AZT oxidative damage in the liver

摘要: Abstract (1) Zidovudine or AZT was the first antiretroviral drug approved by FDA in 1987 and is most common administered to HIV-infected patients with high efficacy controlling retrovirus proliferation but important secondary toxic effects on muscular hepatic tissue. (2) This azo-deoxythymidine analog may induce genetic alterations of nuclear DNA concomitant consequences, also damage mitochondrial that result biosynthesis abnormal respiratory complexes impaired oxidative energy production. (3) The toxicity can be attributed its direct inhibition generation, particularly complex I, leading production reactive oxygen species. (4) In liver tissue, ROS induced administration involved fat accumulation (liver steatosis) inflammation. (5) Since induces an apparent “antioxidant” cell proliferation, it results difficult conciliate main mechanism underlying rests solely generation oxidant/nitrosative stress.