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Antimycin A-induced cell death depends on AIF translocation through NO production and PARP activation and is not involved in ROS generation, cytochrome c release and caspase-3 activation in HL-60 cells.
J Antibiot (Tokyo). 2009 Mar; 62(3):145-52.JA

Abstract

A respiratory inhibitor, antimycin A (AA), induced an apoptotic-like cell death characterized by nuclear and DNA fragmentation in human leukemia HL-60 cells. This cell death was significantly restricted by a nitric oxide synthase (NOS) inhibitor, N(G)-monomethyl-L-arginine (L-NMMA), and a poly(ADP-ribose) polymerase (PARP) inhibitor, 5-aminoisoquinoline (AIQ). Indeed, NO production and PARP overactivation were detected in the cells treated with AA. On the one hand, L-NMMA partly eliminated NO production and on the other, AIQ and L-NMMA also restricted PARP activation. Excessive signals related to PARP overactivation induce the translocation of an apoptosis-inducing factor (AIF) from the mitochondria to the nuclei, resulting in DNA fragmentation. In AA-treated cells, the nuclear translocation of AIF occurred. This translocation was restricted by pretreatment with AIQ and L-NMMA. Although pretreatment with ascorbic acid eliminated the reactive oxygen species (ROS) generation induced by the blockade of complex III by AA, the pretreatment did not protect the cells from AA-induced cell death. Furthermore, cytochrome c release or caspase-3 activation was not observed in the cells treated with AA. These results suggest that AA-induced cell death does not depend on respiratory inhibition and the succeeding cascades, but on NO production, PARP overactivation and AIF translocation.

Authors+Show Affiliations

Department of Biology and Geosciences, Graduate School of Science, Osaka City University, Sumiyoshi-ku, Osaka, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19229286

Citation

Ogita, Masaki, et al. "Antimycin A-induced Cell Death Depends On AIF Translocation Through NO Production and PARP Activation and Is Not Involved in ROS Generation, Cytochrome C Release and Caspase-3 Activation in HL-60 Cells." The Journal of Antibiotics, vol. 62, no. 3, 2009, pp. 145-52.
Ogita M, Ogita A, Usuki Y, et al. Antimycin A-induced cell death depends on AIF translocation through NO production and PARP activation and is not involved in ROS generation, cytochrome c release and caspase-3 activation in HL-60 cells. J Antibiot (Tokyo). 2009;62(3):145-52.
Ogita, M., Ogita, A., Usuki, Y., Fujita, K., & Tanaka, T. (2009). Antimycin A-induced cell death depends on AIF translocation through NO production and PARP activation and is not involved in ROS generation, cytochrome c release and caspase-3 activation in HL-60 cells. The Journal of Antibiotics, 62(3), 145-52. https://doi.org/10.1038/ja.2009.2
Ogita M, et al. Antimycin A-induced Cell Death Depends On AIF Translocation Through NO Production and PARP Activation and Is Not Involved in ROS Generation, Cytochrome C Release and Caspase-3 Activation in HL-60 Cells. J Antibiot (Tokyo). 2009;62(3):145-52. PubMed PMID: 19229286.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Antimycin A-induced cell death depends on AIF translocation through NO production and PARP activation and is not involved in ROS generation, cytochrome c release and caspase-3 activation in HL-60 cells. AU - Ogita,Masaki, AU - Ogita,Akira, AU - Usuki,Yoshinosuke, AU - Fujita,Ken-ichi, AU - Tanaka,Toshio, Y1 - 2009/02/20/ PY - 2009/2/21/entrez PY - 2009/2/21/pubmed PY - 2009/10/20/medline SP - 145 EP - 52 JF - The Journal of antibiotics JO - J Antibiot (Tokyo) VL - 62 IS - 3 N2 - A respiratory inhibitor, antimycin A (AA), induced an apoptotic-like cell death characterized by nuclear and DNA fragmentation in human leukemia HL-60 cells. This cell death was significantly restricted by a nitric oxide synthase (NOS) inhibitor, N(G)-monomethyl-L-arginine (L-NMMA), and a poly(ADP-ribose) polymerase (PARP) inhibitor, 5-aminoisoquinoline (AIQ). Indeed, NO production and PARP overactivation were detected in the cells treated with AA. On the one hand, L-NMMA partly eliminated NO production and on the other, AIQ and L-NMMA also restricted PARP activation. Excessive signals related to PARP overactivation induce the translocation of an apoptosis-inducing factor (AIF) from the mitochondria to the nuclei, resulting in DNA fragmentation. In AA-treated cells, the nuclear translocation of AIF occurred. This translocation was restricted by pretreatment with AIQ and L-NMMA. Although pretreatment with ascorbic acid eliminated the reactive oxygen species (ROS) generation induced by the blockade of complex III by AA, the pretreatment did not protect the cells from AA-induced cell death. Furthermore, cytochrome c release or caspase-3 activation was not observed in the cells treated with AA. These results suggest that AA-induced cell death does not depend on respiratory inhibition and the succeeding cascades, but on NO production, PARP overactivation and AIF translocation. SN - 1881-1469 UR - https://www.unboundmedicine.com/medline/citation/19229286/Antimycin_A_induced_cell_death_depends_on_AIF_translocation_through_NO_production_and_PARP_activation_and_is_not_involved_in_ROS_generation_cytochrome_c_release_and_caspase_3_activation_in_HL_60_cells_ L2 - https://doi.org/10.1038/ja.2009.2 DB - PRIME DP - Unbound Medicine ER -