scholarly journals Reactive Oxygen Species-Mediated Cellular Stress Response and Lipid Accumulation in Oleaginous Microorganisms: The State of the Art and Future Perspectives

2017 ◽  
Vol 8 ◽  
Author(s):  
Kun Shi ◽  
Zhen Gao ◽  
Tian-Qiong Shi ◽  
Ping Song ◽  
Lu-Jing Ren ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stress Response ◽  
Lipid Accumulation ◽  
State Of The Art ◽  
Cellular Stress ◽  
Reactive Oxygen ◽  
The State ◽  
Cellular Stress Response ◽  
Oxygen Species ◽  
Future Perspectives

scholarly journals Prodrug strategies for targeted therapy triggered by reactive oxygen species

MedChemComm ◽  
2019 ◽  
Vol 10 (9) ◽  
pp. 1531-1549 ◽  
Author(s):  
Jorge Peiró Cadahía ◽  
Viola Previtali ◽  
Nikolaj S. Troelsen ◽  
Mads H. Clausen
Keyword(s):  
Reactive Oxygen Species ◽  
Targeted Therapy ◽  
State Of The Art ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Future Perspectives ◽  
Comprehensive Review

A comprehensive review of ROS-activated produg strategies for targeted therapy, including state-of-the-art and future perspectives.

scholarly journals The Roles of Mitochondrial Reactive Oxygen Species in Cellular Signaling and Stress Response in Plants

2016 ◽  
Vol 171 (3) ◽  
pp. 1551-1559 ◽  
Author(s):  
Shaobai Huang ◽  
Olivier Van Aken ◽  
Markus Schwarzländer ◽  
Katharina Belt ◽  
A. Harvey Millar
Keyword(s):  
Reactive Oxygen Species ◽  
Stress Response ◽  
Cellular Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

scholarly journals Lipid droplets alleviate cadmium induced cytotoxicity in Saccharomyces cerevisiae

2017 ◽  
Vol 6 (1) ◽  
pp. 30-41 ◽  
Author(s):  
Selvaraj Rajakumar ◽  
Vasanthi Nachiappan
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Lipid Accumulation ◽  
Lipid Droplets ◽  
Reactive Oxygen ◽  
Oxygen Species

Cadmium (Cd) induces oxidative stress that generates reactive oxygen species (ROS) and increased lipid accumulation.

scholarly journals Caffeic acid reduces lipid accumulation and reactive oxygen species production in adipocytes

2018 ◽  
Vol 12 (20) ◽  
pp. 263-268 ◽  
Author(s):  
Brito Dantas Mariana ◽  
Lima Sampaio Tiago ◽  
Róseo Paula Pessoa Bezerra de Menezes Ramon ◽  
Magalhães Ferreira Jamile ◽  
Sousa Melo Tiago ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Caffeic Acid ◽  
Lipid Accumulation ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Species Production

scholarly journals Nifedipine Modulates Renal Lipogenesis via the AMPK-SREBP Transcriptional Pathway

2019 ◽  
Vol 20 (7) ◽  
pp. 1570 ◽  
Author(s):  
Yen-Chung Lin ◽  
Mai-Szu Wu ◽  
Yuh-Feng Lin ◽  
Chang-Rong Chen ◽  
Chang-Yu Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Accumulation ◽  
Coenzyme A ◽  
Surrogate Marker ◽  
Reactive Oxygen ◽  
Fatty Acyl ◽  
Acid Oxidation ◽  
Oxygen Species ◽  
Atp Production ◽  
Renal Tubular Cells

Lipid accumulation in renal cells has been implicated in the pathogenesis of obesity-related kidney disease, and lipotoxicity in the kidney can be a surrogate marker for renal failure or renal fibrosis. Fatty acid oxidation provides energy to renal tubular cells. Ca2+ is required for mitochondrial ATP production and to decrease reactive oxygen species (ROS). However, how nifedipine (a calcium channel blocker) affects lipogenesis is unknown. We utilized rat NRK52E cells pre-treated with varying concentrations of nifedipine to examine the activity of lipogenesis enzymes and lipotoxicity. A positive control exposed to oleic acid was used for comparison. Nifedipine was found to activate acetyl Coenzyme A (CoA) synthetase, acetyl CoA carboxylase, long chain fatty acyl CoA elongase, ATP-citrate lyase, and 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG CoA) reductase, suggesting elevated production of cholesterol and phospholipids. Nifedipine exposure induced a vast accumulation of cytosolic free fatty acids (FFA) and stimulated the production of reactive oxygen species, upregulated CD36 and KIM-1 (kidney injury molecule-1) expression, inhibited p-AMPK activity, and triggered the expression of SREBP-1/2 and lipin-1, underscoring the potential of nifedipine to induce lipotoxicity with renal damage. To our knowledge, this is the first report demonstrating nifedipine-induced lipid accumulation in the kidney.

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