scholarly journals Effects of Propranolol on Growth, Lipids and Energy Metabolism and Oxidative Stress Response of Phaeodactylum tricornutum

Biology ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 478
Author(s):  
Bernardo Duarte ◽  
Eduardo Feijão ◽  
Ricardo Cruz de Carvalho ◽  
Irina A. Duarte ◽  
Marisa Silva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Energy Production ◽  
Respiratory Activity ◽  
Oxygen Production ◽  
Transport Chain ◽  
Adrenoceptor Blocker ◽  
And Oxidative Stress

Present demographic trends suggest a rise in the contributions of human pharmaceuticals into coastal ecosystems, underpinning an increasing demand to evaluate the ecotoxicological effects and implications of drug residues in marine risk assessments. Propranolol, a non-selective β-adrenoceptor blocker, is used worldwide to treat high blood pressure conditions and other related cardiovascular conditions. Although diatoms lack β-adrenoceptors, this microalgal group presents receptor-like kinases and proteins with a functional analogy to the animal receptors and that can be targeted by propranolol. In the present work, the authors evaluated the effect of this non-selective β-adrenoceptor blocker in diatom cells using P. tricornutum as a model organism, to evaluate the potential effect of this compound in cell physiology (growth, lipids and energy metabolism and oxidative stress) and its potential relevance for marine ecosystems. Propranolol exposure leads to a significant reduction in diatom cell growth, more evident in the highest concentrations tested. This is likely due to the observed impairment of the main primary photochemistry processes and the enhancement of the mitochondrial respiratory activity. More specifically, propranolol decreased the energy transduction from photosystem II (PSII) to the electron transport chain, leading to an increase in oxidative stress levels. Cells exposed to propranolol also exhibited high-dissipated energy flux, indicating that this excessive energy is efficiently diverted, to some extent, from the photosystems, acting to prevent irreversible photoinhibition. As energy production is impaired at the PSII donor side, preventing energy production through the electron transport chain, diatoms appear to be consuming storage lipids as an energy backup system, to maintain essential cellular functions. This consumption will be attained by an increase in respiratory activity. Considering the primary oxygen production and consumption pathways, propranolol showed a significant reduction of the autotrophic O2 production and an increase in the heterotrophic mitochondrial respiration. Both mechanisms can have negative effects on marine trophic webs, due to a decrease in the energetic input from marine primary producers and a simultaneous oxygen production decrease for heterotrophic species. In ecotoxicological terms, bio-optical and fatty acid data appear as highly efficient tools for ecotoxicity assessment, with an overall high degree of classification when these traits are used to build a toxicological profile, instead of individually assessed.

Abstract 665: Cryofluorescence 3D Imaging Shows Mutation of p67phox Improves Metabolic Function and Reduces Oxidative Stress in the Renal Medulla of the Dahl Salt-sensitive Rat

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Allen W Cowley ◽  
Fahimeh Salehpour ◽  
Chun Yang ◽  
Theresa Kurth ◽  
Mahsa Ranji
Keyword(s):  
Oxidative Stress ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Substantial Reduction ◽  
Renal Medulla ◽  
Metabolic Function ◽  
Protective Effects ◽  
3D Images ◽  
Transport Chain ◽  
And Oxidative Stress

The Dahl salt-sensitive (SS) rat exhibits increased renal production of reactive oxygen species (ROS) especially in the renal outer medulla (OM) which is known to contribute importantly to the salt-induced hypertension. We have identified increased expression of the p67 phox cytosolic subunit of NAD(P)H oxidase and enhanced enzyme activity in the OM of Dahl salt-sensitive (SS). We found that ZFN knock down of the NADPH-oxidase cytosolic subunit p67 phox in SS rats (SS p67phox-/- ) resulted in a 40% reduction of hypertension and a substantial reduction of renal injury. To determine whether these protective effects were associated with alterations of regional metabolism and oxidative stress, a custom designed cryoimager was used to acquire multi-channel fluorescent images of sequential serial sections with a z-resolution of 30 μm yielding 400 slices per kidney. Computer reconstruction of the stacked sections provided a 3D image of regional changes of metabolic function and oxidative stress within the kidney. Kidneys obtained from SS and SS p67phox-/- rats fed a high salt diet (4% NaCl) for 21 days were flash frozen in liquid N 2 and fluorescent images of the mitochondrial electron transport chain carriers NADH and FAD were acquired. The naturally fluorescent NADH and FAD levels were acquired to provide a 3D representation of the metabolic state of the tissue and oxidative stress. The mean NADH redox ratio (NADH/FAD RR) was significantly higher in kidneys of SS p67phox-/- rats (1.46 ± 0.11 NADH/FAD RR; n=7) compared to SS kidneys (1.00 ± 0.07 NADH/FAD RR; n=4). This represents an average 46% increase in the electron transport chain metabolic activity and a reduction of oxidative stress in kidneys of SS p67phox-/- rats compared to the SS kidneys. Importantly, this was observed only in the region of the renal medulla as revealed by the 3D images of these kidneys. We conclude that p67(phox) is critically involved in cell energetics and ROS production in the renal medulla.

Alterations of mitochondrial electron transport chain and oxidative stress induced by alkaloid-like α-aminonitriles on Aedes aegypti larvae

2018 ◽  
Vol 144 ◽  
pp. 64-70 ◽  
Author(s):  
Mayra A. Borrero Landazabal ◽  
Aurora L. Carreño Otero ◽  
Vladimir V. Kouznetsov ◽  
Jonny E. Duque Luna ◽  
Stelia C. Mendez-Sanchez
Keyword(s):  
Oxidative Stress ◽  
Electron Transport ◽  
Aedes Aegypti ◽  
Electron Transport Chain ◽  
Mitochondrial Electron Transport Chain ◽  
Transport Chain ◽  
And Oxidative Stress

Mitochondrial Disorder for Muscle Biopsy

2013 ◽  
Author(s):  
J. Fay Jou ◽  
Lori A Aronson ◽  
Jacqueline W Morillo-Delerme
Keyword(s):  
Energy Metabolism ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Disease ◽  
Electron Transport Chain ◽  
Mitochondrial Disorder ◽  
Metabolic Complications ◽  
Transport Chain ◽  
Increased Risk ◽  
Anesthetic Considerations

Mitochondrial disease (mtD) is a genetically, biochemically, and clinically heterogeneous group of disorders that arise most commonly from defects in the oxidative phosphorylation or electron transport chain involved in energy metabolism. These patients have an increased risk for cardiac, respiratory, neurologic, and metabolic complications from anesthesia. Consequently, there are several anesthetic considerations for patients with mtD.

scholarly journals Tissue Factor Decryption By Oxidative Stress-Induced Lipid Peroxidation: Potential Mechanisms

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 125-125
Author(s):  
Shabbir Ansari ◽  
Usha R Pendurthi ◽  
L. Vijaya Mohan Rao
Keyword(s):  
Oxidative Stress ◽  
Electron Transport ◽  
P38 Mapk ◽  
Electron Transport Chain ◽  
Thioredoxin Reductase ◽  
Dependent Manner ◽  
Mapk Activation ◽  
Downstream Signaling ◽  
Transport Chain

Abstract Cellular lipid peroxidation is known to contribute to the initiation and propagation of atherothrombosis. Recently, we showed that 4-hydroxynonenal (HNE), one of the most abundant reactive aldehydes generated from the oxidation of ω-6 fatty acids, enhanced tissue factor (TF) activity on monocytic cells by externalizing phosphatidylserine (PS) in p38 MAPK activation-dependent manner. However, at present, the link between HNE-induced oxidative stress and p38 MAPK activation and the relation of p38 MAPK activation to PS externalization is not fully known. In the present study, we investigated the role of mitochondrial electron transport chain and reactive oxygen species (ROS) generation in HNE-mediated TF decryption. In addition, we also investigated the thioredoxin reductase-thioredoxin-ASK-1 axis in regulating p38 MAPK activation and PS externalization in decrypting TF. To elucidate potential mechanisms of HNE-induced TF decryption, we first determined the role of specific mitochondrial electron transport chain complexes in regulating TF activity. Since THP-1 cells used in the study had a measurable basal TF activity, they were not further treated with LPS or other agonists to induce TF synthesis. The electron transport chain in these cells was disrupted by specific inhibitors and cell surface TF activity was measured by factor X activation assay. Inhibition of complex I and complex IV by rotenone and sodium azide, respectively, enhanced the procoagulant activity of basal level TF. However, the inhibition of complex I and IV had no significant effect on the HNE-mediated increase in TF activity. Interestingly, inhibition of ATP synthase/complex V by oligomycin significantly inhibited the HNE-mediated enhanced TF activity, indicating that HNE-mediated TF decryption may involve the generation of ATP. In agreement with earlier published studies in monocytes/macrophages, stimulation of THP-1 cells with ATP increased cell surface TF activity. However, at present, it is yet to be shown that HNE treatment actually increased the production of ATP and that this ATP is responsible for the HNE-mediated TF decryption. It is also possible that HNE, either through a generation of ROS in mitochondria or directly, can affect the activity of thioredoxin either by intracellular signaling or by directly forming an adduct with it. Therefore, we next investigated the effect of HNE on the activity of thioredoxin reductase, the enzyme known to regulate thioredoxin activity in the cell. Our data showed that HNE treatment inhibited the activity of thioredoxin reductase in a concentration-dependent manner, 40 µM of HNE inhibiting 50% of the activity and a complete inhibition at 80µM of HNE. To further determine the downstream signaling cascade involved in the PS externalization and TF decryption on exposure to HNE, we analyzed the effect of HNE on the activation of MKK3 and MKK6, the protein kinases known to activate p38 MAPK and the downstream signaling activator of thioredoxin/thioredoxin reductase pathway. HNE treatment increased the phosphorylation of MKK3 and MKK6 in a time-dependent manner. In summary, our data suggest that HNE may mediate TF decryption via modulation of thioredoxin/thioredoxin reductase system, which results in activation of MKK3/MKK6, which in turn activates p38 MAPK that is responsible for PS externalization. The study highlights the potential role of oxidative stress in regulating TF activity in thrombotic disorders and provides a mechanistic link between disorders associated with cellular oxidative stress and thrombosis. Disclosures No relevant conflicts of interest to declare.

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