title: Hepatoprotective role of liver fatty acid binding protein in acetaminophen induced toxicity.
abstract: BACKGROUND
  FABP1 has been reported to possess strong antioxidant properties. Upon successful transfection of the Chang cell line, which has undetectable FABP1 mRNA levels, with human FABP1 cDNA, the Chang cells were shown to express FABP1. Using the transfected and control (normal) Chang cells and subjecting them to oxidative stress, transfected cells were reported to be associated with enhanced cell viability. This study extends those observations by investigating the effect of FABP1 on acetaminophen (AAP)-induced hepatotoxicity. We hypothesized that presence of FABP1 would enhance cell viability compared to control cells (vector transfected cells).
  
  
  METHODS
  Following AAP treatment of Chang FABP1 transfected and control cells, cell viability, oxidative stress, and apoptosis were evaluated using lactate dehydrogenase (LDH) release, the fluorescent probe DCF, and Bax expression, respectively.
  
  
  RESULTS
  FABP1 cDNA transfected cells showed greater resistance against AAP toxicity than vector transfected cells. Significantly lower LDH levels (p < 0.05) were observed as were lower DCF fluorescence intensity (p < 0.05) in FABP1 cDNA transfected cells compared to vector transfected cells. FABP1 expression also attenuated the expression of Bax following AAP induced toxicity.
  
  
  CONCLUSIONS
  FABP1 attenuated AAP-induced toxicity and may be considered a cytoprotective agent in this in vitro model of drug induced oxidative stress.
authors.forename: Yu
authors.initials: Y
authors.lastname: Gong
authors.forename: Guqi
authors.initials: G
authors.lastname: Wang
authors.forename: Yuewen
authors.initials: Y
authors.lastname: Gong
authors.forename: Jing
authors.initials: J
authors.lastname: Yan
authors.forename: Yufei
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Faculty of Pharmacy, University of Manitoba, 750 McDermot Avenue, Winnipeg, MB R3E 0T5, Canada. burczyn@cc.umanitoba.ca.
authors.forename: Frank J
authors.initials: FJ
authors.lastname: Burczynski
mesh_terms: D000082:Acetaminophen / Q000633:toxicity*; D018712:Analgesics, Non-Narcotic / Q000633:toxicity*; D017209:Apoptosis; D002470:Cell Survival; D002478:Cells, Cultured; D019610:Cytoprotection; D050556:Fatty Acid-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D005452:Fluoresceins; D005453:Fluorescence; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism* / Q000503:physiopathology; D018384:Oxidative Stress; D014162:Transfection; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D018712:Analgesics, Non-Narcotic; C494826:BAX protein, human; C493319:FABP1 protein, human; D050556:Fatty Acid-Binding Proteins; D005452:Fluoresceins; D051028:bcl-2-Associated X Protein; C029569:diacetyldichlorofluorescein; D000082:Acetaminophen; D007770:L-Lactate Dehydrogenase