scholarly journals Antimicrobial Susceptibility and Antibacterial Mechanism of Limonene against Listeria monocytogenes

Molecules ◽  
2019 ◽  
Vol 25 (1) ◽  
pp. 33 ◽  
Author(s):  
Yingjie Han ◽  
Zhichang Sun ◽  
Wenxue Chen
Keyword(s):  
Listeria Monocytogenes ◽  
Cell Membrane ◽  
Respiratory Chain ◽  
Antimicrobial Susceptibility ◽  
Chain Complex ◽  
Cell Membrane Permeability ◽  
Wall Structure ◽  
Antibacterial Mechanism ◽  
Respiratory Chain Complex ◽  
Complex Activity

Limonene is a monoterpenoid compound, which is founded in a lot of plants’ essential oils with good antibacterial activity against food-borne pathogens, but it has an ambiguous antimicrobial susceptibility and mechanism against Listeria monocytogenes (L. monocytogenes). In this study, the antimicrobial susceptibility of Limonene to L. monocytogenes was studied, and some new sights regarding its antibacterial mechanism were further explored. Scanning electron microscopy (SEM) verified that limonene caused the destruction of the cell integrity and wall structure of L. monocytogenes. The increase in conductivity and the leakage of intracellular biomacromolecules (nucleic acids and proteins) confirmed that limonene had an obvious effect on cell membrane permeability. The results of Propidium Iodide (PI) fluorescence staining were consistent with the results of the conductivity measurements. This indicated that limonene treatment caused damage to the L. monocytogenes cell membrane. Furthermore, the decrease in ATP content, ATPase (Na+K+-ATPase, Ca2+-ATPase) activity and respiratory chain complex activity indicated that limonene could hinder ATP synthesis by inhibiting the activity of the respiratory complex and ATPase. Finally, differential expression of proteins in the respiratory chain confirmed that limonene affected respiration and energy metabolism by inhibiting the function of the respiratory chain complex.

scholarly journals Glutathione and respiratory chain complex activity in duodenal mitochondria of broilers with low and high feed efficiency

2005 ◽  
Vol 84 (5) ◽  
pp. 782-788 ◽  
Author(s):  
C. Ojano-Dirain ◽  
M. Iqbal ◽  
T. Wing ◽  
M. Cooper ◽  
W. Bottje
Keyword(s):  
Respiratory Chain ◽  
Feed Efficiency ◽  
Chain Complex ◽  
Respiratory Chain Complex ◽  
Complex Activity ◽  
High Feed

Exercise can induce temporary mitochondrial and contractile dysfunction linked to impaired respiratory chain complex activity

Metabolism ◽  
2012 ◽  
Vol 61 (1) ◽  
pp. 117-126 ◽  
Author(s):  
Maria Schoepe ◽  
Andrea Schrepper ◽  
Michael Schwarzer ◽  
Moritz Osterholt ◽  
Torsten Doenst
Keyword(s):  
Respiratory Chain ◽  
Chain Complex ◽  
Contractile Dysfunction ◽  
Respiratory Chain Complex ◽  
Complex Activity

Biochemical Assays of Respiratory Chain Complex Activity

2007 ◽  
pp. 93-119 ◽  
Author(s):  
Denise M. Kirby ◽  
David R. Thorburn ◽  
Douglass M. Turnbull ◽  
Robert W. Taylor
Keyword(s):  
Respiratory Chain ◽  
Chain Complex ◽  
Respiratory Chain Complex ◽  
Complex Activity ◽  
Biochemical Assays

scholarly journals Identification of novel genes involved in apoptosis of HIV-infected macrophages using unbiased genome-wide screening

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Simon X. M. Dong ◽  
Frederick S. Vizeacoumar ◽  
Kalpana K. Bhanumathy ◽  
Nezeka Alli ◽  
Cristina Gonzalez-Lopez ◽  
...  
Keyword(s):  
T Cells ◽  
Hiv Infection ◽  
Respiratory Chain ◽  
Cd4 T Cells ◽  
Chain Complex ◽  
Respiratory Chain Complex ◽  
Complex Ii ◽  
Genome Wide ◽  
Latently Infected ◽  
Induced Apoptosis

Abstract Background Macrophages, besides resting latently infected CD4+ T cells, constitute the predominant stable, major non-T cell HIV reservoirs. Therefore, it is essential to eliminate both latently infected CD4+ T cells and tissue macrophages to completely eradicate HIV in patients. Until now, most of the research focus is directed towards eliminating latently infected CD4+ T cells. However, few approaches have been directed at killing of HIV-infected macrophages either in vitro or in vivo. HIV infection dysregulates the expression of many host genes essential for the survival of infected cells. We postulated that exploiting this alteration may yield novel targets for the selective killing of infected macrophages. Methods We applied a pooled shRNA-based genome-wide approach by employing a lentivirus-based library of shRNAs to screen novel gene targets whose inhibition should selectively induce apoptosis in HIV-infected macrophages. Primary human MDMs were infected with HIV-eGFP and HIV-HSA viruses. Infected MDMs were transfected with siRNAs specific for the promising genes followed by analysis of apoptosis by flow cytometry using labelled Annexin-V in HIV-infected, HIV-exposed but uninfected bystander MDMs and uninfected MDMs. The results were analyzed using student’s t-test from at least four independent experiments. Results We validated 28 top hits in two independent HIV infection models. This culminated in the identification of four target genes, Cox7a2, Znf484, Cstf2t, and Cdk2, whose loss-of-function induced apoptosis preferentially in HIV-infected macrophages. Silencing these single genes killed significantly higher number of HIV-HSA-infected MDMs compared to the HIV-HSA-exposed, uninfected bystander macrophages, indicating the specificity in the killing of HIV-infected macrophages. The mechanism governing Cox7a2-mediated apoptosis of HIV-infected macrophages revealed that targeting respiratory chain complex II and IV genes also selectively induced apoptosis of HIV-infected macrophages possibly through enhanced ROS production. Conclusions We have identified above-mentioned novel genes and specifically the respiratory chain complex II and IV genes whose silencing may cause selective elimination of HIV-infected macrophages and eventually the HIV-macrophage reservoirs. The results highlight the potential of the identified genes as targets for eliminating HIV-infected macrophages in physiological environment as part of an HIV cure strategy.

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