Effect of Bovine Serum Albumin on Mitochondrial Respiration in the Brain and Liver of Mice and Rats

Panov, Alexander; Вавилин, В. А.; Lyakhovich, V. V.; Brooks, Benjamin; Bonkovsky, Herbert L.

doi:10.1007/s10517-010-0904-5

Cited by 24 publications

(15 citation statements)

References 13 publications

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“…Rotenone, however, inhibits succinate-stimulated ROS production by RET. It has been suggested that RET is physiologically regulated by several mechanisms, 1) by control of succinate dehydrogenase activity in the citric acid cycle (39), 2) by fatty acids (40), 3) and by mitochondrial membrane potential (35). Thus RET is not an "artifact" and rotenone supplementation may produce an artificially improved mitochondrial functions.…”

Section: Discussionmentioning

confidence: 99%

Nox2 as a potential target of mitochondrial superoxide and its role in endothelial oxidative stress

Nazarewicz

Dikalova

Bikineyeva

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Superoxide (O2(·-)) production by the NADPH oxidases is implicated in the pathogenesis of many cardiovascular diseases, including hypertension. We have previously shown that activation of NADPH oxidases increases mitochondrial O2(·-) which is inhibited by the ATP-sensitive K(+) channel (mitoKATP) inhibitor 5-hydroxydecanoic acid and that scavenging of mitochondrial or cytoplasmic O2(·-) inhibits hypertension. We hypothesized that mitoKATP-mediated mitochondrial O2(·-) potentiates cytoplasmic O2(·-) by stimulation of NADPH oxidases. In this work we studied Nox isoforms as a potential target of mitochondrial O2(·-). We tested contribution of reverse electron transfer (RET) from complex II to complex I in mitochondrial O2(·-) production and NADPH oxidase activation in human aortic endothelial cells. Activation of mitoKATP with low dose of diazoxide (100 nM) decreased mitochondrial membrane potential (tetramethylrhodamine methyl ester probe) and increased production of mitochondrial and cytoplasmic O2(·-) measured by site-specific probes and mitoSOX. Inhibition of RET with complex II inhibitor (malonate) or complex I inhibitor (rotenone) attenuated the production of mitochondrial and cytoplasmic O2(·-). Supplementation with a mitochondria-targeted SOD mimetic (mitoTEMPO) or a mitochondria-targeted glutathione peroxidase mimetic (mitoEbselen) inhibited production of mitochondrial and cytoplasmic O2(·-). Inhibition of Nox2 (gp91ds) or Nox2 depletion with small interfering RNA but not Nox1, Nox4, or Nox5 abolished diazoxide-induced O2(·-) production in the cytoplasm. Treatment of angiotensin II-infused mice with RET inhibitor dihydroethidium (malate) significantly reduced blood pressure. Our study suggests that mitoKATP-mediated mitochondrial O2(·-) stimulates cytoplasmic Nox2, contributing to the development of endothelial oxidative stress and hypertension.

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Section: Discussionmentioning

confidence: 99%

Nox2 as a potential target of mitochondrial superoxide and its role in endothelial oxidative stress

Nazarewicz

Dikalova

Bikineyeva

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…The degree of this intrinsic SDH inhibition varies strongly between the species. In other words, it depends on the metabolic phenotype of the BM [62, 126]. …”

Section: Isolated Brain Mitochondria Have Strongly Inhibited Succmentioning

confidence: 99%

“…Therefore, most researchers traditionally isolate BM and SCM in the presence of defatted BSA [126], which significantly improved oxidation of succinate (Figure 7(b)). Figure 7(b) shows, however, that even with the BSA-BM oxidizing succinate, it required more than a minute for the membrane potential to reach the maximum.…”

Section: Isolated Brain Mitochondria Have Strongly Inhibited Succmentioning

confidence: 99%

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Fatty Acids in Energy Metabolism of the Central Nervous System

Panov

Orynbayeva

Вавилин

et al. 2014

BioMed Research International

163

144

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In this review, we analyze the current hypotheses regarding energy metabolism in the neurons and astroglia. Recently, it was shown that up to 20% of the total brain's energy is provided by mitochondrial oxidation of fatty acids. However, the existing hypotheses consider glucose, or its derivative lactate, as the only main energy substrate for the brain. Astroglia metabolically supports the neurons by providing lactate as a substrate for neuronal mitochondria. In addition, a significant amount of neuromediators, glutamate and GABA, is transported into neurons and also serves as substrates for mitochondria. Thus, neuronal mitochondria may simultaneously oxidize several substrates. Astrocytes have to replenish the pool of neuromediators by synthesis de novo, which requires large amounts of energy. In this review, we made an attempt to reconcile β-oxidation of fatty acids by astrocytic mitochondria with the existing hypothesis on regulation of aerobic glycolysis. We suggest that, under condition of neuronal excitation, both metabolic pathways may exist simultaneously. We provide experimental evidence that isolated neuronal mitochondria may oxidize palmitoyl carnitine in the presence of other mitochondrial substrates. We also suggest that variations in the brain mitochondrial metabolic phenotype may be associated with different mtDNA haplogroups.

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“…However, absolute rates respiration at the State 4 and State 3, are also very important for understanding the mitochondrial energetics. Generally, in mitochondria from normal tissues isolated in the presence of bovine serum albumin, the RCR values are higher with the NAD-dependent substrates than with succinate [51]. …”

Section: Resultsmentioning

confidence: 99%

Bioenergetic and Antiapoptotic Properties of Mitochondria from Cultured Human Prostate Cancer Cell Lines PC-3, DU145 and LNCaP

Panov

Orynbayeva

2013

PLoS ONE

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The purpose of this work was to reveal the metabolic features of mitochondria that might be essential for inhibition of apoptotic potential in prostate cancer cells. We studied mitochondria isolated from normal prostate epithelial cells (PrEC), metastatic prostate cancer cell lines LNCaP, PC-3, DU145; and non-prostate cancer cells - human fibrosarcoma HT1080 cells; and normal human lymphoblastoid cells. PrEC cells contained 2 to 4 times less mitochondria per gram of cells than the three PC cell lines. Respiratory activities of PrEC cell mitochondria were 5-20-fold lower than PC mitochondria, depending on substrates and the metabolic state, due to lower content and lower activity of the respiratory enzyme complexes. Mitochondria from the three metastatic prostate cancer cell lines revealed several features that are distinctive only to these cells: low affinity of Complex I for NADH, 20-30 mV higher electrical membrane potential (ΔΨ). Unprotected with cyclosporine A (CsA) the PC-3 mitochondria required 4 times more Ca2+ to open the permeability transition pore (mPTP) when compared with the PrEC mitochondria, and they did not undergo swelling even in the presence of alamethicin, a large pore forming antibiotic. In the presence of CsA, the PC-3 mitochondria did not open spontaneously the mPTP. We conclude that the low apoptotic potential of the metastatic PC cells may arise from inhibition of the Ca2+-dependent permeability transition due to a very high ΔΨ and higher capacity to sequester Ca2+. We suggest that due to the high ΔΨ, mitochondrial metabolism of the metastatic prostate cancer cells is predominantly based on utilization of glutamate and glutamine, which may promote development of cachexia.

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Effect of Bovine Serum Albumin on Mitochondrial Respiration in the Brain and Liver of Mice and Rats

Cited by 24 publications

References 13 publications

Nox2 as a potential target of mitochondrial superoxide and its role in endothelial oxidative stress

Nox2 as a potential target of mitochondrial superoxide and its role in endothelial oxidative stress

Fatty Acids in Energy Metabolism of the Central Nervous System

Bioenergetic and Antiapoptotic Properties of Mitochondria from Cultured Human Prostate Cancer Cell Lines PC-3, DU145 and LNCaP

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