Abstract Title:

Melatonin abated Bisphenol A-induced neurotoxicity via p53/PUMA/Drp-1 signaling.

Abstract Source:

Environ Sci Pollut Res Int. 2021 Jan 5. Epub 2021 Jan 5. PMID: 33398767

Abstract Author(s):

Ayesha Ishtiaq, Tahir Ali, Attia Bakhtiar, Robina Bibi, Kinza Bibi, Iram Mushtaq, Shupeng Li, Wajiha Khan, Uzma Khan, Riffat Aysha Anis, Mariam Anees, Aneesa Sultan, Iram Murtaza

Article Affiliation:

Ayesha Ishtiaq


Bisphenol A (BPA), an endocrine disruptor, is widely used in the manufacture of different daily life products. Accumulating evidence supports the association between the increasing incidence of neurodegenerative diseases and the BPA level in the environment. In the present study, we aimed to evaluate the neuroprotective role of melatonin against BPA-induced mitochondrial dysfunction-mediated apoptosis in the brain. Herein, adult Sprague Dawley rats were administrated (subcutaneously) with BPA (100μg/kg BW, 1 mg/kg BW, and 10 mg/kg BW) and melatonin (4 mg/kg BW) for 16 days. Our results showed BPA exposure significantly increased the oxidative stress as demonstrated by increased free radicals (ROS), TBARs level, disrupted cellular architecture, and decreased antioxidant enzymes including SOD, CAT, APX, POD, and GSH levels. Additionally, BPA treatment increased the expression of PUMA, p53, and Drp-1 resulting in apoptosis in the brain tissue of rats. However, melatonin treatment significantly attenuated BPA-induced toxic effects by scavenging ROS, boosting antioxidant enzyme activities,and interestingly enervated brain apoptosis by normalizing p53, PUMA, and Drp-1 expressions at both transcriptional and translational level. Moreover, the brain tissue histology also revealed the therapeutic potential of melatonin by normalizing the cellular architecture. Conclusively, our findingsuggests that melatonin could alleviate oxidative stress and mitochondrial dysfunction-linked apoptosis, rendering its neuroprotective potential against BPA-induced toxicity.

Study Type : Animal Study

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