The Effect of Ginkgo biloba Extract on Mitochondrial Oxidative Phosphorylation in the Normal and Ischemic Rat Heart

2011 ◽  
Vol 25 (7) ◽  
pp. 1054-1060 ◽  
Author(s):  
Jurga Bernatoniene ◽  
Daiva Majiene ◽  
Rimantas Peciura ◽  
Ale Laukeviciene ◽  
Ruta Bernatoniene ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Ginkgo Biloba ◽  
Rat Heart ◽  
Ginkgo Biloba Extract ◽  
Mitochondrial Oxidative Phosphorylation

scholarly journals Influence of ubiquinone on the inhibitory effect of adriamycin on mitochondrial oxidative phosphorylation

1984 ◽  
Vol 217 (2) ◽  
pp. 493-498 ◽  
Author(s):  
H Muhammed ◽  
C K R Kurup
Keyword(s):  
Oxidative Phosphorylation ◽  
Rat Heart ◽  
Liver Mitochondria ◽  
Inhibitory Effect ◽  
Oxidative Activity ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Succinate Oxidation ◽  
Exogenous Addition

The inhibition of succinate oxidation in both heart and liver mitochondria by the cardiotoxic anticancer antibiotic adriamycin in vitro was reversed to a large extent by exogenous ubiquinone-45. Inhibition of the oxidation of NAD+-linked substrates in heart and liver mitochondria responded differently to ubiquinone, the inhibition being reversed only in liver organelles. Administration of adriamycin inhibited oxidative phosphorylation in rat heart, kidney and liver mitochondria, the inhibition being highest in the heart organelles (about 50% for both NAD+-linked substrates and succinate). Exogenous addition of ubiquinone to mitochondria isolated from drug-treated animals did not reverse the inhibition. Administration of ubiquinone along with adriamycin did not change effectively the pattern of drug-mediated decrease in oxidative activity of the organelles, particularly in the heart.

scholarly journals SIRT-3 Modulation by Resveratrol Improves Mitochondrial Oxidative Phosphorylation in Diabetic Heart through Deacetylation of TFAM

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 235 ◽  
Author(s):  
Pankaj Bagul ◽  
Parmeshwar Katare ◽  
Paramesha Bugga ◽  
Amit Dinda ◽  
Sanjay K. Banerjee
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dna ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Function ◽  
Rat Heart ◽  
Diabetic Rat ◽  
H9c2 Cells ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Acetylation Status ◽  
Protein Deacetylase

Background and Purpose: Mitochondrial dysfunction remains the crucial cause for many heart diseases including diabetic cardiomyopathy (DCM). Sirtuin-3 (SIRT-3) is a protein deacetylase localized in the mitochondria and regulates mitochondrial function. Being a noteworthy mitochondrial protein deacetylase enzyme, the role of SIRT-3 in DCM is yet to be explored. Experimental Approach: Diabetes mellitus (Type-I, T1DM) was induced using streptozotocin (STZ, 50 mg/kg) in male Sprague Dawley (SD) rats. Rats with >200 mg/dL blood glucose levels were then divided randomly into two groups, DIA and DIA + RESV, where vehicle and resveratrol (25 mg/kg/day) were administered orally in both groups, respectively. Cardiac oxidative stress, fibrosis, and mitochondrial parameters were evaluated. H9c2 cells were transfected with SIRT-3 siRNA and shRNA, and ORF plasmid for silencing and overexpression, respectively. Key Results: After eight weeks, diabetic rat heart showed reduced cardiac cell size, increased oxidative stress and reduction of the activities of enzymes involved in mitochondrial oxidative phosphorylation (OXPHOS). There was reduced expression and activity of SIRT-3 and mitochondrial transcription factor (TFAM) in diabetic heart. Reduced SIRT-3 expression is also correlated with increased acetylation, decreased mitochondrial DNA (mtDNA) binding activity of TFAM, and reduced transcription of mitochondrial DNA encoded genes. Administration of resveratrol prevented the decrease in SIRT-3 and TFAM activity, which was corresponding to the reduced acetylation status of TFAM. Silencing SIRT-3 using siRNA in H9C2 cells showed increased acetylation of TFAM. Conclusion and Implications: Together our data shows that resveratrol activates SIRT-3, regulates the acetylation status of TFAM and preserves the mitochondrial function along with cellular size in diabetic rat heart.

scholarly journals Ginkgo Biloba Extract Ameliorates Oxidative Phosphorylation Performance and Rescues Aβ-Induced Failure

PLoS ONE ◽  
2010 ◽  
Vol 5 (8) ◽  
pp. e12359 ◽  
Author(s):  
Virginie Rhein ◽  
Maria Giese ◽  
Ginette Baysang ◽  
Fides Meier ◽  
Stefania Rao ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract

scholarly journals Therapeutic Effect of Ginkgo Biloba Extract on Rat Heart Failure Induced by Isoprenaline

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Hongwei Yi ◽  
Yongqing Wang ◽  
Fuyun Ding ◽  
Ling Meng ◽  
Xudong Wu
Keyword(s):  
Heart Failure ◽  
Therapeutic Effect ◽  
Ginkgo Biloba ◽  
Rat Heart ◽  
Ginkgo Biloba Extract

Effect of Ginkgo biloba extract on the rat heart mitochondrial function

2007 ◽  
Vol 111 (3) ◽  
pp. 512-516 ◽  
Author(s):  
Sonata Trumbeckaite ◽  
Jurga Bernatoniene ◽  
Daiva Majiene ◽  
Valdas Jakštas ◽  
Arunas Savickas ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Ginkgo Biloba ◽  
Rat Heart ◽  
Ginkgo Biloba Extract

Dependence of Platelet Adenyl Cyclase System on Oxidative Phosphorylation

1975 ◽  
Vol 34 (01) ◽  
pp. 042-049 ◽  
Author(s):  
Shuichi Hashimoto ◽  
Sachiko Shibata ◽  
Bokro Kobayashi
Keyword(s):  
Cyclic Amp ◽  
Oxidative Phosphorylation ◽  
Sodium Succinate ◽  
Potassium Cyanide ◽  
Adenyl Cyclase ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Adenyl Cyclase Activity ◽  
Intact Rabbit ◽  
Adenyl Cyclase System ◽  
Cyclic Amp Synthesis

SummaryThe radioactive adenosine 3′,5′-monophosphate (cyclic AMP) level derived from 8-14C adenine in intact rabbit platelets decreased in the presence of mitochondrial inhibitor (potassium cyanide) or uncoupler (sodium azide), and markedly increased by the addition of NaF, monoiodoacetic acid (MIA), or 2-deoxy-D-glucose. The stimulative effect of the glycolytic inhibitors was distinctly enhanced by the simultaneous addition of sodium succinate. MIA did neither directly stimulate the adenyl cyclase activity nor inhibit the phosphodiesterase activity. These results suggest that cyclic AMP synthesis in platelets is closely linked to mitochondrial oxidative phosphorylation.

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