Photocatalytic TiO2/CdS/ZnS nanocomposite induces Bacillus subtilis cell death by disrupting its metabolism and membrane integrity

2021 ◽  
Author(s):  
Naveen Kumar ◽  
Anuj Mittal ◽  
Monika Yadav ◽  
Shankar Sharma ◽  
Tarun Kumar ◽  
...  
Keyword(s):  
Cell Death ◽  
Bacillus Subtilis ◽  
Membrane Integrity ◽  
Subtilis Cell ◽  
Photocatalytic Tio2

Quercetin in attenuation of ischemic/reperfusion injury: A review

2020 ◽  
Vol 13 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Saeed Samarghandian ◽  
Kiavash Hushmandi ◽  
Amirhossein Zabolian ◽  
Md Shahinozzaman ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Membrane ◽  
Blood Supply ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Membrane Integrity ◽  
Therapeutic Effects ◽  
Molecular Pathways ◽  
Cell Membrane Integrity ◽  
Cell Membrane Disruption

Background: Ischemia/reperfusion (I/R) injury is a serious pathologic event that occurs due to restriction in blood supply to an organ, followed by hypoxia. This condition leads to enhanced levels of pro-inflammatory cytokines such as IL-6 and TNF-, and stimulation of oxidative stress via enhancing reactive oxygen species (ROS) levels. Upon reperfusion, blood supply increases, but it deteriorates condition, and leads to generation of ROS, cell membrane disruption and finally, cell death. Plant derived-natural compounds are well-known due to their excellent antioxidant and anti-inflammatory activities. Quercetin is a flavonoid exclusively found in different vegetables, herbs, and fruits. This naturally occurring compound possesses different pharmacological activities making it appropriate option in disease therapy. Quercetin can also demonstrate therapeutic effects via affecting molecular pathways such as NF-B, PI3K/Akt and so on. Methods: In the present review, we demonstrate that quercetin administration is beneficial in ameliorating I/R injury via reducing ROS levels, inhibition of inflammation, and affecting molecular pathways such as TLR4/NF-B, MAPK and so on. Results and conclusion: Quercetin can improve cell membrane integrity via decreasing lipid peroxidation. Apoptotic cell death is inhibited by quercetin via down-regulation of Bax, and caspases, and upregulation of Bcl-2. Quercetin is able to modulate autophagy (inhibition/induction) in decreasing I/R injury. Nanoparticles have been applied for delivery of quercetin, enhancing its bioavailability and efficacy in alleviation of I/R injury. Noteworthy, clinical trials have also confirmed the capability of quercetin in reducing I/R injury.

scholarly journals Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 845
Author(s):  
Anja Sadžak ◽  
Ignacija Vlašić ◽  
Zoran Kiralj ◽  
Marijana Batarelo ◽  
Nada Oršolić ◽  
...  
Keyword(s):  
Cell Death ◽  
Intracellular Signaling ◽  
Chromatin Condensation ◽  
Membrane Integrity ◽  
Toxic Effects ◽  
Trypan Blue Exclusion ◽  
Atp Production ◽  
Mtt Method ◽  
Biophysical Approach ◽  
Induced Changes

Oxidative stress (OS) induced by the disturbed homeostasis of metal ions is one of the pivotal factors contributing to neurodegeneration. The aim of the present study was to investigate the effects of flavonoid myricetin on copper-induced toxicity in neuroblastoma SH-SY5Y cells. As determined by the MTT method, trypan blue exclusion assay and measurement of ATP production, myricetin heightened the toxic effects of copper and exacerbated cell death. It also increased copper-induced generation of reactive oxygen species, indicating the prooxidative nature of its action. Furthermore, myricetin provoked chromatin condensation and loss of membrane integrity without caspase-3 activation, suggesting the activation of both caspase-independent programmed cell death and necrosis. At the protein level, myricetin-induced upregulation of PARP-1 and decreased expression of Bcl-2, whereas copper-induced changes in the expression of p53, p73, Bax and NME1 were not further affected by myricetin. Inhibitors of ERK1/2 and JNK kinases, protein kinase A and L-type calcium channels exacerbated the toxic effects of myricetin, indicating the involvement of intracellular signaling pathways in cell death. We also employed atomic force microscopy (AFM) to evaluate the morphological and mechanical properties of SH-SY5Y cells at the nanoscale. Consistent with the cellular and molecular methods, this biophysical approach also revealed a myricetin-induced increase in cell surface roughness and reduced elasticity. Taken together, we demonstrated the adverse effects of myricetin, pointing out that caution is required when considering powerful antioxidants for adjuvant therapy in copper-related neurodegeneration.

Accumulation of a recombinant Aspergillus oryzae lipase artificially localized on the Bacillus subtilis cell surface

2000 ◽  
Vol 90 (4) ◽  
pp. 422-425 ◽  
Author(s):  
Gota Kobayashi ◽  
Jinichi Toida ◽  
Takashi Akamatsu ◽  
Hiroki Yamamoto ◽  
Toshio Shida ◽  
...  
Keyword(s):  
Bacillus Subtilis ◽  
Cell Surface ◽  
Aspergillus Oryzae ◽  
Subtilis Cell

scholarly journals Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production

Blood ◽  
2012 ◽  
Vol 119 (10) ◽  
pp. 2368-2375 ◽  
Author(s):  
Guilherme B. Fortes ◽  
Leticia S. Alves ◽  
Rosane de Oliveira ◽  
Fabianno F. Dutra ◽  
Danielle Rodrigues ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Critical Role ◽  
Membrane Integrity ◽  
Iron Chelation ◽  
Heme Oxygenase 1 ◽  
Cytotoxic Effects ◽  
Interacting Protein ◽  
Free Heme ◽  
Necrosis Factor

Abstract Diseases that cause hemolysis or myonecrosis lead to the leakage of large amounts of heme proteins. Free heme has proinflammatory and cytotoxic effects. Heme induces TLR4-dependent production of tumor necrosis factor (TNF), whereas heme cytotoxicity has been attributed to its ability to intercalate into cell membranes and cause oxidative stress. We show that heme caused early macrophage death characterized by the loss of plasma membrane integrity and morphologic features resembling necrosis. Heme-induced cell death required TNFR1 and TLR4/MyD88-dependent TNF production. Addition of TNF to Tlr4−/− or to Myd88−/− macrophages restored heme-induced cell death. The use of necrostatin-1, a selective inhibitor of receptor-interacting protein 1 (RIP1, also known as RIPK1), or cells deficient in Rip1 or Rip3 revealed a critical role for RIP proteins in heme-induced cell death. Serum, antioxidants, iron chelation, or inhibition of c-Jun N-terminal kinase (JNK) ameliorated heme-induced oxidative burst and blocked macrophage cell death. Macrophages from heme oxygenase-1 deficient mice (Hmox1−/−) had increased oxidative stress and were more sensitive to heme. Taken together, these results revealed that heme induces macrophage necrosis through 2 synergistic mechanisms: TLR4/Myd88-dependent expression of TNF and TLR4-independent generation of ROS.

scholarly journals Gene-dependent yeast cell death pathway requires AP-3 vesicle trafficking leading to vacuole membrane permeabilization

2021 ◽  
Author(s):  
Zachary D Stolp ◽  
Madhura Kulkarni ◽  
Yining Liu ◽  
Chengzhang Zhu ◽  
Alizay Jalisi ◽  
...  
Keyword(s):  
Cell Death ◽  
Yeast Cell ◽  
Vesicle Trafficking ◽  
Membrane Integrity ◽  
Time Lapse ◽  
Membrane Permeabilization ◽  
Cell Death Pathway ◽  
Sequence Of Events ◽  
A Genome ◽  
Lysosome Membrane

Unicellular eukaryotes are suggested to undergo self-inflicted destruction. However, molecular details are sparse by comparison to the mechanisms of cell death known for human cells and animal models. Here we report a molecular pathway in Saccharomyces cerevisiae leading to vacuole/lysosome membrane permeabilization and cell death. Following exposure to heat-ramp conditions, a model of environmental stress, we observed that yeast cell death occurs over several hours, suggesting an ongoing molecular dying process. A genome-wide screen for death-promoting factors identified all subunits of the AP-3 adaptor complex. AP-3 promotes stress-induced cell death through its Arf1-GTPase-dependent vesicle trafficking function, which is required to transport and install proteins on the vacuole/lysosome membrane, including a death-promoting protein kinase Yck3. Time-lapse microscopy revealed a sequence of events where AP-3-dependent vacuole permeability occurs hours before the loss of plasma membrane integrity. An AP-3-dependent cell death pathway appears to be conserved in the human pathogen Cryptococcus neoformans.

Mechanisms of death induced by cisplatin in proximal tubular epithelial cells: apoptosis vs. necrosis

1996 ◽  
Vol 270 (4) ◽  
pp. F700-F708 ◽  
Author(s):  
W. Lieberthal ◽  
V. Triaca ◽  
J. Levine
Keyword(s):  
Cell Death ◽  
Dna Cleavage ◽  
Primary Cultures ◽  
Cell Monolayer ◽  
Membrane Integrity ◽  
Ladder Pattern ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
High Concentrations ◽  
Induced Apoptosis

We have examined the mechanisms of cell death induced by cisplatin in primary cultures of mouse proximal tubular cells. High concentrations of cisplatin (800 microM) led to necrotic cell death over a few hours. Much lower concentrations of cisplatin (8 microM) led to apoptosis, which caused loss of the cell monolayer over several days. Necrosis was characterized by a cytosolic swelling and early loss of plasma membrane integrity. In contrast, early features of cells undergoing apoptosis included cell shrinkage and loss of attachment to the monolayers. Nuclear chromatin became condensed and fragmented in apoptosing cells. These features were absent in necrotic cells. DNA electrophoresis of cells exposed to 800 microM cisplatin yielded a "smear" pattern, due to random DNA degradation. In contrast, the DNA of apoptosing cells demonstrated a "ladder" pattern resulting from internucleosomal DNA cleavage. Antioxidants delayed cisplatin-induced apoptosis but not necrosis. Thus the mechanism of cell death induced by cisplatin is concentration dependent. Reactive oxygen species play a role in mediating apoptosis but not necrosis induced by cisplatin.

Repeated use of Bacillus subtilis cell walls for copper binding

1994 ◽  
Vol 10 (4) ◽  
pp. 472-474 ◽  
Author(s):  
R. J. C. McLean ◽  
A. M. Campbell ◽  
P. T. Khu ◽  
A. T. Persaud ◽  
L. E. Bickerton ◽  
...  
Keyword(s):  
Bacillus Subtilis ◽  
Cell Walls ◽  
Copper Binding ◽  
Subtilis Cell ◽  
Repeated Use

scholarly journals Bacillus subtilis cell diameter is determined by the opposing actions of two distinct cell wall synthetic systems

2019 ◽  
Vol 4 (8) ◽  
pp. 1294-1305 ◽  
Author(s):  
Michael F. Dion ◽  
Mrinal Kapoor ◽  
Yingjie Sun ◽  
Sean Wilson ◽  
Joel Ryan ◽  
...  
Keyword(s):  
Cell Wall ◽  
Bacillus Subtilis ◽  
Cell Diameter ◽  
Subtilis Cell ◽  
Distinct Cell
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