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Effect of metal ions on apoptosis of PC‐12 cells
Author(s) -
Tessalee Elisha,
Goswami Raj,
Mungre Shubhangee
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a507-d
Subject(s) - staurosporine , apoptosis , ceramide , glutathione , trypan blue , chemistry , oxidative stress , glutathione reductase , programmed cell death , caspase , catalase , microbiology and biotechnology , viability assay , enzyme , biochemistry , biology , protein kinase c , glutathione peroxidase
Neurodegenerative diseases are characterized by neuronal death leading to a loss of function. Metals such as cobalt and manganese have been reported to play a role in neuronal degeneration. The mechanisms of metal‐induced toxicity continue to be of interest given the ubiquitous nature of these contaminants. Suggested mechanism involves oxidative stress to cells. Chronic hypoxia has been reported to increase the production of TNF alpha, which in turn increases ceramide production and activates apoptotic pathways. We studied the effect of metal ions on the viability of PC‐12 cells. There was significant cell death when cells were treated with CoCl 2 and MnCl 2 , as observed by MTT assay and trypan blue exclusion. We also studied the effect of metal ions on enzymes of the apoptotic pathway including glutathione reductase, caspases and catalase. The activity of caspase‐3 increased within 6 hours of treatment. Glutathione levels decreased within 24 hours. Results obtained were comparable to those seen with staurosporine, a compound known to increase ceramide levels in cells. These results indicate that metals may act via a TNF alpha like mechanism.