Ethidium Bromide Inhibits Mitochondrial Phosphorylating Oxidation

Higgins, Edwin S.; Dunlavey, Brenda L.; Friend, Wilson H.; Rogers, Kenneth S.

doi:10.3181/00379727-149-38957

Cited by 4 publications

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“…Cell treatment with EthBr showed the same outcome on the mitochondrial stress profile as the treatment with SSL. EthBr treatment is used to deplete cells from mtDNA by its ability to inhibit mitochondrial RNA synthesis , but it also directly affects oxidative phosphorylation and ATP synthesis . These different effects of SSL and EthBr versus UVC on mitochondrial function is consistent with the findings of Furda et al who showed that H 2 O 2 , but not the DNA alkylating agent MMS, did cause mitochondrial dysfunction .…”

Section: Discussionsupporting

confidence: 79%

Shortwave UV-Induced Damage as Part of the Solar Damage Spectrum Is Not a Major Contributor to Mitochondrial Dysfunction

Gebhard

Matt

Bürger

et al. 2014

J Biochem Mol Toxicol

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Because of the absence of a nucleotide excision repair in mitochondria, ultraviolet (UV)-induced bulky mitochondrial DNA (mtDNA) lesions persist for several days before they would eventually be removed by mitophagy. Long persistence of this damage might disturb mitochondrial functions, thereby contributing to skin ageing. In this study, we examined the influence of shortwave UV-induced damage on mitochondrial parameters in normal human skin fibroblasts. We irradiated cells with either sun-simulating light (SSL) or with ultraviolet C to generate bulky DNA lesions. At equivalent antiproliferative doses, both irradiation regimes induced gene expression of mitochondrial transcription factor A (TFAM) and matrix metallopeptidase 1 (MMP-1). Only irradiation with SSL, however, caused significant changes in mtDNA copy number and a decrease in mitochondrial respiration. Our results indicate that shortwave UV-induced damage as part of the solar spectrum is not a major contributor to mitochondrial dysfunction.

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Section: Discussionsupporting

confidence: 79%

Shortwave UV-Induced Damage as Part of the Solar Damage Spectrum Is Not a Major Contributor to Mitochondrial Dysfunction

Gebhard

Matt

Bürger

et al. 2014

J Biochem Mol Toxicol

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“…Variation in mitochondrial function might reflect the reported variations in the capacities of these tissues for protein and DNA syntheses (2,3). We have already shown that inhibition of protein synthesis in rat liver by ethidium bromide was in part due to inhibition of phosphorylating oxidation in the mitochondria (4).…”

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confidence: 98%

Heterogeneity of Renal Mitochondria of the Rat

Higgins

Seibel

Friend

et al. 1978

Experimental Biology and Medicine

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Recently, we have examined organ differences in mitochondrial capacities for conversion of reducing equivalents to phosphate bond energy potential and have related these differences to lipophilic properties of the mitochondrial inner membrane (1). The lipophilic (hydrophobic) nature of NADH dehydrogenase and succinate dehydrogenase sites differed in mitochondria from heart, spleen, liver, kidney and brain. These differences were not correlated with the embryonic origin of the tissues.In this communication, we wish to extend our work to the morphologically distinct tissues within one organ, the kidney. Variation in respiratory control as well as in NADH dehydrogenase lipophilicities were monitored for mitochondria isolated from renal cortex, red medulla and white medulla tissues. Variation in mitochondrial function might reflect the reported variations in the capacities of these tissues for protein and DNA syntheses (2, 3). We have already shown that inhibition of protein synthesis in rat liver by ethidium bromide was in part due to inhibition of phosphorylating oxidation in the mitochondria (4). Materials and methods.Renal mitochondria were prepared from male Sprague-Dawley rats as described previously (1). A Stadie-Riggs apparatus having 0.5 mm clearance was used to prepare slices which were dissected into cortex, red medulla, and white medulla (2). Respiratory rates, respiratory control ratios (RCR) and mitochondrial protein were determined as previously reported (1). Tetrabutylammonium bromide was a product a Eastman Organic Chemicals. Substrates and other biochemicals were purchased from Sigma Chemical Company.Results. The yields of mitochondrial protein obtained from each dissected renal tissue were 12.6 mg per g of decapsulated intact kidney, 12.2 mg/g of cortex, 8.5 mg/g of red medulla, and 1.3 mg/g of white medulla. Electron micrographs (Fig. 1) showed relatively few mitochondria in the isolated pellet of white medulla mitochondria (inset 6) and in the tissue slice of white medulla (inset 5 ) from the decapsulated kidney. Considerably more red medulla and cortical mitochondria were found in either the pellet preparations (insets 2 and 4, respectively) or tissue slices (insets 1 and 3, respectively). Mitochondria isolated from red medulla (inset 2) were somewhat larger and more spherical than those from cortex (inset 4).Variation in respiratory properties were recorded for the mitochondrial preparations in Table I. Cortical mitochondrial respiration was not significantly different from that of the intact kidney. This was not unexpected since the bulk of the kidney was composed of cortical tissue (84%), whereas only 13% was red medulla and 3% was white medulla (2,3). The response of mitochondria from red medulla to stimulation by ADP (state 3 respiration) was about 1.4 times that of organelles from cortex or whole kidney ( P < 0.05). This indicated that the former were more efficient and tightly coupled (higher RCR, P < 0.05).Although only one experiment was conducted with white medulla (kidneys from 28 rat...

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Influence of Dietary Cholesterol on Mitochondrial Function in the Rat

Rogers

Higgins

Grogan

1980

The Journal of Nutrition

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Rat-liver mitochondrial cholesterol ester levels were increased nine-fold and free cholesterol levels were doubled by feeding 10% lard and 2% cholesterol with Purina rabbit chow pellets to weanling male Sprague-Dawley rats for 5 weeks. This resulted in depression of State 3 (ADP-stimulated) glutamate respiration and reduced sensitivity to inhibition of phosphyorylation by tetrabutylammonium bromide and oligomycin. Brain, heart, lung, spleen, kidney and testis mitochondrial functions were not responsive to changes in dietary cholesterol nor were increases noted in free cholesterol content; mitochondrial cholesterol esters in these six tissues remained at extremely low levels regardless of treatment. Inclusion of 0.01% oleyl-p-decylbenzene sulfonate (a hypocholesterolemic agent) in the 10% lard and 2% cholesterol diet prevented elevation of rat-liver cholesterol esters and restored "normal" mitochondrial functions of respiratory control. This compound had no lowering effect on the raised level of liver mitochondrial free cholesterol nor on the reduced mitochondrial sensitivity to the phosphorylation inhibitors. We concluded that cholesterol esters were associated with depression of liver mitochondrial respiratory control and that free cholesterol was related to desensitization of mitochondria to the phosphorylation inhibitors.

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Ethidium Bromide Inhibits Mitochondrial Phosphorylating Oxidation

Cited by 4 publications

References 0 publications

Shortwave UV-Induced Damage as Part of the Solar Damage Spectrum Is Not a Major Contributor to Mitochondrial Dysfunction

Shortwave UV-Induced Damage as Part of the Solar Damage Spectrum Is Not a Major Contributor to Mitochondrial Dysfunction

Heterogeneity of Renal Mitochondria of the Rat

Influence of Dietary Cholesterol on Mitochondrial Function in the Rat

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