Tags

Type your tag names separated by a space and hit enter

Involvement of mitochondrial alteration and reactive oxygen species generation in Taiwan cobra cardiotoxin-induced apoptotic death of human neuroblastoma SK-N-SH cells.
Toxicon. 2008 Aug 01; 52(2):361-8.T

Abstract

Naja naja atra cardiotoxin 3 (CTX3) induced apoptotic death on human neuroblastoma SK-N-SH cells. The apoptosis signals of CTX3 included reactive oxygen species (ROS) generation, disruption of mitochondrial membrane potential (DeltaPsim), cytochrome c release to the cytosol and activation of caspase-9 and -3. However, CTX3-induced increase in mitochondrial permeability transition was not initiated by proteins of the Bcl-2 family. The collapse of DeltaPsim, release of cytosolic cytochrome c, production of ROS and subsequent apoptotic cell death in CTX-treated cells could not be completely abolished by either N-acetylcysteine (ROS scavenger) or cyclosporin A (an inhibitor of mitochondrial permeability transition). Co-incubation with rotenone, an inhibitor of mitochondrial electron transport chain complexes I, resulted in partial inhibition of CTX3-induced ROS generation but not the loss of DeltaPsim. Obviously, the dissipation of DeltaPsim was not an upstream event for ROS generation or vice versa. Given that CTX3 was able to induce the leakage of isolated mitochondria, our data indicate that CTX3-induced apoptotic death of SK-N-SH cells is mediated through mitochondrial alteration and ROS generation.

Authors+Show Affiliations

Institute of Biomedical Sciences, National Sun Yat-Sen University-Kaohsiung Medical University Joint Research Center, National Sun Yat-Sen University, Kaohsiung 804, Taiwan.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18619991

Citation

Chen, Ku-Chung, et al. "Involvement of Mitochondrial Alteration and Reactive Oxygen Species Generation in Taiwan Cobra Cardiotoxin-induced Apoptotic Death of Human Neuroblastoma SK-N-SH Cells." Toxicon : Official Journal of the International Society On Toxinology, vol. 52, no. 2, 2008, pp. 361-8.
Chen KC, Lin SR, Chang LS. Involvement of mitochondrial alteration and reactive oxygen species generation in Taiwan cobra cardiotoxin-induced apoptotic death of human neuroblastoma SK-N-SH cells. Toxicon. 2008;52(2):361-8.
Chen, K. C., Lin, S. R., & Chang, L. S. (2008). Involvement of mitochondrial alteration and reactive oxygen species generation in Taiwan cobra cardiotoxin-induced apoptotic death of human neuroblastoma SK-N-SH cells. Toxicon : Official Journal of the International Society On Toxinology, 52(2), 361-8. https://doi.org/10.1016/j.toxicon.2008.06.013
Chen KC, Lin SR, Chang LS. Involvement of Mitochondrial Alteration and Reactive Oxygen Species Generation in Taiwan Cobra Cardiotoxin-induced Apoptotic Death of Human Neuroblastoma SK-N-SH Cells. Toxicon. 2008 Aug 1;52(2):361-8. PubMed PMID: 18619991.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of mitochondrial alteration and reactive oxygen species generation in Taiwan cobra cardiotoxin-induced apoptotic death of human neuroblastoma SK-N-SH cells. AU - Chen,Ku-Chung, AU - Lin,Shinne-Ren, AU - Chang,Long-Sen, Y1 - 2008/06/24/ PY - 2008/04/02/received PY - 2008/06/08/revised PY - 2008/06/09/accepted PY - 2008/7/16/pubmed PY - 2008/10/29/medline PY - 2008/7/16/entrez SP - 361 EP - 8 JF - Toxicon : official journal of the International Society on Toxinology JO - Toxicon VL - 52 IS - 2 N2 - Naja naja atra cardiotoxin 3 (CTX3) induced apoptotic death on human neuroblastoma SK-N-SH cells. The apoptosis signals of CTX3 included reactive oxygen species (ROS) generation, disruption of mitochondrial membrane potential (DeltaPsim), cytochrome c release to the cytosol and activation of caspase-9 and -3. However, CTX3-induced increase in mitochondrial permeability transition was not initiated by proteins of the Bcl-2 family. The collapse of DeltaPsim, release of cytosolic cytochrome c, production of ROS and subsequent apoptotic cell death in CTX-treated cells could not be completely abolished by either N-acetylcysteine (ROS scavenger) or cyclosporin A (an inhibitor of mitochondrial permeability transition). Co-incubation with rotenone, an inhibitor of mitochondrial electron transport chain complexes I, resulted in partial inhibition of CTX3-induced ROS generation but not the loss of DeltaPsim. Obviously, the dissipation of DeltaPsim was not an upstream event for ROS generation or vice versa. Given that CTX3 was able to induce the leakage of isolated mitochondria, our data indicate that CTX3-induced apoptotic death of SK-N-SH cells is mediated through mitochondrial alteration and ROS generation. SN - 0041-0101 UR - https://www.unboundmedicine.com/medline/citation/18619991/Involvement_of_mitochondrial_alteration_and_reactive_oxygen_species_generation_in_Taiwan_cobra_cardiotoxin_induced_apoptotic_death_of_human_neuroblastoma_SK_N_SH_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0041-0101(08)00384-X DB - PRIME DP - Unbound Medicine ER -