Kinetics of xylem loading, membrane potential maintenance, and sensitivity of K+-permeable channels to reactive oxygen species: physiological traits that differentiate salinity tolerance between pea and barley

Background: Reserpine, an indole alkaloid commonly used for hypertension, is found in the roots of Rauwolfia serpentina. Although the root extract has been used for the treatment of cancer, the molecular mechanism of its anti-cancer activity on hormonal independent prostate cancer remains elusive. Methods: we evaluated the cytotoxicity of reserpine and other indole alkaloids, yohimbine and ajmaline on Prostate Cancer cells (PC3) using MTT assay. We investigated the mechanism of apoptosis using a combination of techniques including acridine orange/ethidium bromide staining, high content imaging of Annexin V-FITC staining, flow cytometric quantification of the mitochondrial membrane potential and Reactive Oxygen Species (ROS) and cell cycle analysis. Results: Our results indicate that reserpine inhibits DNA synthesis by arresting the cells at the G2 phase and showed all standard sequential features of apoptosis including, destabilization of mitochondrial membrane potential, reduced production of reactive oxygen species and DNA ladder formation. Our in silico analysis further confirmed that indeed reserpine docks to the catalytic cleft of anti-apoptotic proteins substantiating our results. Conclusion: Collectively, our findings suggest that reserpine can be a novel therapeutic agent for the treatment of androgen-independent prostate cancer.

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Ischemic preconditioning preserves mitochondrial membrane potential and limits reactive oxygen species production

Journal of Surgical Research ◽

10.1016/j.jss.2012.05.090 ◽

2012 ◽

Vol 178 (1) ◽

pp. 8-17 ◽

Cited By ~ 13

Author(s):

Ricardo Quarrie ◽

Daniel S. Lee ◽

Gregory Steinbaugh ◽

Brandon Cramer ◽

Warren Erdahl ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Ischemic Preconditioning ◽

Mitochondrial Membrane ◽

Reactive Oxygen Species Production ◽

Reactive Oxygen ◽

Oxygen Species ◽

Species Production

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Wheat Oxophytodienoate Reductase Gene TaOPR1 Confers Salinity Tolerance via Enhancement of Abscisic Acid Signaling and Reactive Oxygen Species Scavenging

PLANT PHYSIOLOGY ◽

10.1104/pp.112.211854 ◽

2013 ◽

Vol 161 (3) ◽

pp. 1217-1228 ◽

Cited By ~ 70

Author(s):

Wei Dong ◽

Mengcheng Wang ◽

Fei Xu ◽

Taiyong Quan ◽

Keqin Peng ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Abscisic Acid ◽

Salinity Tolerance ◽

Reactive Oxygen ◽

Oxygen Species ◽

Abscisic Acid Signaling ◽

Reductase Gene

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Abstract 062: Mitoubiquinone Decreases Reactive Oxygen Species Production and Improves Cardiac Efficiency in Chronic Volume Overload

Circulation Research ◽

10.1161/res.113.suppl_1.a062 ◽

2013 ◽

Vol 113 (suppl_1) ◽

Author(s):

Danielle M Yancey ◽

James D Gladden ◽

Jason L Guichard ◽

Victor M Darley-Usmar ◽

Louis J Dell’Italia ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Membrane Potential ◽

Systolic Pressure ◽

Reactive Oxygen ◽

Volume Overload ◽

Left Ventricular ◽

Ros Production ◽

Oxygen Species ◽

Cardiac Efficiency ◽

Lv Dysfunction

Background: The hemodynamic stress of left ventricular (LV) volume overload (VO) produces LV dysfunction accompanied by mitochondrial and cytoskeletal disruption in cardiomyocytes. Because mitochondria are both a source and target of reactive oxygen species (ROS), we hypothesize myocyte damage and LV dysfunction are mediated by mitochondrially produced ROS and can be attenuated by the mitochondrially targeted antioxidant, mitoubiquinone (MitoQ). Methods: Aortocaval fistula (ACF) was induced for 8 weeks in adult rats ± MitoQ. Echocardiography and high-fidelity LV pressure catheter recordings were used to study the LV end-systolic pressure-volume relationship and cardiac efficiency. Isolated cardiomyocytes were loaded with Carboxy-H2DFFDA (CM-DCF) and tetramethylrhodamine (TMRM) to measure mitochondrial ROS production and membrane potential. Results: Isolated cardiomyocyte studies demonstrated increased ROS production and decreased mitochondrial membrane potential in VO animals, both of which were attenuated with MitoQ. Treatment with MitoQ demonstrated a strong trend toward improvement in LV contractility, as cardiac efficiency improved significantly in MitoQ-treated VO animals. Untreated VO animals exhibited mitochondrial swelling and myofibrillar disruption that was prevented by MitoQ. Conclusion: These studies suggest an early interplay between mitochondrial-derived ROS production and cardiac ultrastructure and function.

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