scholarly journals Quercetin Protects Rat L6 Myocytes from Antimycin A-Induced Mitochondrial Dysfunction

2016 ◽  
Vol 06 (01) ◽  
Author(s):  
Vijay M Kale
2019 ◽  
Vol 1715 ◽  
pp. 94-105 ◽  
Author(s):  
Katherine R. Stanford ◽  
Stephen H. Hadley ◽  
Ivan Barannikov ◽  
Joanne M. Ajmo ◽  
Parmvir K. Bahia ◽  
...  

Molecules ◽  
2021 ◽  
Vol 26 (20) ◽  
pp. 6289
Author(s):  
Sinenhlanhla X. H. Mthembu ◽  
Christo J. F. Muller ◽  
Phiwayinkosi V. Dludla ◽  
Evelyn Madoroba ◽  
Abidemi P. Kappo ◽  
...  

The current study investigated the physiological effects of flavonoids found in daily consumed rooibos tea, aspalathin, isoorientin, and orientin on improving processes involved in mitochondrial function in C2C12 myotubes. To achieve this, C2C12 myotubes were exposed to a mitochondrial channel blocker, antimycin A (6.25 µM), for 12 h to induce mitochondrial dysfunction. Thereafter, cells were treated with aspalathin, isoorientin, and orientin (10 µM) for 4 h, while metformin (1 µM) and insulin (1 µM) were used as comparators. Relevant bioassays and real-time PCR were conducted to assess the impact of treatment compounds on some markers of mitochondrial function. Our results showed that antimycin A induced alterations in the mitochondrial respiration process and mRNA levels of genes involved in energy production. In fact, aspalathin, isoorientin, and orientin reversed such effects leading to the reduced production of intracellular reactive oxygen species. These flavonoids further enhanced the expression of genes involved in mitochondrial function, such as Ucp 2, Complex 1/3, Sirt 1, Nrf 1, and Tfam. Overall, the current study showed that dietary flavonoids, aspalathin, isoorientin, and orientin, have the potential to be as effective as established pharmacological drugs such as metformin and insulin in protecting against mitochondrial dysfunction in a preclinical setting; however, such information should be confirmed in well-established in vivo disease models.


2012 ◽  
Vol 302 (10) ◽  
pp. R1134-R1142 ◽  
Author(s):  
Sergey I. Dikalov ◽  
Wei Li ◽  
Abdulrahman K. Doughan ◽  
Raul R. Blanco ◽  
A. Maziar Zafari

Production of superoxide (O2·−) by NADPH oxidases contributes to the development of hypertension and atherosclerosis. Factors responsible for activation of NADPH oxidases are not well understood; interestingly, cardiovascular disease is associated with both altered NADPH oxidase activity and age-associated mitochondrial dysfunction. We hypothesized that mitochondrial dysfunction may contribute to activation of NADPH oxidase. The effect of mitochondrial inhibitors on phagocytic NADPH oxidase in human lymphoblasts and whole blood was measured at the basal state and upon PKC-dependent stimulation with PMA using extracellular 1-hydroxy-2,2,6,6-tetramethylpiperidin-4-yl-trimethylammonium or mitochondria-targeted 1-hydroxy-4-[2-triphenylphosphonio)-acetamido]-2,2,6,6-tetramethylpiperidine spin probes and electron spin resonance (ESR). Intracellular cytosolic calcium [Ca2+]iwas measured spectrofluorometrically using fura-2 AM. Incubation of lymphoblasts with the mitochondrial inhibitors rotenone, antimycin A, CCCP, or ruthenium red (an inhibitor of mitochondrial Ca2+uniporter) did not significantly change basal activity of NADPH oxidase. In contrast, preincubation with the mitochondrial inhibitors prior to PMA stimulation of lymphoblasts resulted in two- to three-fold increase of NADPH oxidase activity compared with stimulation with PMA alone. Most notably, the intracellular Ca2+-chelating agent BAPTA-AM abolished the effect of mitochondrial inhibitors on NADPH oxidase activity. Cytosolic Ca2+measurements with fura-2 AM showed that the mitochondrial inhibitors increased [Ca2+]i, while BAPTA-AM abolished the increase in [Ca2+]i. Furthermore, depletion of cellular Ca2+with thapsigargin attenuated CCCP- and antimycin A-mediated activation of NADPH oxidase in the presence of PMA by 42% and 31%, correspondingly. Our data suggest that mitochondria regulate PKC-dependent activation of phagocytic NADPH oxidase. In summary, increased mitochondrial O2·−and impaired buffering of cytosolic Ca2+by dysfunctional mitochondria result in enhanced NADPH oxidase activity, which may contribute to the development of cardiovascular diseases.


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
A-Rang Im ◽  
Young-Hwa Kim ◽  
Md. Romij Uddin ◽  
Hye Won Lee ◽  
Seong Wook Chae ◽  
...  

Antimycin A (AMA) damages mitochondria by inhibiting mitochondrial electron transport and can produce reactive oxygen species (ROS). ROS formation, aging, and reduction of mitochondrial biogenesis contribute to mitochondrial dysfunction. The present study sought to investigate extracts ofScutellaria baicalensisand its flavonoids (baicalin, baicalein, and wogonin), whether they could protect mitochondria against oxidative damage. The viability of L6 cells treated with AMA increased in the presence of flavonoids and extracts ofS. baicalensis. ATP production decreased in the AMA treated group, but increased by 50% in cells treated with flavonoids (except wogonin) and extracts ofS. baicalensiscompared to AMA-treated group. AMA treatment caused a significant reduction (depolarized) in mitochondrial membrane potential (MMP), whereas flavonoid treatment induced a significant increase in MMP. Mitochondrial superoxide levels increased in AMA treated cells, whereas its levels decreased when cells were treated with flavonoids or extracts ofS. baicalensis. L6 cells treated with flavonoids and extracts ofS. baicalensisincreased their levels of protein expression compared with AMA-treated cells, especially water extracts performed the highest levels of protein expression. These results suggest that theS. baicalensisextracts and flavonoids protect against AMA-induced mitochondrial dysfunction by increasing ATP production, upregulating MMP, and enhancing mitochondrial function.


2013 ◽  
Vol 153 (1-3) ◽  
pp. 428-436 ◽  
Author(s):  
Kwang Sik Suh ◽  
Young Soon Lee ◽  
Seung Hwan Seo ◽  
Young Seol Kim ◽  
Eun Mi Choi

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Maria Hytti ◽  
Eveliina Korhonen ◽  
Juha M. T. Hyttinen ◽  
Heidi Roehrich ◽  
Kai Kaarniranta ◽  
...  

Mitochondrial dysfunction has been implicated in a wide variety of degenerative diseases, including age-related macular degeneration. Damage to mitochondria and mitochondrial DNA accumulates with age in the postmitotic retinal pigment epithelium (RPE), which could lead to RPE cell death and trigger disease. One possible mechanism for cells to avoid cell death is mitophagy, the targeted clearance of damaged mitochondria by autophagy. Here, we induced mitochondrial damage in human RPE cells (ARPE-19 and hRPE), using antimycin A, an inhibitor of complex III of the electron transport chain, and investigated cellular viability, mitochondrial structure and function, and autophagy activity. We observed that antimycin A evoked dose-dependent cell death, a rapid loss in mitochondrial membrane potential, and a collapse of oxidative phosphorylation. Mitochondria appeared swollen and there was clear damage to their cristae structure. At the same time, cells were undergoing active autophagy and were sensitive to autophagy inhibition by bafilomycin A1 or chloroquine. These results indicate that mitochondrial dysfunction can cause significant RPE damage and that autophagy is an important survival mechanism for cells suffering from mitochondrial damage.


2013 ◽  
Vol 36 (1) ◽  
pp. 19-29 ◽  
Author(s):  
A-Rang Im ◽  
Young-Hwa Kim ◽  
Md. Romij Uddin ◽  
Seong Wook Chae ◽  
Hye Won Lee ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document