PMID- 28285737
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 0928-4680 (Print)
IS  - 0928-4680 (Linking)
VI  - 24
IP  - 2
DP  - 2017 Jun
TI  - Lung injury induced by Bisphenol A: A food contaminant, is ameliorated by 
      selenium supplementation.
PG  - 81-89
LID - S0928-4680(17)30006-8 [pii]
LID - 10.1016/j.pathophys.2017.02.003 [doi]
AB  - Bisphenol A (BPA), a widely used industrial chemical, is known to disrupt 
      endocrine function. This study aimed to investigate the impact of chronic 
      exposure to BPA on the lung tissue of adult male rats as well as any possible 
      alleviating effects resulting from selenium (Se) treatment. Chronic exposure to 
      BPA resulted in prominent inflammation and oxidative stress responses as 
      evidenced by an increase in levels of malondialdehyde (MDA), reduced 
      concentrations of superoxide dismutase (SOD), and upregulation of Interleukin-18 
      (IL-18) expression in lung tissue. In addition, chronic exposure led to 
      modulation of the fibrosis-related gene expression, as we observed augmented 
      follistatin-like1 (FSTL1) expression and diminished a disintegrin and 
      metalloproteinase with thrombospondin motif 5 (ADAMTS5) expression. Se treatment 
      remarkably mitigated changes in the expression of these dysregulated markers of 
      lung injury. The biochemical changes were consistent with the histopathological 
      findings, where cellular infiltration and inflammatory fibrotic changes were 
      observed following BPA administration and a lessening of these effects with 
      concomitant Se treatment. Taken together, the results from the study reveal that 
      chronic exposure to BPA may promote the development of pulmonary inflammatory 
      diseases with possible induction of lung fibrosis. Se treatment effectively 
      suppressed oxidative stress, inflammation, and fibrosis, suggesting that Se has 
      the potential to be used as a therapeutic agent in the treatment of pulmonary 
      inflammatory diseases.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Abedelhaffez, Azza S
AU  - Abedelhaffez AS
AD  - Department of Medical physiology, Faculty of Medicine, Assiut University, Assiut, 
      P.O. Box No. 71526, Assiut, Egypt. Electronic address: azzasalah10@hotmail.com.
FAU - El-Aziz, Ebtihal A Abd
AU  - El-Aziz EAA
AD  - Department of Medical physiology, Faculty of Medicine, Assiut University, Assiut, 
      P.O. Box No. 71526, Assiut, Egypt. Electronic address: ebthal2@gmail.com.
FAU - Aziz, Mohamed A Abdel
AU  - Aziz MAA
AD  - Department of Biochemistry, Faculty of Pharmacy, Al-Azhar University, Assiut 
      Branch, Assiut, P.O. Box No. 71524, Assiut, Egypt. Electronic address: 
      dr_manwar@yahoo.com.
FAU - Ahmed, Asmaa M
AU  - Ahmed AM
AD  - Department of Pathology, Faculty of Medicine, Assiut University, Assiut, P.O. Box 
      No. 71526, Assiut, Egypt. Electronic address: dr.asmaamhm@yahoo.com.
LA  - eng
PT  - Journal Article
DEP - 20170212
PL  - Switzerland
TA  - Pathophysiology
JT  - Pathophysiology : the official journal of the International Society for 
      Pathophysiology
JID - 9433813
OTO - NOTNLM
OT  - A disintegrin and metalloproteinase with thrombospondin motif 5
OT  - Bisphenol A
OT  - Follistatin-like 1
OT  - Lung fibrosis
OT  - Lung inflammation
OT  - Oxidative stress
OT  - Selenium
EDAT- 2017/03/14 06:00
MHDA- 2017/03/14 06:01
CRDT- 2017/03/14 06:00
PHST- 2016/07/21 00:00 [received]
PHST- 2017/01/27 00:00 [revised]
PHST- 2017/02/04 00:00 [accepted]
PHST- 2017/03/14 06:00 [pubmed]
PHST- 2017/03/14 06:01 [medline]
PHST- 2017/03/14 06:00 [entrez]
AID - S0928-4680(17)30006-8 [pii]
AID - 10.1016/j.pathophys.2017.02.003 [doi]
PST - ppublish
SO  - Pathophysiology. 2017 Jun;24(2):81-89. doi: 10.1016/j.pathophys.2017.02.003. Epub 
      2017 Feb 12.