Early interconnectivity between metabolic and defense events against oxidative stress induced by cadmium in roots of four citrus rootstocks

2016 ◽  
Vol 43 (10) ◽  
pp. 973 ◽  
Author(s):  
Griselda Podazza ◽  
Marta Arias ◽  
Fernando E. Prado
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Plasma Membrane ◽  
Membrane Damage ◽  
Soluble Phenolics ◽  
Rangpur Lime ◽  
Plasma Membrane Damage ◽  
H2o2 Accumulation ◽  
Volkamer Lemon ◽  
Main Driver

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.

scholarly journals Ferroptotic pores induce Ca2+ fluxes and ESCRT-III activation to modulate cell death kinetics

2020 ◽  
Author(s):  
Lohans Pedrera ◽  
Rafael A. Espiritu ◽  
Uris Ros ◽  
Josephine Weber ◽  
Anja Schmitt ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Plasma Membrane ◽  
Membrane Damage ◽  
Protective Mechanism ◽  
Membrane Repair ◽  
Membrane Rupture ◽  
Plasma Membrane Damage ◽  
Regulated Necrosis ◽  
Sustained Increase

AbstractFerroptosis is an iron-dependent form of regulated necrosis associated with lipid peroxidation. Despite its key role in the inflammatory outcome of ferroptosis, little is known about the molecular events leading to the disruption of the plasma membrane during this type of cell death. Here we show that a sustained increase in cytosolic Ca2+ is a hallmark of ferroptosis that precedes complete bursting of the cell. We report that plasma membrane damage leading to ferroptosis is associated with membrane nanopores of a few nanometers in radius and that ferroptosis, but not lipid peroxidation, can be delayed by osmoprotectants. Importantly, Ca2+ fluxes during ferroptosis induce the activation of the ESCRT-III-dependent membrane repair machinery, which counterbalances the kinetics of cell death and modulates the immunological signature of ferroptosis. Our findings with ferroptosis provide a unifying concept that sustained increase of cytosolic Ca2+ prior to plasma membrane rupture is a common feature of regulated types of necrosis and position ESCRT-III activation as a general protective mechanism in these lytic cell death pathways.

scholarly journals Ferroptotic pores induce Ca2+ fluxes and ESCRT-III activation to modulate cell death kinetics

2019 ◽  
Author(s):  
Lohans Pedrera ◽  
Rafael A. Espiritu ◽  
Uris Ros ◽  
Anja Schmitt ◽  
Stephan Hailfinger ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Plasma Membrane ◽  
Membrane Damage ◽  
Protective Mechanism ◽  
Membrane Repair ◽  
Plasma Membrane Damage ◽  
Molecular Events ◽  
Regulated Necrosis ◽  
Dependent Form

SummaryFerroptosis is an iron-dependent form of regulated necrosis associated with lipid peroxidation. Despite its key role in the inflammatory outcome of ferroptosis, little is known about the molecular events leading to the disruption of the plasma membrane during this type of cell death. Here we show that a sustained increase in cytosolic Ca2+ is a hallmark of ferroptosis that precedes complete bursting of the cell. We report that plasma membrane damage leading to ferroptosis is associated with membrane nanopores of few nanometers in radius and that ferroptosis, but not lipid peroxidation, can be delayed by osmoprotectants. Importantly, Ca2+ fluxes during ferroptosis correlate with the activation of ESCRT-III-mediated membrane repair, which counterbalances the kinetics of cell death and modulates the inflammatory signature of ferroptosis. Our findings with ferroptosis provide a unifying concept that sustained high levels of cytosolic Ca2+ prior to plasma membrane disruption are a common feature of regulated necrosis and position ESCRT-III as a general protective mechanism in these inflammatory cell death pathways.

scholarly journals A cryo–electron tomography workflow reveals protrusion-mediated shedding on injured plasma membrane

2021 ◽  
Vol 7 (13) ◽  
pp. eabc6345
Author(s):  
Shrawan Kumar Mageswaran ◽  
Wei Yuan Yang ◽  
Yogaditya Chakrabarty ◽  
Catherine M. Oikonomou ◽  
Grant J. Jensen
Keyword(s):  
Plasma Membrane ◽  
Molecular Mechanisms ◽  
Electron Tomography ◽  
Membrane Damage ◽  
Light And Electron Microscopy ◽  
Actin Dynamics ◽  
Endosomal Sorting ◽  
Plasma Membrane Damage ◽  
Cryo Electron Tomography ◽  
Vacuolar Protein

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.

scholarly journals Plasma membrane integrity: implications for health and disease

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Dustin A. Ammendolia ◽  
William M. Bement ◽  
John H. Brumell
Keyword(s):  
Plasma Membrane ◽  
Membrane Damage ◽  
Membrane Integrity ◽  
Whole Body ◽  
Plasma Membrane Integrity ◽  
Plasma Membrane Damage ◽  
Cellular Environment ◽  
Health And Disease ◽  
Repair Pathways ◽  
The Impact

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.

scholarly journals Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane pore

Biology Open ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. bio035287 ◽  
Author(s):  
Lars Nygård Skalman ◽  
Mikkel R. Holst ◽  
Elin Larsson ◽  
Richard Lundmark
Keyword(s):  
Plasma Membrane ◽  
Membrane Damage ◽  
Listeriolysin O ◽  
Membrane Pore ◽  
Plasma Membrane Damage

scholarly journals Benzoyl Peroxide Increases UVA-Induced Plasma Membrane Damage and Lipid Oxidation in Murine Leukemia L1210 Cells

1998 ◽  
Vol 110 (1) ◽  
pp. 79-83 ◽  
Author(s):  
Sally H. Ibbotson ◽  
Christopher R. Lambert ◽  
Michael N. Moran ◽  
Mary C. Lynch ◽  
Irene E. Kochevar
Keyword(s):  
Plasma Membrane ◽  
Lipid Oxidation ◽  
Benzoyl Peroxide ◽  
Membrane Damage ◽  
Plasma Membrane Damage ◽  
L1210 Cells ◽  
Murine Leukemia

scholarly journals Plasma membrane damage causes NLRP3 activation and pyroptosis during Mycobacterium tuberculosis infection

2019 ◽  
Author(s):  
Kai S. Beckwith ◽  
Marianne S. Beckwith ◽  
Sindre Ullmann ◽  
Ragnhild Sætra ◽  
Haelin Kim ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Plasma Membrane ◽  
Membrane Damage ◽  
Common Mechanism ◽  
Mycobacterium Tuberculosis Infection ◽  
Plasma Membrane Damage ◽  
Cytosolic Side ◽  
Infected Cells ◽  
Mediated Contact ◽  
Spread Of Infection

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

Membrane outer leaflet is the primary regulator of membrane damage induced by silica nanoparticles in vesicles and erythrocytes

2019 ◽  
Vol 6 (4) ◽  
pp. 1219-1232 ◽  
Author(s):  
Saeed Nazemidashtarjandi ◽  
Amir M. Farnoud
Keyword(s):  
Plasma Membrane ◽  
Silica Nanoparticles ◽  
Membrane Damage ◽  
Engineered Nanoparticles ◽  
Cell Toxicity ◽  
Outer Leaflet ◽  
Plasma Membrane Damage

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

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