Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic cell death of human myeloid leukemia HL-60 cells by a dietary compound withaferin A with concomitant protection by N-acetyl cysteine.

Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic cell death of human myeloid leukemia HL-60 cells by a dietary compound withaferin A with concomitant protection by N-acetyl cysteine. Research Abstract Details 

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Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic cell death of human myeloid leukemia HL-60 cells by a dietary compound withaferin A with concomitant protection by N-acetyl cysteine. Abstract Text:

Fayaz Malik,Ajay Kumar,Shashi Bhushan,Sheema Khan,Aruna Bhatia,Krishan Avtar Suri,Ghulam Nabi Qazi,Jaswant Singh,Fayaz Malik,Ajay Kumar,Shashi Bhushan,Sheema Khan,Aruna Bhatia,Krishan Avtar Suri,Ghulam Nabi Qazi,Jaswant Singh,

Induction of apoptosis in cancer cells has become the major focus of anti-cancer therapeutics development. WithaferinA, a major chemical constituent of Withania somnifera, reportedly shows cytotoxicity in a variety of tumor cell lines while its molecular mechanisms of action are not fully understood. We observed that withaferinA primarily induces oxidative stress in human leukemia HL-60 cells and in several other cancer cell lines. The withanolide induced early ROS generation and mitochondrial membrane potential (Deltapsi(mt)) loss, which preceded release of cytochrome c, translocation of Bax to mitochondria and apoptosis inducing factor to cell nuclei. These events paralleled activation of caspases -9, -3 and PARP cleavage. WA also activated extrinsic pathway significantly as evidenced by time dependent increase in caspase-8 activity vis-à-vis TNFR-1 over expression. WA mediated decreased expression of Bid may be an important event for cross talk between intrinsic and extrinsic signaling. Furthermore, withaferinA inhibited DNA binding of NF-kappaB and caused nuclear cleavage of p65/Rel by activated caspase-3. N-acetyl-cysteine rescued all these events suggesting thereby a pro-oxidant effect of withaferinA. The results of our studies demonstrate that withaferinA induced early ROS generation and mitochondrial dysfunction in cancer cells trigger events responsible for mitochondrial -dependent and -independent apoptosis pathways.

Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic cell death of human myeloid leukemia HL-60 cells by a dietary compound withaferin A with concomitant protection by N-acetyl cysteine. Publishing Authors By Initials

F Malik,A Kumar,S Bhushan,S Khan,A Bhatia,KA Suri,GN Qazi,J Singh,F Malik,A Kumar,S Bhushan,S Khan,A Bhatia,KA Suri,GN Qazi,J Singh,

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Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic cell death of human myeloid leukemia HL-60 cells by a dietary compound withaferin A with concomitant protection by N-acetyl cysteine. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Apoptosis : an international journal on programmed

VOLUME: 12

Page Numbers: 2115-33

Journal Abbreviation: Apoptosis

ISSN: 1360-8185

DAY: 1

MONTH: Nov

YEAR: 2007

Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic cell death of human myeloid leukemia HL-60 cells by a dietary compound withaferin A with concomitant protection by N-acetyl cysteine. Information

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LANGUAGE: eng

NlmUniqueID: 9712129

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Grant and Affiliation Information for Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic cell death of human myeloid leukemia HL-60 cells by a dietary compound withaferin A with concomitant protection by N-acetyl cysteine.

AFFILIATION: Division of Pharmacology, Indian Institute of Integrative Medicine, Council of Scientific and Industrial Research, Canal Road, Jammu-Tawi 180001, India.

Country: United States

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MEDLINETA: Apoptosis

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