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Cadmium-induced apoptotic death of human retinal pigment epithelial cells is mediated by MAPK pathway.
Exp Eye Res. 2009 Oct; 89(4):494-502.EE

Abstract

Cadmium (Cd), released from cigarette smoke and metal industrial activities, is known to accumulate in human body organs including retina and is particularly higher in retinal tissues of age-related macular degeneration (AMD) eyes compared to non-AMD eyes. We have determined the cytotoxic effects of Cd on human retinal pigment epithelial (RPE) cells. Upon Cd treatment, there was a dose- and time-dependent decline in ARPE-19 cell viability as well as early apoptotic changes such as altered mitochondrial membrane potential (MMP) and Cytochrome C release in cytosol. Depletion of GSH by buthionine-[S,R]-sulfoximine (BSO) resulted in increased Cd toxicity in ARPE-19 cells. Cadmium also caused reactive oxygen species (ROS) generation and activation of mitogen-activated protein kinases (MAPKs) pathway including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (Erk1/2), and p38 in ARPE-19 cells. Antioxidants such as N-acetylcysteine (NAC) significantly reduced Cd-induced toxicity. These results indicate that elevated ROS-induced activation of the MAPK signaling pathway could be associated with Cd-induced RPE cell apoptosis, one of the major contributing factors in AMD. The toxic effects of Cd on ARPE-19 cells indicate that environmental heavy metals such as Cd could be important potential factors in RPE cells death associated retinal diseases particularly related to smoking.

Authors+Show Affiliations

Department of Ophthalmology & Visual Sciences, University of Texas Medical Branch, Galveston, TX 77555, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19524565

Citation

Kalariya, Nilesh M., et al. "Cadmium-induced Apoptotic Death of Human Retinal Pigment Epithelial Cells Is Mediated By MAPK Pathway." Experimental Eye Research, vol. 89, no. 4, 2009, pp. 494-502.
Kalariya NM, Wills NK, Ramana KV, et al. Cadmium-induced apoptotic death of human retinal pigment epithelial cells is mediated by MAPK pathway. Exp Eye Res. 2009;89(4):494-502.
Kalariya, N. M., Wills, N. K., Ramana, K. V., Srivastava, S. K., & van Kuijk, F. J. (2009). Cadmium-induced apoptotic death of human retinal pigment epithelial cells is mediated by MAPK pathway. Experimental Eye Research, 89(4), 494-502. https://doi.org/10.1016/j.exer.2009.05.011
Kalariya NM, et al. Cadmium-induced Apoptotic Death of Human Retinal Pigment Epithelial Cells Is Mediated By MAPK Pathway. Exp Eye Res. 2009;89(4):494-502. PubMed PMID: 19524565.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cadmium-induced apoptotic death of human retinal pigment epithelial cells is mediated by MAPK pathway. AU - Kalariya,Nilesh M, AU - Wills,Nancy K, AU - Ramana,Kota V, AU - Srivastava,Satish K, AU - van Kuijk,Frederik J G M, Y1 - 2009/06/12/ PY - 2009/04/08/received PY - 2009/05/06/revised PY - 2009/05/12/accepted PY - 2009/6/16/entrez PY - 2009/6/16/pubmed PY - 2010/1/28/medline SP - 494 EP - 502 JF - Experimental eye research JO - Exp Eye Res VL - 89 IS - 4 N2 - Cadmium (Cd), released from cigarette smoke and metal industrial activities, is known to accumulate in human body organs including retina and is particularly higher in retinal tissues of age-related macular degeneration (AMD) eyes compared to non-AMD eyes. We have determined the cytotoxic effects of Cd on human retinal pigment epithelial (RPE) cells. Upon Cd treatment, there was a dose- and time-dependent decline in ARPE-19 cell viability as well as early apoptotic changes such as altered mitochondrial membrane potential (MMP) and Cytochrome C release in cytosol. Depletion of GSH by buthionine-[S,R]-sulfoximine (BSO) resulted in increased Cd toxicity in ARPE-19 cells. Cadmium also caused reactive oxygen species (ROS) generation and activation of mitogen-activated protein kinases (MAPKs) pathway including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (Erk1/2), and p38 in ARPE-19 cells. Antioxidants such as N-acetylcysteine (NAC) significantly reduced Cd-induced toxicity. These results indicate that elevated ROS-induced activation of the MAPK signaling pathway could be associated with Cd-induced RPE cell apoptosis, one of the major contributing factors in AMD. The toxic effects of Cd on ARPE-19 cells indicate that environmental heavy metals such as Cd could be important potential factors in RPE cells death associated retinal diseases particularly related to smoking. SN - 1096-0007 UR - https://www.unboundmedicine.com/medline/citation/19524565/Cadmium_induced_apoptotic_death_of_human_retinal_pigment_epithelial_cells_is_mediated_by_MAPK_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(09)00153-5 DB - PRIME DP - Unbound Medicine ER -