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the exposure to Alcausedcell death , Al(3
The release of cytochrome c from mitochondriacan causecell death ( apoptosis
the mitochondria [ R(passive) caused bycell death ( apoptosis
cancer cellscausingcell death ( apoptosis
these granules ... in turnwill causecell death ( apoptosis
The virus invades the small gutsubsequently causecell death ( apoptosis
that are not folded correctlycould ... causecell death ( apoptosis
Cd in kidneycould causecell death ( cytotoxicity
endogenous ROS levels ... if not resolvedcan causecell death [ 43][44
a membrane disruption effectcausescell death [ 95,96
cell detachmentcausescell death , anoikis
This condition ... the GSH productioncausesdopaminergic cell death
Although autophagy induction can function as a survival mechanism in response to cellular stress such as ROS , excessive autophagic activity is knownto causecell death
the mode by whichcausesNSCLC cell death
This state of oxidative stress ... all the important cellular components like proteins , DNA and membrane lipidscan causecell death
all the important cellular components like proteins , DNA and membrane lipidscan causecell death
However , overproduction of ROS or a decreased ability of the cell to remove ROS can result in increased levels of ROS , ... , oxidative DNA changes and protein and enzyme inactivationcausingcell death
During the third phase of apoptosis , free radicals and activated enzymes attack the cell protein structure and thereforecausingcell death
the reactive oxidation product to bind cellular components such as proteins , lipids , and DNAcausingcell death
that the substantial modification of the structure of mitochondria leads to disruption of their function , leading to a shutdown of the cellular activity and release of pro - apoptotic factorscausingcell death
Dysfunctional and damaged mitochondria generate excess ROS , which damage proteins , membrane lipids , nucleic acids , adjacent mitochondria and release proapoptotic proteins into the cytosolcausingcell death
ROS , which are able to damage plasma membranes , mitochondria and DNAcausingcell death
DNA and proteins ... the cellswill causecell death
Such oxidative and/or nitrative stress can damage the lipids , proteins and nucleic acids of cells and mitochondriapotentially causingcell death
protein response ( UPR ... different cellular pathwayscan causecell death
The formation of free radicals from oxidative stress can set off a chain reaction that damages DNA or cell membranesoften causingcell death
Through an oxidative stress which leads to production of high levels of reactive oxygen species , the normal cellular physiological pathways disruptedcausecell death
the progression of energy failure in the cell , as well as the severe cell swelling and accumulation of intracellular calciumcausecell death
tumour cells against the excessive accumulation of DNA damagewould ... causecell death
injury ... oxidizing proteins , DNA and membrane lipidscan causecell death
by calcium and ROS - induced mitochondrial disruption(passive) caused bycell death
important roles ... oxidative stress - induced cellular injury and apoptosiscausecell death
mitochondrial damage or caspase activation alone ... sufficientto causecell death
protein complexes known as caspases , which are required for the activation of other genescausecell death
The drug targets cells and breaks down their DNAcausingcell death
proteins , DNA and membrane lipidscan causecell death
When the defense mechanism fails , membranes , DNA , and proteins may be damagedcausingcell death
radiation damage biological protein and genetic material DNAcausingcell death
cellular proteins and DNAcausescell death
induced apoptosis through intracellular and extracellular apoptosis pathwaysto causecell death
to the development of liver fibrosisleadto the development of liver fibrosis
organ damagemay causeorgan damage
the development of embryonic abnormalitiescausesthe development of embryonic abnormalities
to tissue deathwill ... leadto tissue death
from ischemic brain injuryresultingfrom ischemic brain injury
from acute cellular injuryresultsfrom acute cellular injury
to the development of mitochondria - directed drugs designed to trigger apoptosis in cancer cellshas ledto the development of mitochondria - directed drugs designed to trigger apoptosis in cancer cells
from acute tissue injuryresultsfrom acute tissue injury
the reduced number of EGFP+ neural cells(passive) was caused bythe reduced number of EGFP+ neural cells
inflammationcausinginflammation
harm blood vesselssetharm blood vessels
from apoptosisresultingfrom apoptosis
in a highly selective apoptotic neuronal death in the dentate granule cell layer of the hippocampusresultsin a highly selective apoptotic neuronal death in the dentate granule cell layer of the hippocampus
from these componentsresultingfrom these components
from oxidative anxietypromptedfrom oxidative anxiety
from oxidative worrycausedfrom oxidative worry
to total organ failurecan leadto total organ failure
diseases(passive) caused bydiseases
to serial killing of host cellsleadsto serial killing of host cells
This decreased viability(passive) was caused byThis decreased viability
DNA damage(passive) caused byDNA damage
to serial killing of host cells " for consideration by eLifeleadsto serial killing of host cells " for consideration by eLife
to viral replicationcontributesto viral replication
in the development of cancereventually resultingin the development of cancer
from cellular damage or infiltration by pathogensresultingfrom cellular damage or infiltration by pathogens
to the widespread and severe NC phenotypes observed in fscn1aMO embryosmay contributeto the widespread and severe NC phenotypes observed in fscn1aMO embryos
to regulated nuclear fragmentation by endonuclease enzymes in a controlled manner that involves DNA fragmentationleadsto regulated nuclear fragmentation by endonuclease enzymes in a controlled manner that involves DNA fragmentation
to controlled inter - nucleosomal cleavage of genomic DNAleadsto controlled inter - nucleosomal cleavage of genomic DNA
a paucity of medial vascular SMCs(passive) caused bya paucity of medial vascular SMCs
to the release of damage - associated molecular patterns ( DAMPsleadingto the release of damage - associated molecular patterns ( DAMPs
to the release of damage - associated molecular patternsleadingto the release of damage - associated molecular patterns
to the release of cellular contents which can promote inflammationleadsto the release of cellular contents which can promote inflammation
from injury or cell stressresultsfrom injury or cell stress
from acute cellular injuryresultsfrom acute cellular injury
by apoptosis , necrosis or autophagic cell deathmay causedby apoptosis , necrosis or autophagic cell death
to loss of such cellsleadingto loss of such cells
from this increase in cell stressresultedfrom this increase in cell stress
to neuronal dysfunction and cell deathmay leadto neuronal dysfunction and cell death
in the release and accumulation of DNAcan resultin the release and accumulation of DNA
to specific activation of the immune systemleadingto specific activation of the immune system