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Reactive oxygen species-induced cell death of rat primary astrocytes through mitochondria-mediated mechanism.
J Cell Biochem. 2009 Aug 01; 107(5):933-43.JC

Abstract

Astrocytes, the most abundant glial cell population in the central nervous system (CNS), play physiological roles in neuronal activities. Oxidative insult induced by the injury to the CNS causes neural cell death through extrinsic and intrinsic pathways. This study reports that reactive oxygen species (ROS) generated by exposure to the strong oxidizing agent, hexavalent chromium (Cr(VI)) as a chemical-induced oxidative stress model, caused astrocytes to undergo an apoptosis-like cell death through a caspase-3-independent mechanism. Although activating protein-1 (AP-1) and NF-kappaB were activated in Cr(VI)-primed astrocytes, the inhibition of their activity failed to increase astrocytic cell survival. The results further indicated that the reduction in mitochondrial membrane potential (MMP) was accompanied by an increase in the levels of ROS in Cr(VI)-primed astrocytes. Moreover, pretreatment of astrocytes with N-acetylcysteine (NAC), the potent ROS scavenger, attenuated ROS production and MMP loss in Cr(VI)-primed astrocytes, and significantly increased the survival of astrocytes, implying that the elevated ROS disrupted the mitochondrial function to result in the reduction of astrocytic cell viability. In addition, the nuclear expression of apoptosis-inducing factor (AIF) and endonuclease G (EndoG) was observed in Cr(VI)-primed astrocytes. Taken together, evidence shows that astrocytic cell death occurs by ROS-induced oxidative insult through a caspase-3-independent apoptotic mechanism involving the loss of MMP and an increase in the nuclear levels of mitochondrial pro-apoptosis proteins (AIF/EndoG). This mitochondria-mediated but caspase-3-independent apoptotic pathway may be involved in oxidative stress-induced astrocytic cell death in the injured CNS.

Authors+Show Affiliations

Department of Life Sciences, National Cheng Kung University, Tainan City, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19459161

Citation

Wang, Chia-Chun, et al. "Reactive Oxygen Species-induced Cell Death of Rat Primary Astrocytes Through Mitochondria-mediated Mechanism." Journal of Cellular Biochemistry, vol. 107, no. 5, 2009, pp. 933-43.
Wang CC, Fang KM, Yang CS, et al. Reactive oxygen species-induced cell death of rat primary astrocytes through mitochondria-mediated mechanism. J Cell Biochem. 2009;107(5):933-43.
Wang, C. C., Fang, K. M., Yang, C. S., & Tzeng, S. F. (2009). Reactive oxygen species-induced cell death of rat primary astrocytes through mitochondria-mediated mechanism. Journal of Cellular Biochemistry, 107(5), 933-43. https://doi.org/10.1002/jcb.22196
Wang CC, et al. Reactive Oxygen Species-induced Cell Death of Rat Primary Astrocytes Through Mitochondria-mediated Mechanism. J Cell Biochem. 2009 Aug 1;107(5):933-43. PubMed PMID: 19459161.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reactive oxygen species-induced cell death of rat primary astrocytes through mitochondria-mediated mechanism. AU - Wang,Chia-Chun, AU - Fang,Kuan-Min, AU - Yang,Chung-Shi, AU - Tzeng,Shun-Fen, PY - 2009/5/22/entrez PY - 2009/5/22/pubmed PY - 2009/10/14/medline SP - 933 EP - 43 JF - Journal of cellular biochemistry JO - J. Cell. Biochem. VL - 107 IS - 5 N2 - Astrocytes, the most abundant glial cell population in the central nervous system (CNS), play physiological roles in neuronal activities. Oxidative insult induced by the injury to the CNS causes neural cell death through extrinsic and intrinsic pathways. This study reports that reactive oxygen species (ROS) generated by exposure to the strong oxidizing agent, hexavalent chromium (Cr(VI)) as a chemical-induced oxidative stress model, caused astrocytes to undergo an apoptosis-like cell death through a caspase-3-independent mechanism. Although activating protein-1 (AP-1) and NF-kappaB were activated in Cr(VI)-primed astrocytes, the inhibition of their activity failed to increase astrocytic cell survival. The results further indicated that the reduction in mitochondrial membrane potential (MMP) was accompanied by an increase in the levels of ROS in Cr(VI)-primed astrocytes. Moreover, pretreatment of astrocytes with N-acetylcysteine (NAC), the potent ROS scavenger, attenuated ROS production and MMP loss in Cr(VI)-primed astrocytes, and significantly increased the survival of astrocytes, implying that the elevated ROS disrupted the mitochondrial function to result in the reduction of astrocytic cell viability. In addition, the nuclear expression of apoptosis-inducing factor (AIF) and endonuclease G (EndoG) was observed in Cr(VI)-primed astrocytes. Taken together, evidence shows that astrocytic cell death occurs by ROS-induced oxidative insult through a caspase-3-independent apoptotic mechanism involving the loss of MMP and an increase in the nuclear levels of mitochondrial pro-apoptosis proteins (AIF/EndoG). This mitochondria-mediated but caspase-3-independent apoptotic pathway may be involved in oxidative stress-induced astrocytic cell death in the injured CNS. SN - 1097-4644 UR - https://www.unboundmedicine.com/medline/citation/19459161/Reactive_oxygen_species_induced_cell_death_of_rat_primary_astrocytes_through_mitochondria_mediated_mechanism_ L2 - https://doi.org/10.1002/jcb.22196 DB - PRIME DP - Unbound Medicine ER -