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Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A
BACKGROUND: Increasing evidence suggests that bisphenol A (BPA) induces liver pathological changes. Further, an association between BPA and circulating vitamin D (VitD) levels were documented. AIM: The role of VitD in BPA-induced liver pathological changes was explored in this study. METHODS: Health...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Faculty of Veterinary Medicine
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9897508/ https://www.ncbi.nlm.nih.gov/pubmed/36777431 http://dx.doi.org/10.5455/OVJ.2023.v13.i1.9 |
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author | Al-Griw, Mohamed A. Zaed, Suhila M. Hdud, Ismail M. Shaibi, Taher |
author_facet | Al-Griw, Mohamed A. Zaed, Suhila M. Hdud, Ismail M. Shaibi, Taher |
author_sort | Al-Griw, Mohamed A. |
collection | PubMed |
description | BACKGROUND: Increasing evidence suggests that bisphenol A (BPA) induces liver pathological changes. Further, an association between BPA and circulating vitamin D (VitD) levels were documented. AIM: The role of VitD in BPA-induced liver pathological changes was explored in this study. METHODS: Healthy 4.5-week-old male (n = 35) and female (n = 35) Swiss albino mice were used in this study. The animals were randomly divided into control and treated groups. The control groups were further divided into sham (no treatment) and vehicle (corn oil), whereas the treated groups were also divided into VitD (2195 U/kg), BPA (50 μg/kg), and BPA + VitD (50 μg/kg + 2195 U/kg) groups. For 6 weeks (twice a week), the animals were dosed intraperitoneally. One week later (at 10.5-weeks-old), the animals were sacrificed for biochemical and histological analyses. RESULTS: BPA produced a considerable rise in the body and liver weights in both genders of mice when compared to control mice. BPA also caused significant increases in the liver damage markers alanine transaminase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT). It also induced liver histopathological changes, including higher apoptotic indices in both genders. On the other hand, treatment with VitD considerably reduced liver damage and slightly decreased the apoptotic index rate. The ALP, ALT, and GGT levels were also markedly reduced. VitD has been proven to have a protective effect on both genders. CONCLUSIONS: According to our findings, VitD protects mice from BPA-induced liver damage, possibly via suppressing liver damage markers. |
format | Online Article Text |
id | pubmed-9897508 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Faculty of Veterinary Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-98975082023-02-09 Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A Al-Griw, Mohamed A. Zaed, Suhila M. Hdud, Ismail M. Shaibi, Taher Open Vet J Original Research BACKGROUND: Increasing evidence suggests that bisphenol A (BPA) induces liver pathological changes. Further, an association between BPA and circulating vitamin D (VitD) levels were documented. AIM: The role of VitD in BPA-induced liver pathological changes was explored in this study. METHODS: Healthy 4.5-week-old male (n = 35) and female (n = 35) Swiss albino mice were used in this study. The animals were randomly divided into control and treated groups. The control groups were further divided into sham (no treatment) and vehicle (corn oil), whereas the treated groups were also divided into VitD (2195 U/kg), BPA (50 μg/kg), and BPA + VitD (50 μg/kg + 2195 U/kg) groups. For 6 weeks (twice a week), the animals were dosed intraperitoneally. One week later (at 10.5-weeks-old), the animals were sacrificed for biochemical and histological analyses. RESULTS: BPA produced a considerable rise in the body and liver weights in both genders of mice when compared to control mice. BPA also caused significant increases in the liver damage markers alanine transaminase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT). It also induced liver histopathological changes, including higher apoptotic indices in both genders. On the other hand, treatment with VitD considerably reduced liver damage and slightly decreased the apoptotic index rate. The ALP, ALT, and GGT levels were also markedly reduced. VitD has been proven to have a protective effect on both genders. CONCLUSIONS: According to our findings, VitD protects mice from BPA-induced liver damage, possibly via suppressing liver damage markers. Faculty of Veterinary Medicine 2023-01 2023-01-15 /pmc/articles/PMC9897508/ /pubmed/36777431 http://dx.doi.org/10.5455/OVJ.2023.v13.i1.9 Text en https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Al-Griw, Mohamed A. Zaed, Suhila M. Hdud, Ismail M. Shaibi, Taher Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A |
title | Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A |
title_full | Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A |
title_fullStr | Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A |
title_full_unstemmed | Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A |
title_short | Vitamin D ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol A |
title_sort | vitamin d ameliorates liver pathology in mice caused by exposure to endocrine disruptor bisphenol a |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9897508/ https://www.ncbi.nlm.nih.gov/pubmed/36777431 http://dx.doi.org/10.5455/OVJ.2023.v13.i1.9 |
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