نتایج جستجو برای: Lysosomes Oxidative stress
تعداد نتایج: 489590 فیلتر نتایج به سال:
this study was conducted to evaluate the cytoprotection of various extracts and bioactive compounds found in pistacia vera againts cytotoxicity, ros formation, lipid peroxidation, protein carbonylation , mitochondrial and lysosomal membrane damages in cell toxicity models of diabetes related carbonyl (glyoxal) and oxidative stress (hydroperoxide). methanol, water and ethyl acetate were used to ...
dacarbazine (dtic) is a synthetic chemical antitumor agent which is used to treat malignant melanoma and hodgkin’s disease. dtic is a prodrug which is converted to an active form undergoing demethylation by liver enzymes. the active form prevents the progress of disease via alkylation of dna strand. in the structure of this drug, the imidazole ring, a triazen chain and carboxamide group exist. ...
chloroacetaldehyde (caa) is a chlorination by-product in finished drinking water and a toxic metabolite of a wide variety of industrial chemicals (e.g. vinyl chloride) and chemotherapeutic agents (e.g. cyclophosphamide and ifosfamide). in this research, the cytotoxic mechanisms of caa in freshly isolated rat hepatocytes were investigated.caa cytotoxicity was associated with reactive oxygen spec...
Graphene-based nanomaterials (GNMs), including graphene, graphene oxide, reduced and quantum dots, may have direct anticancer activity or be used as nanocarriers for antitumor drugs. GNMs usually enter tumor cells by endocytosis can accumulate in lysosomes. This accumulation prevents drugs bound to from reaching their targets, suppressing effects. A number of chemical modifications are made fac...
1 2 Cover picture: confocal microscopy images of APPswe cells double immunostained for Aβ oligomers (A11 antibody, red fluorescence) and LAMP-2 (green fluorescence). Nuclei were stained by DAPI (blue fluorescence). All previously published papers were reproduced with permission from the publisher. ABSTRACT Alzheimer's disease (AD), the major cause of senile dementia, is associated with progress...
The C-ETS2-TFEB Axis Promotes Neuron Survival under Oxidative Stress by Regulating Lysosome Activity
Excessive reactive oxygen species/reactive nitrogen species (ROS/RNS) produced as a result of ageing causes damage to macromolecules and organelles or leads to interference of cell signalling pathways, which in turn results in oxidative stress. Oxidative stress occurs in many neurodegenerative diseases (e.g., Parkinson's disease) and contributes to progressive neuronal loss. In this study, we s...
Background: Insulin downregulates GLUT4 by accelerating degradation in lysosomes. Results: Insulin through H2O2 production dissociates retromer from LDM membrane in a protein kinase CK2-dependent manner. Conclusion: Insulin switches GLUT4 traffic route toward lysosomes via retromer inhibition. Significance: This revealed a unique oxidative stress-mediated insulin signal cascade that regulates t...
The introduction of apo-ferritin or the iron chelator DFO (desferrioxamine) conjugated to starch into the lysosomal compartment protects cells against oxidative stress, lysosomal rupture and ensuing apoptosis/necrosis by binding intralysosomal redox-active iron, thus preventing Fenton-type reactions and ensuing peroxidation of lysosomal membranes. Because up-regulation of MTs (metallothioneins)...
Lysosomes, the cell's recycling center, undergo nutrient-sensitive adaptive changes in function and biogenesis, i.e., lysosomal adaptation. We recently discovered that lysosomes also mediate the cell's "survival" response (i.e., autophagy) to oxidative stress through the activation of TFEB (transcription factor EB), a master regulator of lysosome biogenesis and autophagy. MCOLN1/TRPML1, the pri...
................................................................................................................... 7 LIST OF PAPERS ........................................................................................................... 9 ABBREVIATIONS ....................................................................................................... 10 INTRODUCTION .......................
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