scholarly journals EFFECTS OF GLYPHOSATE ON GERMINATION AND PHOTOSYNTHESIS IN Prosopis alba G.: A BIOCHEMICAL APPROACH

2022 ◽  
Vol 7 (1) ◽  
pp. 9
Author(s):  
Diego Ariel Meloni ◽  
María José Nieva ◽  
Carlos Alberto Martínez
Keyword(s):  
Fluorescence Emission ◽  
Antioxidant Response ◽  
Complex Iii ◽  
Native Forest ◽  
Native Flora ◽  
Prosopis Alba ◽  
Transport Chain ◽  
Mean Germination Time ◽  
High Production ◽  
High Doses

In recent decades, the phytogeographic region of the Western Chaco has been subjected to heavy deforestation. The native forest was gradually replaced by agricultural crops using high doses of herbicides. Glyphosate is the most widely used herbicide, and its impact on the surrounding native flora is unknown. The aim of this work was to determine the effect of glyphosate on the germination of Prosopis alba seeds and the photosynthesis of seedlings.  Seeds were placed between paper towels, moistened with solutions of 0, 10, 20, 20, 30 and 40 mg a.i. glyphosate l-1, in a growth chamber at 25 oC and a 12 h photoperiod. The percentage of germinated seeds and the mean germination time were calculated. The respiratory rate was measured in these seeds, and the activity of complexes I and III of the respiratory chain was quantified. The shikimate concentration and antioxidant response of the seeds were also quantified. Chlorophyll a fluorescence emission variables were measured in the cotyledons. It was concluded that glyphosate inhibits germination in P. alba seeds and decreases the speed of the process.  This effect can partly be explained by inhibition of respiration, mainly at the level of complex III of the mitochondrial electron transport chain. It is also due to oxidative stress produced by the herbicide, since the antioxidant response of the seeds fails to compensate for the high production of reactive oxygen species. Glyphosate inhibits the photochemical stage of photosynthesis on P. alba cotyledons.

scholarly journals AB0031 T HELPER 17 CELLS WERE SIGNIFICANTLY DECREASED BY MITOCHONDRIAL ELECTRON TRANSPORT CHAIN COMPLEX INHIBITOR IN PATIENTS WITH RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1318.2-1318
Author(s):  
H. R. Lee ◽  
S. J. Yoo ◽  
J. Kim ◽  
I. S. Yoo ◽  
C. K. Park ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Electron Transport ◽  
Disease Activity ◽  
Th17 Cells ◽  
Electron Transport Chain ◽  
Chain Complex ◽  
Complex Iii ◽  
Mitochondrial Electron Transport Chain ◽  
Transport Chain ◽  
Healthy Control

Background:Reactive oxygen species (ROS) and T helper 17 (TH17) cells have been known to play an important role in the pathogenesis of rheumatoid arthritis (RA). However, the interrelationship between ROS and TH17 remains unclear in RAObjectives:To explore whether ROS affect TH17 cells in peripheral blood mononuclear cells (PBMC) of RA patients, we analyzed ROS expressions among T cell subsets following treatment with mitochondrial electron transport chain complex inhibitors.Methods:Blood samples were collected from 40 RA patients and 10 healthy adult volunteers. RA activity was divided according to clinical parameter DAS28. PBMC cells were obtained from the whole blood using lymphocyte separation medium density gradient centrifugation. Following PBMC was stained with Live/Dead stain dye, cells were incubated with antibodies for CD3, CD4, CD8, and CD25. After fixation and permeabilization, samples were stained with antibodies for FoxP3 and IL-17A. MitoSox were used for mitochondrial specific staining.Results:The frequency of TH17 cells was increased by 4.83 folds in moderate disease activity group (5.1>DAS28≥3.2) of RA patients compared to healthy control. Moderate RA activity patients also showed higher ratio of TH17/Treg than healthy control (3.57 folds). All RA patients had elevated expression of mitochondrial specific ROS than healthy control. When PBMC cells were treated with 2.5uM of antimycin A (mitochondrial electron transport chain complex III inhibitor) for 16 h, the frequency of TH17 cells was significantly decreased.Conclusion:The mitochondrial electron transport chain complex III inhibitor markedly downregulated the frequency of TH17 cells in moderate disease activity patients with RA. These findings provide a novel approach to regulate TH17 function in RA through mitochondrial metabolism related ROS production.References:[1]Szekanecz, Z., et al., New insights in synovial angiogenesis. Joint Bone Spine, 2010. 77(1): p. 13-9.[2]Prevoo, M.L., et al., Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum, 1995. 38(1): p. 44-8.Disclosure of Interests:None declared

scholarly journals New Insights into the Chemical and Biochemical Basis of the “Yang-Invigorating” Action of Chinese Yang-Tonic Herbs

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Jihang Chen ◽  
Hoi Shan Wong ◽  
Pou Kuan Leong ◽  
Hoi Yan Leung ◽  
Wing Man Chan ◽  
...  
Keyword(s):  
Functional Capacity ◽  
Antioxidant Response ◽  
Mitochondrial Uncoupling ◽  
Biochemical Basis ◽  
Age Related ◽  
Mitochondrial Ros ◽  
Transport Chain ◽  
Median Lifespan ◽  
Bodily Function ◽  
Increased Activity

In the practice of traditional Chinese medicine, many Yang-tonic herbs have been used for retarding the decline in bodily function and delaying the onset of age-related diseases. Our earlier studies have demonstrated that Yang-invigorating herbs/formulations protect against oxidative injury in various organs and also extend the median lifespan in mice. This lifespan extension was associated with an upregulation of cellular antioxidant status including that of mitochondria whose functional capacity is also increased by “Yang-invigorating” herbs/formulations. In this paper, we propose that triterpenes and phytosterols, which are ubiquitously found in Yang-tonic herbs, may be the chemical entities responsible for enhancing mitochondrial functional and antioxidant capacity and thus the “Yang-invigorating” action. The biochemical mechanism underlying this “Yang-invigorating” action may involve a sustained production of low levels of mitochondrial reactive oxygen species (ROS) secondary to an increased activity of the electron transport chain, with the possible involvement of mitochondrial uncoupling. The increase in mitochondrial functional capacity can retard the decline in bodily function during aging, whereas the mitochondrial ROS production is instrumental in eliciting a glutathione antioxidant response via redox-sensitive signaling pathways, which can delay the onset of age-related diseases.

scholarly journals A Chemogenomic Screen in Saccharomyces cerevisiae Uncovers a Primary Role for the Mitochondria in Farnesol Toxicity and Its Regulation by the Pkc1 Pathway

2006 ◽  
Vol 282 (7) ◽  
pp. 4868-4874 ◽  
Author(s):  
Gregory D. Fairn ◽  
Kendra MacDonald ◽  
Christopher R. McMaster
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Electron Transport ◽  
Signaling Pathway ◽  
Electron Transport Chain ◽  
Reactive Oxygen ◽  
Complex Iii ◽  
Oxygen Species ◽  
Transport Chain

The isoprenoid farnesol has been shown to preferentially induce apoptosis in cancerous cells; however, the mode of action of farnesol-induced death is not established. We used chemogenomic profiling using Saccharomyces cerevisiae to probe the core cellular processes targeted by farnesol. This screen revealed 48 genes whose inactivation increased sensitivity to farnesol. The gene set indicated a role for the generation of oxygen radicals by the Rieske iron-sulfur component of complex III of the electron transport chain as a major mediator of farnesol-induced cell death. Consistent with this, loss of mitochondrial DNA, which abolishes electron transport, resulted in robust resistance to farnesol. A genomic interaction map predicted interconnectedness between the Pkc1 signaling pathway and farnesol sensitivity via regulation of the generation of reactive oxygen species. Consistent with this prediction (i) Pkc1, Bck1, and Mkk1 relocalized to the mitochondria upon farnesol addition, (ii) inactivation of the only non-essential and non-redundant member of the Pkc1 signaling pathway, BCK1, resulted in farnesol sensitivity, and (iii) expression of activated alleles of PKC1, BCK1, and MKK1 increased resistance to farnesol and hydrogen peroxide. Sensitivity to farnesol was not affected by the presence of the osmostabilizer sorbitol nor did farnesol affect phosphorylation of the ultimate Pkc1-responsive kinase responsible for controlling the cell wall integrity pathway, Slt2. The data indicate that the generation of reactive oxygen species by the electron transport chain is a primary mechanism by which farnesol kills cells. The Pkc1 signaling pathway regulates farnesol-mediated cell death through management of the generation of reactive oxygen species.

Activity of complex III of the mitochondrial electron transport chain is essential for early heart muscle cell differentiation

2004 ◽  
Vol 18 (11) ◽  
pp. 1300-1302 ◽  
Author(s):  
Dimitry Spitkovsky ◽  
Philipp Sasse ◽  
Eugen Kolossov ◽  
Cornelia Böttinger ◽  
Bernd K. Fleischmann ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Electron Transport ◽  
Muscle Cell ◽  
Heart Muscle ◽  
Electron Transport Chain ◽  
Complex Iii ◽  
Mitochondrial Electron Transport Chain ◽  
Heart Muscle Cell ◽  
Muscle Cell Differentiation ◽  
Transport Chain

scholarly journals Inhibition of Mitochondrial Complex III in Candida Albicans ADH1 Deletion Mutant Attenuates Its Pathogenicity Significantly

2021 ◽  
Author(s):  
Hui Guo ◽  
Yi Shan Zhang ◽  
Yan Jun Song ◽  
Ya Jing Zhao ◽  
Shui Xiu Li ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Alternative Oxidase ◽  
Oxidase Inhibitor ◽  
Complex Iii ◽  
Ros Production ◽  
Mitochondrial Complex ◽  
Aerobic Growth ◽  
Transport Chain ◽  
Atp Generation

Abstract Fermentation and aerobic respiration in mitochondria are coordinately regulated and compensated either when C. albicans grows in vitro or in the hosts, and the creature gain the strong viability. It’s insufficient to influent the growth, reproduction and pathogenicity of C. albicans by inhibiting the electron transport chain (ECT) CI, CII, CIII, CV, or fermentation related gene ADH1. Our study showed that the induction of AA (inhibitor of complex III) rather than SHAM (alternative oxidase inhibitor) abolishes the mitochondrial function completely （96% less ATP generation, 59% reduction in MMP), and increases ROS production significantly in ADH1-deleted mutant ( adh1Δ/ adh1Δ ) that in turn becomes hypersensitive to azole and apoptosis, less viable and more difficult to form hyphae. At the same time, the expression of virulence related genes ALS3 and HWP1 were significantly lower than that of WT under AA induction. Under the induction of AA, the mitochondrial function of WT was slightly damaged and cell apoptosis increased slightly，ROS production and sensitivity of azoles increased significantly, but mycelium formation and the growth of cells were not affected. Under aerobic growth, we observed an ADH1 - dependent mitochondrial effect in C. albicans demonstrated by 64% less ATP generation, 58% reduction in MMP and significant elevations of the ROS and apoptosis in ADH1 -deleted mutant. However, mycelium formation and azole susceptibility are not affected. Our results suggested that ADH1 plus CIII played an important role in antifungal activity by damaging mitochondrial function, inhibiting cell growth and hyphae formation, promoting apoptosis and reducing pathogenicity.

scholarly journals Differential remodeling of the electron transport chain is required to support TLR3 and TLR4 signaling and cytokine production in macrophages

2019 ◽  
Author(s):  
Duale Ahmed ◽  
David Roy ◽  
Allison Jaworski ◽  
Alex Edwards ◽  
Alfonso Abizaid ◽  
...  
Keyword(s):  
Electron Transport ◽  
Immune Responses ◽  
Electron Transport Chain ◽  
Cytokine Production ◽  
Critical Role ◽  
Innate Immune ◽  
Fine Tuning ◽  
Complex Iii ◽  
Innate Immune Responses ◽  
Transport Chain

AbstractIncreasing evidence suggests that mitochondria play a critical role in driving innate immune responses against bacteria and viruses. However, it is unclear if differential reprogramming of mitochondrial function contributes to the fine tuning of pathogen specific immune responses. Here, we found that TLR3 and TLR4 engagement on murine bone marrow derived macrophages was associated with differential remodeling of electron transport chain complex expression. This remodeling was associated with differential accumulation of mitochondrial and cytosolic ROS, which were required to support ligand specific inflammatory and antiviral cytokine production. We also found that the magnitude of TLR3, but not TLR4, responses were modulated by glucose availability. Under conditions of low glucose conditions, TLR3 engagement was associated with increased ETC complex III expression, increased mitochondrial and cytosolic ROS and increased inflammatory and antiviral cytokine production. This amplification was selectively reversed by targeting superoxide production from the outer Q-binding site of the ETC complex III. These results suggest that ligand specific modulation of the ETC may act as a rheostat that fine-tunes innate immune responses via mitochondrial ROS production. Modulation of these processes may represent a novel mechanism to modulate the nature as well as the magnitude of antiviral versus inflammatory immune responses.

scholarly journals Inositol hexakisphosphate kinase-2 determines cellular energy dynamics by regulating creatine kinase-B

2021 ◽  
Vol 118 (6) ◽  
pp. e2020695118
Author(s):  
Latika Nagpal ◽  
Michael D. Kornberg ◽  
Lauren K. Albacarys ◽  
Solomon H. Snyder
Keyword(s):  
Creatine Kinase ◽  
Energy Homeostasis ◽  
Combined Treatment ◽  
Complex Iii ◽  
Inositol Hexakisphosphate ◽  
Transport Chain ◽  
Creatine Kinase B ◽  
Protein Interactome ◽  
Key Enzyme ◽  
Cellular Apoptosis

Inositol hexakisphosphate kinases (IP6Ks) regulate various biological processes. IP6Ks convert IP6 to pyrophosphates such as diphosphoinositol pentakisphosphate (IP7) and bis-diphosphoinositol tetrakisphosphate (IP8). IP7 is produced in mammals by a family of inositol hexakisphosphate kinases, IP6K1, IP6K2, and IP6K3, which have distinct biological functions. The inositol hexakisphosphate kinase 2 (IP6K2) controls cellular apoptosis. To explore roles for IP6K2 in brain function, we elucidated its protein interactome in mouse brain revealing a robust association of IP6K2 with creatine kinase-B (CK-B), a key enzyme in energy homeostasis. Cerebella of IP6K2-deleted mice (IP6K2-knockout [KO]) produced less phosphocreatine and ATP and generated higher levels of reactive oxygen species and protein oxidative damage. In IP6K2-KO mice, mitochondrial dysfunction was associated with impaired expression of the cytochrome-c1 subunit of complex III of the electron transport chain. We reversed some of these effects by combined treatment with N-acetylcysteine and phosphocreatine. These findings establish a role for IP6K2–CK-B interaction in energy homeostasis associated with neuroprotection.

Assessment of Impacts of Coal Mining–Induced Subsidence on Native Flora and Native Forest Land: A Brief Review

2020 ◽  
pp. 141-152
Author(s):  
Ashish Kumar Vishwakarma ◽  
Rajesh Rai ◽  
Ashwani Kumar Sonkar ◽  
Tusarkanta Behera ◽  
Bal Krishna Shrivastva
Keyword(s):  
Coal Mining ◽  
Native Forest ◽  
Forest Land ◽  
Native Flora
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