Thiol oxidation-mediated cell death in Aplysia cultured sensory neurons

Chang, Deok-Jin; Lee, Seung‐Hee; Lim, Chae‐Seok; Jang, Dong-Hyuk; Lee, Chi-Hoon; Lee, Young‐Don; Kaang, Bong‐Kiun

doi:10.1016/j.brainres.2003.12.053

Cited by 3 publications

(2 citation statements)

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“…Interestingly, we did not observe increased ROS levels following diamide treatment, indicating that the diamide-induced electrophysiological effects may in part be independent of ROS levels. These results support the notion that ROS scavengers do not block diamide-induced injury in Aplysia neurons (Chang et al 2004). Collectively, our data suggest that KB may exert both ROS-dependent and independent effects on oxidative stress-induced hyperexcitability.…”

Section: Discussionsupporting

confidence: 89%

Ketone bodies are protective against oxidative stress in neocortical neurons

Kim

Davis

Sullivan

et al. 2007

Journal of Neurochemistry

177

120

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Ketone bodies (KB) have been shown to prevent neurodegeneration in models of Parkinson's and Alzheimer's diseases, but the mechanisms underlying these effects remain unclear. One possibility is that KB may exert antioxidant activity. In the current study, we explored the effects of KB on rat neocortical neurons exposed to hydrogen peroxide (H 2 O 2 ) or diamide -a thiol oxidant and activator of mitochondrial permeability transition (mPT). We found that: (i) KB completely blocked large inward currents induced by either H 2 O 2 or diamide; (ii) KB significantly decreased the number of propidium iodide-labeled cells in neocortical slices after exposure to H 2 O 2 or diamide; (iii) KB significantly decreased reactive oxygen species (ROS) levels in dissociated neurons and in isolated neocortical mitochondria; (iv) the electrophysiological effects of KB in neurons exposed to H 2 O 2 or diamide were mimicked by bongkrekic acid and cyclosporin A, known inhibitors of mPT, as well as by catalase and DLdithiothreitol, known antioxidants; (v) diamide alone did not significantly alter basal ROS levels in neurons, supporting previous studies indicating that diamide-induced neuronal injury may be mediated by mPT opening; and (vi) KB significantly increased the threshold for calcium-induced mPT in isolated mitochondria. Taken together, our data suggest that KB may prevent mPT and oxidative injury in neocortical neurons, most likely by decreasing mitochondrial ROS production.

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Section: Discussionsupporting

confidence: 89%

Ketone bodies are protective against oxidative stress in neocortical neurons

Kim

Davis

Sullivan

et al. 2007

Journal of Neurochemistry

177

120

View full text Add to dashboard Cite

show abstract

“…Interestingly, V-ATPases are overexpressed in several metastatic cancers (Sennoune et al, 2004) and the overexpression of proteasome sub-units leads to increased survival rate of human cell lines following oxidative stress, due to a higher proteasome degradation of oxidized modified protein (Chondrogianni et al, 2005). Other human orthologs related with the oxidative stress response ( PRDX2 , PRDX3 , GSR , GCLC , GSS , SOD1 , and SOD2 ), have been involved in the onset and progression of neurodegenerative diseases, namely Parkinson’s disease, by protecting the cell, acting as anti-oxidant agents and neuroprotectors (Chang et al, 2004; Ihara et al, 2005; Cumming et al, 2007). Besides, PAK1 , MAP2K1 , and LCP1 , three other genes described as being involved in tumor development and invasiveness (Wang et al, 2006a,b), are orthologs of yeast determinants of mancozeb resistance CLA4 , PBS2 , and SAC6 (Dias et al, 2010).…”

Section: Yeast Toxicogenomics Applied To Environmental Pollutants Andmentioning

confidence: 99%

Yeast toxicogenomics: genome-wide responses to chemical stresses with impact in environmental health, pharmacology, and biotechnology

Santos¹

2012

Front. Gene.

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The emerging transdisciplinary field of Toxicogenomics aims to study the cell response to a given toxicant at the genome, transcriptome, proteome, and metabolome levels. This approach is expected to provide earlier and more sensitive biomarkers of toxicological responses and help in the delineation of regulatory risk assessment. The use of model organisms to gather such genomic information, through the exploitation of Omics and Bioinformatics approaches and tools, together with more focused molecular and cellular biology studies are rapidly increasing our understanding and providing an integrative view on how cells interact with their environment. The use of the model eukaryote Saccharomyces cerevisiae in the field of Toxicogenomics is discussed in this review. Despite the limitations intrinsic to the use of such a simple single cell experimental model, S. cerevisiae appears to be very useful as a first screening tool, limiting the use of animal models. Moreover, it is also one of the most interesting systems to obtain a truly global understanding of the toxicological response and resistance mechanisms, being in the frontline of systems biology research and developments. The impact of the knowledge gathered in the yeast model, through the use of Toxicogenomics approaches, is highlighted here by its use in prediction of toxicological outcomes of exposure to pesticides and pharmaceutical drugs, but also by its impact in biotechnology, namely in the development of more robust crops and in the improvement of yeast strains as cell factories.

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