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PRINT ISSN : 2319-7692
Online ISSN : 2319-7706 Issues : 12 per year Publisher : Excellent Publishers Email : editorijcmas@gmail.com / submit@ijcmas.com Editor-in-chief: Dr.M.Prakash Index Copernicus ICV 2018: 95.39 NAAS RATING 2020: 5.38 |
Presence of carcinogens, like Polycyclic Aromatic Hydrocarbons (PAH), in the form of cigarette smoke, vehicular emission and industrial emissions in our immediate surroundings is a potent health hazard. Arsenic, a carcinogenic metalloid, omnipresent in the environment, can act as co-carcinogen, where it enhances the carcinogenicity of other carcinogens. In the present study, the co-carcinogenic effect of Arsenic has been investigated, upon the 7,12-dimethylbenz[a]-anthracene (DMBA), a PAH, induced skin cancer model, in Swiss albino mice. Histological analysis revealed earlier development of invasive carcinoma in the DMBA and arsenic treated group in comparison to the DMBA treated mice alone. To understand this phenomena, ROS generation, DNA damage, lipid peroxidation, protein carbonyl content, total antioxidant capacity and activity of pro-inflammatory cytokines (TNF-α, IL6, IL17a, IL22) and their downstream modulators (NF-κB) was assessed. The results suggested that arsenic in the presence of DMBA induced higher ROS generation, greater DNA damage, elevated lipid peroxidation, increased protein carbonyl content, upregulated activity of pro-inflammatory cytokines and their downstream regulators as well as down regulated the total antioxidant capacity in comparison to DMBA alone. These findings hint at the co-carcinogenic potential of arsenic, as it significantly enhances the carcinogenicity of DMBA and hastens carcinogenesis.