Antioxidants effectively prevent oxidation-induced protein damage in OLN 93 cells
Archives of Biochemistry and Biophysics, ISSN: 0003-9861, Vol: 421, Issue: 1, Page: 54-60
2004
- 27Citations
- 15Captures
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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.
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Metrics Details
- Citations27
- Citation Indexes26
- 26
- CrossRef17
- Policy Citations1
- 1
- Captures15
- Readers15
- 15
Article Description
Oxidative stress is supposed to play an important role in demyelinating diseases. Oligodendrocytes are the myelin-forming cells in the brain and are highly susceptible to oxidative stress due to their low antioxidative defense systems and high metabolic rate. In the present work, we tested the response of the oligodendrocyte cell line OLN 93 to oxidative stress. OLN 93 cell cultures are characterized by a loss of cell viability after oxidation. This loss of cell viability is accompanied by an increase in protein oxidation and consequently an elevated overall proteolysis. To minimize the oxidative damage, we tested the effects of the antioxidants α-lipoic acid and coenzyme Q 10. Both compounds were able to elevate cell viability and to decrease intracellular protein turnover and oxidant induced protein oxidation. Therefore, we concluded that the excessive oxidative damage of oligodendrocytes and their protein pool can be prevented by the usage of antioxidants.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0003986103005666; http://dx.doi.org/10.1016/j.abb.2003.10.008; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0346848905&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/14678784; https://linkinghub.elsevier.com/retrieve/pii/S0003986103005666; https://dx.doi.org/10.1016/j.abb.2003.10.008
Elsevier BV
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