Synergistic combination of direct plasma membrane damage and oxidative stress as a cause of antifungal activity of polyol macrolide antibiotic niphimycin

2002 ◽  
Vol 94 (3) ◽  
pp. 207-211 ◽  
Author(s):  
Keiji Nakayama ◽  
Takafumi Yamaguchi ◽  
Takeshi Doi ◽  
Yoshinosuke Usuki ◽  
Makoto Taniguchi ◽  
...  
2010 ◽  
Vol 61 (4) ◽  
pp. 274-279 ◽  
Author(s):  
Jia Liu ◽  
Yuanyuan Zong ◽  
Guozheng Qin ◽  
Boqiang Li ◽  
Shiping Tian

2016 ◽  
Vol 43 (10) ◽  
pp. 973 ◽  
Author(s):  
Griselda Podazza ◽  
Marta Arias ◽  
Fernando E. Prado

The effect of cadmium on roots of four citrus rootstocks was studied to assess the relationships between oxidative stress, carbohydrates, phenolics and antioxidant responses. Swingle citrumelo (SC), Rangpur lime (RL), Troyer citrange (TC) and Volkamer lemon (VL) genotypes were exposed to 0, 5 and 10 µM Cd over 7 days, after which Cd accumulation was markedly higher in roots compared with stems and leaves. Malondialdehyde (MDA) and lipoxygenase (LOX) activity increased in Cd-treated SC and RL roots, suggesting that a lipid peroxidation is the main driver of plasma membrane damage. In contrast, in TC and VL genotypes, LOX-mediated lipid peroxidation does not appear to play a key role in Cd-induced lipid peroxidation, but H2O2 accumulation seems to be responsible of less plasma membrane damage. Catalase (CAT), superoxide dismutase (SOD) and guaiacol and syringaldazine peroxidases (G-POD and S-POD respectively) were differentially affected by Cd. Lipid profile and ATPase-dependant proton extrusion indicated higher disfunctionalities of root plasma membrane in SC and RL genotypes than in TC and VL genotypes. Differences in carbohydrates and phenolic compounds were also observed. Histochemical analysis of G-POD activity and lignin and suberin deposition revealed differences among genotypes. A model to explain the relationships among carbohydrates, soluble phenolics, lipid peroxidation and H2O2 accumulation in Cd-exposed roots was proposed.


2021 ◽  
Vol 7 (13) ◽  
pp. eabc6345
Author(s):  
Shrawan Kumar Mageswaran ◽  
Wei Yuan Yang ◽  
Yogaditya Chakrabarty ◽  
Catherine M. Oikonomou ◽  
Grant J. Jensen

Cryo–electron tomography (cryo-ET) provides structural context to molecular mechanisms underlying biological processes. Although straightforward to implement for studying stable macromolecular complexes, using it to locate short-lived structures and events can be impractical. A combination of live-cell microscopy, correlative light and electron microscopy, and cryo-ET will alleviate this issue. We developed a workflow combining the three to study the ubiquitous and dynamic process of shedding in response to plasma membrane damage in HeLa cells. We found filopodia-like protrusions enriched at damage sites and acting as scaffolds for shedding, which involves F-actin dynamics, myosin-1a, and vacuolar protein sorting 4B (a component of the ‘endosomal sorting complex required for transport’ machinery). Overall, shedding is more complex than current models of vesiculation from flat membranes. Its similarities to constitutive shedding in enterocytes argue for a conserved mechanism. Our workflow can also be adapted to study other damage response pathways and dynamic cellular events.


BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Dustin A. Ammendolia ◽  
William M. Bement ◽  
John H. Brumell

AbstractPlasma membrane integrity is essential for cellular homeostasis. In vivo, cells experience plasma membrane damage from a multitude of stressors in the extra- and intra-cellular environment. To avoid lethal consequences, cells are equipped with repair pathways to restore membrane integrity. Here, we assess plasma membrane damage and repair from a whole-body perspective. We highlight the role of tissue-specific stressors in health and disease and examine membrane repair pathways across diverse cell types. Furthermore, we outline the impact of genetic and environmental factors on plasma membrane integrity and how these contribute to disease pathogenesis in different tissues.


Biology Open ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. bio035287 ◽  
Author(s):  
Lars Nygård Skalman ◽  
Mikkel R. Holst ◽  
Elin Larsson ◽  
Richard Lundmark

1998 ◽  
Vol 110 (1) ◽  
pp. 79-83 ◽  
Author(s):  
Sally H. Ibbotson ◽  
Christopher R. Lambert ◽  
Michael N. Moran ◽  
Mary C. Lynch ◽  
Irene E. Kochevar

2019 ◽  
Author(s):  
Kai S. Beckwith ◽  
Marianne S. Beckwith ◽  
Sindre Ullmann ◽  
Ragnhild Sætra ◽  
Haelin Kim ◽  
...  

AbstractMycobacterium tuberculosis (Mtb) is a major global health problem and causes extensive cytotoxicity in patient cells and tissues. Here we define an NLRP3, caspase-1 and gasdermin D-mediated pathway to pyroptosis in human monocytes following exposure to Mtb. We demonstrate an ESX-1 mediated, contact-induced plasma membrane (PM) damage response that occurs during phagocytosis or from the cytosolic side of the PM after phagosomal rupture in Mtb infected cells. This PM injury in turn causes K+ efflux and activation of NLRP3 dependent IL-1β release and pyroptosis, facilitating the spread of Mtb to neighbouring cells. Further we reveal a dynamic interplay of pyroptosis with ESCRT-mediated PM repair. Collectively, these findings reveal a novel mechanism for pyroptosis and spread of infection acting through dual PM disturbances both during and after phagocytosis. We also highlight dual PM damage as a common mechanism utilized by other NLRP3 activators that have previously been shown to act through lysosomal damage.Graphical abstract


2019 ◽  
Vol 6 (4) ◽  
pp. 1219-1232 ◽  
Author(s):  
Saeed Nazemidashtarjandi ◽  
Amir M. Farnoud

Plasma membrane damage is one of the primary mechanisms through which engineered nanoparticles induce cell toxicity.


Sign in / Sign up

Export Citation Format

Share Document