Protective effects of a polyherbal medicine, Majoon Suranjan against bisphenol-A induced genetic, oxidative and tissue damages

Abstract

Bisphenol-A (BPA) is a toxic chemical largely produced and used in polycarbonate plastics worldwide. Majoon Suranjan (MS), a polyherbal formulation, is used as an anti-inflammatory medicine against rheumatoid arthritis. The present study aimed to evaluate BPA-induced toxicity and its possible amelioration by MS. To test our hypothesis, we performed gas chromatography-mass spectrometry (GC-MS) analysis, DNA interaction studies, genotoxicity tests, oxidative stress parameters, and histopathological examinations. GC-MS profiling of MS revealed the presence of various anti-oxidant compounds. DNA interaction studies showed that both chemicals intercalate between DNA base pairs. Next, we observed BPA-induced genotoxicity and oxidative damage. The observed effects might be due to BPA-induced reactive oxygen species production. Further, BPA changed the anti-oxidant enzyme activities, increased the malondialdehyde, alanine aminotransferase, alkaline phosphatase, and total bilirubin levels, and caused gross damage to the liver and kidney. Interestingly, these effects were significantly reversed by MS. In conclusion, MS shows protective effects against BPA-induced toxicity and could be a potential alternative medicine against BPA toxicity, especially in third-world countries where BPA uses are not strictly regulated.

Highlights:

• Bisphenol-A (BPA) induces multiple toxic effects.

• BPA induces genotoxicity, oxidative and tissue damage.

• Majoon Suranjan (MS) ameliorates the BPA induced toxic effects.

• GC-MS profiling show various active anti-oxidant compounds in MS.

• MS is anti-genotoxic, anti-oxidant, and hepato-renal protective

Graphical Abstract

Keywords:

• Bisphenol-A
• Majoon Suranjan
• DNA interaction
• genotoxicity
• oxidative and tissue damages
• amelioration

Acknowledgements

The authors thank the Department of Zoology, AMU, Aligarh, for providing the necessary facilities. MAK (09/112(0599)/2018-EMR-I); DS (524/(UGC NET JUNE 2019)) express their gratitude to the CSIR, UGC, India for fellowships, respectively. HRS is thankful to the UGC (grant no. F0.30-377/2017(BSR)) and DST-SERB (grant no. EMR/20l7/001758), New Delhi, for providing financial help.

Author contributions

Genotoxicity, oxidative parameters and histopathology study: DS, MAK, HRS. DNA interaction studies: DS, MAK, SP. Data acquisition: DS, MAK, SR, KMYA, HRS. Data analysis and interpretation: DS, MAK, KA, HRS. Writing of the manuscript: DS, MAK, HRS. Conception and supervision: HRS.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by the (#UGC) under grant (F0.30-377/2017(BSR)) and the (#DST-SERB) under grant [EMR/20l7/001758].