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While extracellular UA has antioxidant effects that may protect normal cells from transformation, entry of UA into cells can generate inflammatory stress that arises from the effects of intracellular UA on ROS/RNS generation and COX-2 activation.
It can be speculated that specific AMPA receptor inhibitors may protect normal neurons against the high glutamate microenvironment of GBM tumors.
Therefore, we propose that Tan IIA may protect normal cells, but inhibit cancer cells.
In this study, we also show that, in principle, all bioactive derivatives of Roc-A may protect normal cells from genotoxin-induced cytotoxicity.
First, because brain tissues are one of the most oxidative environments and therefore susceptible to radiation damage, antioxidants may protect normal brain tissues from radiation damage and lead to better survival [ 39].
Paradoxically, while robustness characteristics may protect normal cells against transformation, they may also at the tumor stage protect the cancer properties or oncogenes (e.g., oncogenic Raf stabilized by HSP90) [ 60].
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It is important to note that VDRff itself does not cause the aggressive phenotype, but due to its increased transcriptional activity of genes implicated in an aggressive phenotype, the VDRff genotype may fail to protect normal cells from oncogenic insults over time.
The normal physiologic role of P-gp is still unknown, but it may serve to protect normal tissues from toxic products and xenobiotics [ 24].
Alternatively, it may be possible to protect normal tissues from responding by switching off bystander interactions.
Gauze swabs may be used to protect normal tissue and mop up excess dye.
Moreover, in susceptible individuals with low Fus1 levels, PM or other antioxidative treatments may be used to protect normal tissues during radiation cancer therapy.
Related(20)
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