Differential effects of route of T-2 toxin exposure on hepatic oxidative damage in mice.

T-2 toxin is the most toxic among mycotoxins and poses a potential health hazard for both humans and animals. At high doses, T-2 toxin can cause shock-like syndrome that can result in death. We evaluated the effect of time course and route of exposure on hepatic oxidative damage in mice and it is only such study so far to compare the effects of dermal and subcutaneous exposure of T-2 toxin. Mice were exposed to 1 LD50 of T-2 toxin either by percutaneous (5.94 mg/kg body weight) or subcutaneous (1.54 mg/kg body weight) route and sacrificed at 0, 1, 3, and 7 days postexposure. Analysis of a number of serum biochemical variables, antioxidant enzymes activity, gene and protein expression by immunoblot assay showed time and route dependent effects of T-2 induced hepatic oxidative damage. Time dependent increase in protein carbonyl content and protein oxidation was seen in serum and liver. Results of our study may provide possible mechanism for developing medical countermeasures against T-2 toxin.
AuthorsManjari Chaudhary, A S B Bhaskar, P V Lakshmana Rao
JournalEnvironmental toxicology (Environ Toxicol) Vol. 30 Issue 1 Pg. 64-73 (Jan 2015) ISSN: 1522-7278 [Electronic] United States
PMID23929680 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2013 Wiley Periodicals, Inc.
Chemical References
  • Antioxidants
  • Biomarkers
  • Catalase
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • T-2 Toxin
  • Administration, Cutaneous
  • Animals
  • Antioxidants (metabolism)
  • Biomarkers (blood)
  • Catalase (genetics, metabolism)
  • Female
  • Gene Expression (drug effects)
  • Glutathione Peroxidase (genetics, metabolism)
  • Injections, Subcutaneous
  • Liver (drug effects, enzymology, metabolism)
  • Mice
  • Oxidative Stress (drug effects)
  • Protein Carbonylation
  • Superoxide Dismutase (genetics, metabolism)
  • T-2 Toxin (toxicity)

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