrast, parathion increased brain regional citrulline (40-47%) and decreased HEPs (18-40%) in rats drinking water, with significantly greater changes in glucose-fed rats (248-363% increase and 31-61% decrease, respectively). We then studied the effects of inhibiting neuronal nitric oxide synthase (nNOS) by 7-nitroindazole (7NI, 30 mg/kg, i.p. x4) on parathion toxicity and its modulation by glucose feeding. Co-exposure to parathion and 7NI led to a marked increase in cholinergic signs of toxicity and lethality, regardless of glucose intake. Thus, glucose feeding enhanced the accumulation of brain nitric oxide following parathion exposure, but inhibition of nitric oxide synthesis was ineffective at counteracting increased parathion toxicity associated with glucose feeding. Evidence is therefore presented to suggest that nitric oxide may play both toxic and protective roles in cholinergic toxicity, and its precise contribution to modulation by glucose feeding requires further investigation.
    • Grant Information:
      ES009119 United States ES NIEHS NIH HHS
    • Accession Number:
      0 (Adenine Nucleotides)
      0 (Cholinesterase Inhibitors)
      29VT07BGDA (Citrulline)
      31C4KY9ESH (Nitric Oxide)
      61G466064D (Parathion)
      EC 1.6.3.- (NADPH Oxidases)
      EC 3.1.1.8 (Cholinesterases)
      IY9XDZ35W2 (Glucose)
      MU72812GK0 (Creatine)
    • Publication Date:
      Date Created: 20061221 Date Completed: 20070329 Latest Revision: 20171116
    • Publication Date:
      20231215
    • Accession Number:
      10.1016/j.taap.2006.11.005
    • Accession Number:
      17178140