Superoxide mediated photomodification and DNA damage induced apoptosis by Benz(a)anthracene via mitochondrial mediated pathway

• Superoxide mediated photomodification of Benz(a)anthracene under sunlight exposure.
• Photosensitized Benz(a)anthracene induced single and double strand breakage as well as CPDs formation.
• p21 regulated apoptosis in HaCaT keratinocytes through up-regulation of pro-apoptotic Bax gene and protein.
• Benz(a)anthracene induce apoptosis through mitochondrial mediated pathway.

Benz(a)anthracene (BA) is an ubiquitous environmental pollutant of polycyclic aromatic hydrocarbon’s (PAHs) family. We showed superoxide (O2−) catalyzed BA photo modification and apoptosis in HaCaT keratinocytes under sunlight exposure. O2− generation was confirmed by quenching through superoxide dismutase (SOD). BA induced photocytotoxicity were investigated through MTT and NRU assay. We proposed DNA insults such as single and double strand breakage and CPDs formation which results in cell cycle arrest and apoptosis by photosensitized BA. BA induced apoptosis was caspase dependent and occurred through a mitochondrial pathway. Reduction of mitochondrial membrane potential, translocation of Bax to mitochondria and cytochrome c release favors involvement of mitochondria in BA phototoxicity. AO/EB double staining and TEM analysis also support apoptotic cell death. We propose a p21 regulated apoptosis via expression of Bax, and cleaved PARP under sunlight exposure. Thus, we conclude that it is imperative to avoid solar radiation during peak hr (between 11 A.M. and 3 P.M.) when the amount of solar radiation is high, in the light of DNA damage which may lead to mutation or skin cancer through photosensitized BA under sunlight exposure. Concomitantly, investigation is urgently required for the photosafety of BA photoproducts reaching in the environment through photomodification.