Difference between revisions of "Dlaskova 2010 Biochim Biophys Acta"
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|journal=Biochim Biophys Acta | |journal=Biochim Biophys Acta | ||
|abstract=We provide evidence that ablation or inhibition of, uncoupling protein 1 increases the rate of reactive oxygen containing species production by mitochondria from brown adipose tissue, no matter what electron transport chain substrate is used (succinate, glycerol-3-phosphate or pyruvate/malate). Consistent with these data are our observations that (a) the mitochondrial membrane potential is maximal when uncoupling protein 1 is ablated or inhibited and (b) oxygen consumption rates in mitochondria from uncoupling protein 1 knock-out mice, are significantly lower than those from wild-type mice, but equivalent to those from wild-type mice in the presence of GDP. In summary, we show that uncoupling protein 1 can affect reactive oxygen containing species production by isolated mitochondria from brown adipose tissue. | |abstract=We provide evidence that ablation or inhibition of, uncoupling protein 1 increases the rate of reactive oxygen containing species production by mitochondria from brown adipose tissue, no matter what electron transport chain substrate is used (succinate, glycerol-3-phosphate or pyruvate/malate). Consistent with these data are our observations that (a) the mitochondrial membrane potential is maximal when uncoupling protein 1 is ablated or inhibited and (b) oxygen consumption rates in mitochondria from uncoupling protein 1 knock-out mice, are significantly lower than those from wild-type mice, but equivalent to those from wild-type mice in the presence of GDP. In summary, we show that uncoupling protein 1 can affect reactive oxygen containing species production by isolated mitochondria from brown adipose tissue. | ||
|keywords= | |keywords=Mitochondria, Reactive oxygen species, Brown adipose tissue, Uncoupling protein 1 | ||
|mipnetlab= | |mipnetlab=IE Dublin Porter RK | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
}} | }} |
Revision as of 16:02, 17 March 2015
Dlaskovรก A, Clarke KJ, Porter RK (2010) The role of UCP 1 in production of reactive oxygen species by mitochondria isolated from brown adipose tissue. Biochim Biophys Acta 1797:1470-6. |
ยป PMID: 20416274; PDF
Dlaskova A, Clarke KJ, Porter RK (2010) Biochim Biophys Acta
Abstract: We provide evidence that ablation or inhibition of, uncoupling protein 1 increases the rate of reactive oxygen containing species production by mitochondria from brown adipose tissue, no matter what electron transport chain substrate is used (succinate, glycerol-3-phosphate or pyruvate/malate). Consistent with these data are our observations that (a) the mitochondrial membrane potential is maximal when uncoupling protein 1 is ablated or inhibited and (b) oxygen consumption rates in mitochondria from uncoupling protein 1 knock-out mice, are significantly lower than those from wild-type mice, but equivalent to those from wild-type mice in the presence of GDP. In summary, we show that uncoupling protein 1 can affect reactive oxygen containing species production by isolated mitochondria from brown adipose tissue. โข Keywords: Mitochondria, Reactive oxygen species, Brown adipose tissue, Uncoupling protein 1
โข O2k-Network Lab: IE Dublin Porter RK
Labels: MiParea: Respiration, Genetic knockout;overexpression
Stress:Oxidative stress;RONS Organism: Mouse Tissue;cell: Fat Preparation: Isolated mitochondria Enzyme: Uncoupling protein
Coupling state: OXPHOS
HRR: Oxygraph-2k