260
arcuate nucleus. Female mice exposed to a high-fat diet, will show a decrease in the
expression of POMC gene in arcuate nucleus upon exposure to high concentration
of BPA. Early life exposure of BPA to both male and female mice causes impairment
for the tolerance of glucose [66].
Conclusion
BPA is a synthetic organic compound and one of the most vulnerable endocrinedisrupting chemicals that is being used in many products of daily uses. Food is the
most common source of BPA exposure. It has been proved that BPA exposed to
humans can cause interaction with many receptors such as estrogen, aryl hydrocarbon, androgen, and peroxisome proliferator-activated receptors and change the
function of leptin, insulin, adiponectin, thyroxin, and other hormones that are
involved in the maintaining of the immune and nervous system. BPA induces the
production of oxidative stress, impairs signaling of cell and changes in DNA due to
inhibition of methylation of DNA. BPA also enhances the risk of coronary heart
diseases and metabolic disorders.
Acknowledgments This work has been financially supported by the research grant (5661/Punjab/
NRPU/R&D/HEC/2016 and 8365/Punjab/NRPU/R&D/HEC/2017) received from the Higher
Education Commission (HEC) of Pakistan.
Conflict of Interest The authors confirm that authors have no conflict of interest.
References
1. Chevalier N, Fenichel P. Endocrine disruptors: a missing link in the pandemy of type 2 diabetes and obesity? Presse Med. 2016;45(1):88–97. Epub 2015/12/15. Obesite, diabete de type 2
et perturbateurs endocriniens. fre.
2. Rochester JR. Bisphenol A and human health: a review of the literature. Reprod Toxicol.
2013;42:132–55. Epub 2013/09/03. eng.
3. Sciences Nioeh. Bisphenol A (BPA). https://www.niehs.nih.gov/health/topics/agents/sya-bpa/
index.cfm.
4. Geens T, Roosens L, Neels H, Covaci A. Assessment of human exposure to Bisphenol-A,
Triclosan and Tetrabromobisphenol-A through indoor dust intake in Belgium. Chemosphere.
2009;76(6):755–60. Epub 2009/06/19. eng.
5. Wetherill YB, Fisher NL, Staubach A, Danielsen M, de Vere White RW, Knudsen
KE. Xenoestrogen action in prostate cancer: pleiotropic effects dependent on androgen receptor status. Cancer Res. 2005;65(1):54–65. Epub 2005/01/25. eng.
6. Hassan ZK, Elobeid MA, Virk P, Omer SA, ElAmin M, Daghestani MH, et al. Bisphenol
A induces hepatotoxicity through oxidative stress in rat model. Oxidative Med Cell Longev.
2012;2012:194829. Epub 2012/08/14. eng.
7. Doherty LF, Bromer JG, Zhou Y, Aldad TS, Taylor HS. In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland:
an epigenetic mechanism linking endocrine disruptors to breast cancer. Hormones Cancer.
2010;1(3):146–55.
K. Irshad et al.
arcuate nucleus. Female mice exposed to a high-fat diet, will show a decrease in the
expression of POMC gene in arcuate nucleus upon exposure to high concentration
of BPA. Early life exposure of BPA to both male and female mice causes impairment
for the tolerance of glucose [66].
Conclusion
BPA is a synthetic organic compound and one of the most vulnerable endocrinedisrupting chemicals that is being used in many products of daily uses. Food is the
most common source of BPA exposure. It has been proved that BPA exposed to
humans can cause interaction with many receptors such as estrogen, aryl hydrocarbon, androgen, and peroxisome proliferator-activated receptors and change the
function of leptin, insulin, adiponectin, thyroxin, and other hormones that are
involved in the maintaining of the immune and nervous system. BPA induces the
production of oxidative stress, impairs signaling of cell and changes in DNA due to
inhibition of methylation of DNA. BPA also enhances the risk of coronary heart
diseases and metabolic disorders.
Acknowledgments This work has been financially supported by the research grant (5661/Punjab/
NRPU/R&D/HEC/2016 and 8365/Punjab/NRPU/R&D/HEC/2017) received from the Higher
Education Commission (HEC) of Pakistan.
Conflict of Interest The authors confirm that authors have no conflict of interest.
References
1. Chevalier N, Fenichel P. Endocrine disruptors: a missing link in the pandemy of type 2 diabetes and obesity? Presse Med. 2016;45(1):88–97. Epub 2015/12/15. Obesite, diabete de type 2
et perturbateurs endocriniens. fre.
2. Rochester JR. Bisphenol A and human health: a review of the literature. Reprod Toxicol.
2013;42:132–55. Epub 2013/09/03. eng.
3. Sciences Nioeh. Bisphenol A (BPA). https://www.niehs.nih.gov/health/topics/agents/sya-bpa/
index.cfm.
4. Geens T, Roosens L, Neels H, Covaci A. Assessment of human exposure to Bisphenol-A,
Triclosan and Tetrabromobisphenol-A through indoor dust intake in Belgium. Chemosphere.
2009;76(6):755–60. Epub 2009/06/19. eng.
5. Wetherill YB, Fisher NL, Staubach A, Danielsen M, de Vere White RW, Knudsen
KE. Xenoestrogen action in prostate cancer: pleiotropic effects dependent on androgen receptor status. Cancer Res. 2005;65(1):54–65. Epub 2005/01/25. eng.
6. Hassan ZK, Elobeid MA, Virk P, Omer SA, ElAmin M, Daghestani MH, et al. Bisphenol
A induces hepatotoxicity through oxidative stress in rat model. Oxidative Med Cell Longev.
2012;2012:194829. Epub 2012/08/14. eng.
7. Doherty LF, Bromer JG, Zhou Y, Aldad TS, Taylor HS. In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland:
an epigenetic mechanism linking endocrine disruptors to breast cancer. Hormones Cancer.
2010;1(3):146–55.
K. Irshad et al.