| First Author | Young A | Year | 2017 |
| Journal | FEBS Lett | Volume | 591 |
| Issue | 16 | Pages | 2426-2438 |
| PubMed ID | 28771687 | Mgi Jnum | J:244408 |
| Mgi Id | MGI:5913187 | Doi | 10.1002/1873-3468.12777 |
| Citation | Young A, et al. (2017) Physiological levels of formate activate mitochondrial superoxide/hydrogen peroxide release from mouse liver mitochondria. FEBS Lett 591(16):2426-2438 |
| abstractText | Here, we found that formate, an essential one-carbon metabolite, activates superoxide (O2.-)/hydrogen peroxide (H2 O2 ) release from mitochondria. Sodium formate (30 mum) induces a significant increase in O2.-/H2 O2 production in liver mitochondria metabolizing pyruvate (50 mum). At concentrations deemed to be toxic, formate does not increase O2.-/H2 O2 production further. It was observed that the formate-mediated increase in O2.-/H2 O2 production is not associated with cytochrome c oxidase (COX) inhibition or changes in membrane potential and NAD(P)H levels. Sodium formate supplementation increases phosphorylating respiration without altering proton leaks. Finally, it was observed that the 2-oxoglutarate dehydrogenase (OGDH) inhibitors 3-methyl-2-oxovaleric acid (KMV) and CPI-613 inhibit the formate-induced increase in pyruvate-driven ROS production. The importance of these findings in one-carbon metabolism and physiology are discussed herein. |
