Among the environmental perturbations that may cause cell necrosis are oxygen deprivation (anoxia), hyperthermia, immunological attack, and exposure to various toxins that inhibit crucial intracellular metabolic processes.
In fact, severe stretching of the axon of neural cells during traumatic brain injury may cause cell death [4].
However, a previous study by the authors showed the capability of basaltic ash to generate the hydroxyl radical, a highly-reactive species which may cause cell damage.
However, prolonged induction periods at elevated temperature, especially at 37 °C, may cause cell lysis, which would decrease productivity and secretion capacity (Mana et al. 2015).
It has also been reported that various types of nanoparticles, in different sizes from 20 to 300 nm and produced from different materials, may cause cell death by apoptosis in the brain tissue [16].
Therefore, the selection of Na+ vs. Ca2+ ions in Nav channels is of particular interest, since Ca2+ ions frequently act as secondary messengers and their cross-membrane leaking may cause cell disorder.
The addition of cryopreservative agents (CPAs) to chondrocytes and natural and engineered cartilage is critical to protect the cells and tissues from freezing damage during cryopreservation, but this may cause cell damage, e.g. by osmotic shock.
Results suggest that 18β-glycyrrhetinic acid may cause cell death in SiHa cells by inducing the mitochondrial membrane permeability change, leading to cytochrome c release and caspase-3 activation.
However, the residual bone defects, between the implant neck and the residual bone walls, may cause cell migration from the connective and epithelial tissue into the defect area, possibly preventing osseointegration [2], and jeopardize the success of immediate implant procedures [3].
Several pathways by which mHtt may cause cell death have been identified.
Excessive activation of glutamate receptors may cause cell vulnerability, in part as a result of intracellular calcium influx [4], [5].
