title: Bisphenol A sulfonation is impaired in metabolic and liver disease.
abstract: BACKGROUND
  Bisphenol A (BPA) is a widely used industrial chemical and suspected endocrine disruptor to which humans are ubiquitously exposed. The liver metabolizes and facilitates BPA excretion through glucuronidation and sulfonation. The sulfotransferase enzymes contributing to BPA sulfonation (detected in human and rodents) is poorly understood.
  
  
  OBJECTIVE
  To determine the impact of metabolic and liver disease on BPA sulfonation in human and mouse livers.
  
  
  METHODS
  The capacity for BPA sulfonation was determined in human liver samples that were categorized into different stages of metabolic and liver disease (including obesity, diabetes, steatosis, and cirrhosis) and in livers from ob/ob mice.
  
  
  RESULTS
  In human liver tissues, BPA sulfonation was substantially lower in livers from subjects with steatosis (23%), diabetes cirrhosis (16%), and cirrhosis (18%), relative to healthy individuals with non-fatty livers (100%). In livers of obese mice (ob/ob), BPA sulfonation was lower (23%) than in livers from lean wild-type controls (100%). In addition to BPA sulfonation activity, Sult1a1 protein expression decreased by 97% in obese mouse livers.
  
  
  CONCLUSIONS
  Taken together these findings establish a profoundly reduced capacity of BPA elimination via sulfonation in obese or diabetic individuals and in those with fatty or cirrhotic livers versus individuals with healthy livers.
authors.affiliation: Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States.
authors.forename: Emine B
authors.initials: EB
authors.lastname: Yalcin
authors.affiliation: Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States.
authors.forename: Supriya R
authors.initials: SR
authors.lastname: Kulkarni
authors.affiliation: Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States. Electronic address: angela_slitt@uri.edu.
authors.forename: Angela L
authors.initials: AL
authors.lastname: Slitt
authors.affiliation: Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States. Electronic address: rking@uri.edu.
authors.forename: Roberta
authors.initials: R
authors.lastname: King
mesh_terms: D000818:Animals; D001559:Benzhydryl Compounds / Q000378:metabolism*; D006801:Humans; D008107:Liver Diseases / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008659:Metabolic Diseases / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008820:Mice, Obese; D010636:Phenols / Q000378:metabolism*; D015238:Sulfotransferases / Q000378:metabolism*; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D010636:Phenols; D015238:Sulfotransferases; C006780:bisphenol A; D000098826:Bisphenol A Compounds
keywords: Bisphenol A; Cirrhosis; Diabetes; Obesity; Phase-II; Steatosis; Sulfotransferase