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However, when ROS homeostasis is disrupted due to various environmental or pathological factors, excessive ROS are accumulated in the mitochondria and cytoplasm – a condition referred to as intracellular oxidative stress, which can cause oxidative damages of cells and disease consequences [ 66- 71].
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The electrostatic connection between NPs with the sulfur-containing proteins present on the surface of bacterial cells causes irreversible changes in cell wall structure resulting in damages of cell wall and membrane [12].
Similarly, mechanical damages of cell wall and other organelles (chloroplasts) due to GO treatments as well as enhanced formation of ROS have been detected in algal cells [180, 181].
Secondary damages of cell membranes, edema, and vascular alterations followed by hemorrhage and necrosis are completing the clinical picture.
Such injuries result from the toxicity and high concentration of cryoprotectants as well as mechanical damage of cells due to ice crystal formation during the cooling and rewarming processes.
These rates were lower than the rates of damage of cells stimulated under the same conditions.
Scandalios ([1993]) reported that SOD and CAT were effective antioxidant enzymes for decreasing oxidant damage of cells by oxidative stress.
For SMC, TNF-α is released from cells when the cells are damaged, and then the free TNF-α will promote the inflammatory damage of cells inversely.
Damaging of cells by transient vapor bubbles generated around nanoparticle accumulations within Bac-1 cells was investigated.
Released to the extracellular space ATP informs about pathological conditions and damage of cells and activates immunological response [ 80].
The freezing treatment that we used presumably led to damage of cells or even death due to severe dehydration.
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CEO of Professional Science Editing for Scientists @ prosciediting.com