Hepatocellular carcinoma is one of the primary liver cancer. Even though the incidence of HCC differs among various geographic regions, ethnicity, gender and age, it is one of the most common malignancies among Asian and African populations. It is well represented as the fourth most common cancer in the world. It is estimated that more than 80% of HCC cases are attributed due to viruses including hepatitis B and C infections. However it is also quite interesting that consumption of hazardous alcohol, dietary exposure of aflatoxin1 and hemochromatosis are also highly associated with the initiation and development of HCC. Risk factors such as AFB1 could alter the DNA upon exposure, modify the proteins and induce oxidative stress and further leading to malignant transformation of the hepatocytes. In this review we narrated the basics of the etiology and molecular mechanisms behind the involvement of AFB1 in the initiation and development of hepatocellular carcinoma.

Ferroptosis is a form of programmed cell death (PCD), distinct from apoptosis, that was identified in 2012. The process is driven by the iron-dependent oxidative degeneration of lipids. Ferroptosis causes cell death through the accumulation of iron-dependent lipid reactive oxygen species. Free radicals cause degradation of lipid molecules by the removal of electrons through oxidation. The process is dependent on intracellular iron as the accumulation of iron acts as a catalyst for converting peroxides into free radicals. The oxidative degradation of lipids occurs when there is depletion of the antioxidant glutathione and a loss of activity of the lipid repair enzyme glutathione peroxidase 4. The lipid peroxidation then leads to cell membrane denaturation. The biochemical mechanism behind the unique iron-dependent programmed cell death with reference to the triple negative breast cancer have been reviewed in this article.