Mechanisms participating in oxidative damage of isolated rat hepatocytes
Archives of Toxicology, ISSN: 0340-5761, Vol: 83, Issue: 4, Page: 363-372
2009
- 23Citations
- 11Captures
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations23
- Citation Indexes23
- 23
- CrossRef16
- Captures11
- Readers11
- 11
Article Description
The aim of the study was to evaluate time course and dose dependence of peroxidative damage induced by tert-butyl hydroperoxide (tBHP) in rat hepatocytes cultured in suspension and in monolayer. At the lowest (0.1 mM) concentration, decrease of cytosolic glutathione and discharge of mitochondrial membrane potential (MMP) could be detected. Significant increases in leakage of lactate dehydrogenase and in malondialdehyde concentrations together with decrease of pyruvate-dependent respiration were detected at higher tBHP concentrations (above 0.5 mM) and after longer periods of incubation. Changes in plasma membrane integrity were observed at 1 mM concentration of tBHP. Succinate-dependent oxidation was most resistant to peroxidative damages. Opening of the mitochondrial permeability transition pore was responsible for the discharge of mitochondria membrane potential. In the presence of cyclosporine A and succinate, the membrane potential could be restored. Our data showed that the most sensitive indicators of the peroxidative damage are changes of cytosolic glutathione concentration and MMP. © 2008 Springer-Verlag.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=64249100504&origin=inward; http://dx.doi.org/10.1007/s00204-008-0385-8; http://www.ncbi.nlm.nih.gov/pubmed/19020865; http://link.springer.com/10.1007/s00204-008-0385-8; http://www.springerlink.com/index/10.1007/s00204-008-0385-8; http://www.springerlink.com/index/pdf/10.1007/s00204-008-0385-8; https://dx.doi.org/10.1007/s00204-008-0385-8; https://link.springer.com/article/10.1007/s00204-008-0385-8
Springer Science and Business Media LLC
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