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Melatonin Ameliorates BPA Induced Oxidative Stress in Human Red Blood Cells: An In vitro Study

[ Vol. 20 , Issue. 8 ]


Saleh M. Abdullah* and Hina Rashid   Pages 1321 - 1327 ( 7 )


Background: Bisphenol A (BPA) is a xenobiotic that causes oxidative stress in various organs in living organisms. Blood cells are also an endpoint where BPA is known to cause oxidative stress. Blood cells, especially red blood cells (RBCs), are crucial for maintaining homeostasis and overall wellbeing of the organism. They are highly susceptible to oxidative stress induced by xenobiotics. However, there is limited data about the oxidative stress induced by BPA in blood, especially in red blood cells. This study was carried out to evaluate BPA induced oxidative stress in human RBCs in vitro and its amelioration by melatonin.

Objective: To find if melatonin exerts a protective effect on the oxidative stress induced by the BPA in human red blood cells in vitro.

Methods: The erythrocyte suspensions (2 ml) were divided into six groups and treated with 0, 50, 100, 150, 200, and 250 μg/ml of BPA. Another set of erythrocyte suspension with similar BPA treatment and 50 μM Melatonin per group was also set. Incubations lasted for 12 hrs in the dark. Lipid peroxidation, glutathione, glutathione reductase, catalase, and superoxide dismutase were measured as indicators of oxidative stress.

Results: BPA caused a significant increase in lipid peroxidation. A decrease in GSH levels was also observed. The activities of all the studied antioxidants also decreased with BPA treatment. Melatonin was seen to mitigate the oxidative stress induced by BPA.

Conclusion: Treatment of red blood cells with BPA caused an increase in oxidative stress, while melatonin decreased the induced oxidative stress.


Bisphenol A, xenobiotic, red blood cells, oxidative stress, melatonin, in vitro.


Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, Jazan University, Jazan, Centre of Research for Development, University of Kashmir, Srinagar, 190 006

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