In the present study, we investigated whether mitochondria are the potential cytoplasmic target of high LET radiation in mediating cellular damage using a mitochondrial DNA (mtDNA) depleted (ρ0) human small airway epithelial (SAE) cell model and a precision charged particle microbeam with a beam width of merely one micron.
ROS can mediate cellular damage through direct interaction with cellular components.
ROS have been known for a long time to induce cell cycle alterations; however, focus was directed towards secondary effects mediating cellular damage [ 51].
In conclusion, our data provides evidence that plasma histones are not only elevated in human sepsis but are associated with sepsis-related organ dysfunction, mediating cellular damage and severe inflammation responses.
Hence, converging lines of evidence indicate that mTOR and its downstream pathway, by transducing nutrient-triggered signals, may mediate cellular damage, through molecular mechanisms largely involving mTOR cross-talk with growth factor-triggered mitogenic and survival cascades.
Oxidative stress triggered by the increased production of ROS and nitrogen reactive species could mediate cellular damages in tissues such as in the heart, brain and liver (Goldbart et al. 2003; Haussinger and Schliess 2008; Joyeux-Faure et al. 2005).
Diverse spectrums of cellular changes that underline dysfunctional signal transduction are attributed to mediate cellular damage associated with their use [ 32].
Lipids, DNA, and proteins have been shown to interact with ROS and mediate cellular damage [ 46], given that it is not surprising that chronic and acute exposure to excessive levels of ROS can induce cell death processes (apoptosis, necrosis, and autophagy) [ 47– 50].
We also discuss instances of non-oxidative stress-mediated cellular damage resulting from direct physical interference of nanomaterials with cellular structures.
FH dysfunction might promote complement-mediated cellular damage and expose intracellular antigens, which cross-react with anti-bacterial antigen antibodies, amplifying and perpetuating the activity of the immune system against the host (Fig. 9).
bar mutants show specific cardiovascular failure due to oxidative stress and ROS-mediated cellular damage.
