ATO induces oxidative stress in APL cells through lipid peroxidat

ATO induces oxidative stress in APL cells through lipid peroxidation, GSH content changed and DNA damage.

It changes mitochondrial membrane potential and modulates expression and translocation of apoptotic proteins, which lead to caspase3 activity and apoptosis in HL-60 cells. Conclusions It can be concluded from the present in vitro study that arsenic trioxide induces mitochondrial pathway of apoptosis in HL-60 cells. Although the exact anti-leukemic molecular mechanism of ATO is not well understood, we have investigated in present study its detailed mechanism of oxidative stress-induced intrinsic pathway of apoptosis by modulation of expression and translocation of apoptotic proteins, changing mitochondrial membrane potential and activation of caspase 3 activity selleck chemicals in HL-60 cells. By elucidating the anti-leukemic mechanisms of action of ATO in HL-60 cells, we are able to provide new insights into the molecular targets, and a rational basis for drug designing for a more prominent APL chemotherapy in the future. Acknowledgments The research described in this publication was made possible by a grant from the National Institutes of Health (Grant No. G12MD007581) through the RCMI Center for Environmental Health at Jackson State University. check details References 1. Powell BL: Arsenic trioxide in acute promyelocytic leukemia: potion not poison. Expert Rev Anticancer Ther 2011, 11:1317–1319.PubMedCrossRef

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