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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Matsebatlela, Thabe M. Anderson, Amy L. Gallicchio, Vincent S. Elford, Howard Rice, Charles D. |
| Description | Country affiliation: South Africa Author Affiliation: Matsebatlela TM ( Department of Biochemistry, Microbiology and Biotechnology, University of Limpopo, South Africa.); Anderson AL ( Department of Biological Sciences, Clemson University, SC, USA.); Gallicchio VS ( Department of Biological Sciences, Clemson University, SC, USA.); Elford H ( Molecules for Health, Richmond, VA, USA.); Rice CD ( Department of Biological Sciences, Clemson University, SC, USA. Electronic address: cdrice@clemson.edu.) |
| Abstract | Didox (3,4-dihydroxy-benzohydroxamic acid), is a synthetic ribonucleotide reductase (RR) inhibitor derived from polyhydroxy-substituted benzohydroxamic acid, and originally developed as an anti-cancer agent. Some studies indicate that didox may have anti-oxidative stress-like properties, while other studies hint that didox may have anti-inflammatory properties. Using nitric oxide production in response to LPS treatment as a sensitive screening assay for anti-inflammatory compounds, we show that didox is very potent at levels as low as 6.25 µM, with maximal inhibition at 100 µM. A qRT-PCR array was then employed to screen didox for other potential anti-inflammatory and anti-oxidative stress-related properties. Didox was very potent in suppressing the expression of these arrayed mRNA in response to LPS, and in some cases didox alone suppressed expression. Using qRT-PCR as a follow up to the array, we demonstrated that didox suppresses LPS-induced mRNA levels of iNOS, IL-6, IL-1, TNF- , NF-κß (p65), and p38- , after 24h of treatment. Treatment with didox also suppresses the secretion of nitric oxide, IL-6, and IL-10. Furthermore, oxidative stress, as quantified by intracellular ROS levels in response to macrophage activators LPS and phorbol ester (PMA), and the glutathione depleting agent BSO, is reduced by treatment with didox. Moreover, we demonstrate that nuclear translocation of NF-κß (p65) in response to LPS is inhibited by didox. These findings were supported by qRT-PCR for oxidative stress genes SOD1 and catalase. Overall, this study supports the conclusion that didox may have a future role in managing acute and chronic inflammatory diseases and oxidative stress due to high production of ROS. |
| File Format | HTM / HTML |
| ISSN | 00092797 |
| e-ISSN | 18727786 |
| DOI | 10.1016/j.cbi.2015.03.027 |
| Journal | Chemico-Biological Interactions |
| Volume Number | 233 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2015-05-25 |
| Publisher Place | Ireland |
| Access Restriction | Open |
| Subject Keyword | Discipline Biochemistry Discipline Pharmacology Anti-inflammatory Agents Pharmacology Free Radical Scavengers Hydroxamic Acids Macrophages Drug Effects Immunology Oxidative Stress Toll-like Receptor 4 Animals Catalase Genetics Cell Line Cyclooxygenase 2 Down-regulation Interleukin-6 Lipopolysaccharides Metabolism Mice Nitric Oxide Synthase Type Ii Reactive Oxygen Species Superoxide Dismutase Tumor Necrosis Factor-alpha Up-regulation Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Toxicology |
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