Abstract
Chronic use of 3′-Azido-3′-deoxythymidine (AZT) to treat HIV/AIDS causes mitochondrial dysfunction and the accumulation of mitochondrial mutations. These toxicities have been attributed to increased oxidative damage among other mechanisms. Palm fruit juice (PFJ), also known as oil palm phenolics (OPP), is a water soluble by-product of oil extraction from the fruit of the oil palm (Elaeis guineensis) that is rich in antioxidants and other phytochemicals. The capacity of PFJ to mitigate AZT mitochondrial genotoxicity (mutagenesis) as well as dose-dependent cytotoxicity were measured in cultured HepG2 cells. In the presence of PFJ, AZT-induced mutations were 35% the number of mutations observed in samples treated with AZT alone in the three regions of themitochondrial genome examined (HV2, CO2, and ND1). Co-treatment with PFJ increased cell survival in the presence of increasing doses of AZT by up to 350%. These effects were not due to degradation or inactivation ofAZT by PFJ. The discovery of the mitigating effects of PFJ provides a potential means of ameliorating AZT-induced mutations and possibly other long-term negative side effects of long-term AZT use
