Quantitation of the signals and normalization with β-actin against the total p53 levels showed that maximal phosphorylation of BAD in HepG2 cells by WM spiked with AFB1 was dependent on the dose of radiation used. The result of the cellular response is influenced by the regulation of p53 target genes, which is strongly dependent on the irradiation dosage utilized . The p53 tumor suppressor protein promotes apoptosis through a variety of mechanisms, including the activation of pro-apoptotic BAX and inhibition of BCL-2, as well as the induction of GADD45 (growth arrest and DNA-damage inducible gene), and numerous p53 inducible genes implicated in oxidative stress responses and apoptosis . found that direct exposure to low doses of UV radiation induced a rapid p53 accumulation followed by a decrease which correlated with a transient cell cycle withdrawal and presumably also DNA repair. On the other hand, high and sustained levels of p53 were observed after a high dose of UV radiation in cells undergoing apoptosis. In contrast, our data (Fig. ) summarizes that as the housekeeping p53 gene was not significantly increased the UV-A doses we delivered on WM is believed to cause no significant stress on the human cell lines. As the pro-apoptotic enzyme BAD is decreased with increasing dose, we can infer that the cells experienced a less toxic environment which may be due to the degradation of aflatoxins. The degradation of aflatoxins under UV-A is proposed to be through hydration/ demethoxylation resulting due to the breakage of the double bond in the lactone ring or by cleavage of the furan ring which is considered to be the primary site of toxicity . Moreover, this data can also be correlated with the formation of FAA and lipid peroxidation. UV-A irradiation at 838 mJ/cm 2 does not lead to formation of toxic by-products that can cause oxidative cell stress. Excess ammonia has been proven in several animal and human studies to be harmful to human cell lines . Because the targeted gene p53 was not considerably altered, we can affirm that UV-A irradiated WM was safe from toxins that lead to oxidative cell stress. These results indicate that a substantial breakdown of AF in WM by UV-A occurs and there is no accumulation of toxic components from protein, lipid, and FAA degradation.