Cytogenotoxicological defense of retinyl palmitate in the front damage of antineoplastics.

Cancer, the multifactorial pathology and to date is the most lethal causes of death in the world. Cyclophosphamide (CPA) and doxorubicin (DOX) are the individually or combindly used two anticancer drugs. The antineoplastic drugs-mediated genetic instability can be overcome by using antioxidants. The study evaluated the cytogenotoxic modulatory potentials of retinyl palmitate (RP) caused by CPA and DOX in Swiss mice. For this, adult Mus musculus of either sex were divided equally regarding to the gender. Toxicogenetic effects were induced by the intraperitoneal (i.p.) administration of the CPA (20mg/kg) and/or DOX (2mg/kg), following to test for comet assay and micronucleus test in bone marrow cells after 48h (DOX) and 7h (CPA) of the administration of RP (100 IU/kg). Both CPA and DOX significantly (p<0.05) increased with the index and frequency of damages, clastogenic and/or aneugenic effects with the augmenting of micronuclei, demonstrating the cytotoxicity interference on the ratio of normochromatic to polychromatic erythrocytes and bone marrow cells of mice, that were found to reduce in RP treatment groups. In conclusion, RP has a modulatory effect on CPA and DOX-mediated cytogenotoxic events. The findings may be a good indication to manage the antioneoplastic drug-induced stress mediated detrimental effects by using RP, especially as a side effect minimizer.