Page 169 - SRPSKO DRUŠTVO ISTRAŽIVAČA RAKA

SDIRSACR Oncology Insights

SESSION 12

TOXIC TRIGGERS: ENVIROMENTAL CHEMICALS AND CANCER RISK

P82

Protective Role of Mangiferin Against Bisphenol A-Induced Toxicity

Ayca Uvez , Emel Durak , Sima Kilic3, Konstantinos Dimas , Elif Ilkay Armutak 1
1
2
4
1Department of Histology and Embryology, Faculty of Veterinary Medicine, Istanbul University- Cerrahpasa, Istanbul, Turkey,
34320, Istanbul, Turkey
2 Institute of Graduate Studies, Istanbul University- Cerrahpasa, Istanbul, Turkey, 34320, Istanbul, Turkey
3Institute of Nanotechnology and Biotechnology, Department of Biotechnology Istanbul University- Cerrahpasa 34320, Istanbul,
Turkey
4Department of Pharmacology, Faculty of Medicine, University of Thessaly, Larissa, Greece

Keywords: Bisphenol A, Mangiferin, Protective effect, Endocrine-disruptor, HUVEC

Background: Bisphenol A (BPA), a widely used industrial compound, is recognized for its endocrine-disrupting
potential and its detrimental effects on multiple organ systems, including the reproductive, neurological, hepatic,
and cardiovascular systems. Chronic exposure to BPA, even at low doses, has been associated with oxidative stress,
inflammation, and metabolic dysfunction. Mangiferin, a natural xanthone glycoside primarily isolated from Mangifera
indica, has demonstrated potent antioxidant, anti-inflammatory, and cytoprotective properties in various experimental
models. This study aims to evaluate the protective effect of mangiferin against BPA-induced cellular and systemic
toxicity in vitro.
Methods: The cytotoxic effect of siramesine on endothelial cells (HUVEC) was examined with the SRB. HUVEC cells
were exposed to Bisphenol A (BPA) at concentrations ranging from 10 to 100 μM. This exposure was conducted in the
presence or absence of Mangiferin, a compound that was administered at concentrations ranging from 10 to 100 μM.
Human Umbilical Vein Endothelial Cell (HUVEC) cells were exposed to bisphenol A (BPA) at concentrations of 5, 45 and
90 μM, 5 μM MNG, and a combination of both, over a 24-48 hour period. This experimental approach was adopted for
cell cycle analysis and wound healing assay. The primary objective of this investigation was to ascertain the protective
effect of MNG.
Results: Mangiferin demonstrated no cytotoxic effect on HUVEC cells within the applied dose range. The investigation
revealed that the presence of bisphenol A resulted in a dose-dependent enhancement in the degree of cytotoxic effect,
within the established range of doses. The Bisphenol A GI50 dose was determined to be 88.01 µM, the TGI dose was
134.34 µM, and the LC50 dose was 179.5 µM. Cell viability increased in the combination of Bisphenol A 90 µM and
Mangiferin 5 µM. The results of the cell cycle and wound healing experiments provide support for cell viability results.
Conclusion: Mangiferin is hypothesized to attenuate BPA-induced cell stress, normalize cell behavior, and preserve
cell integrity. Our results will provide critical insights into the protective efficacy of mangiferin against BPA toxicity and
contribute to the development of plant-derived interventions for environmental toxicant exposure.

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