Tissue superoxide dismutases (T‐SOD)—referring generally to the family of SOD enzymes (e.g., SOD1, SOD2, and SOD3) responsible for detoxifying reactive oxygen species (ROS)—in the context of cancer.
Superoxide dismutases (SODs) are antioxidant enzymes that catalyze the conversion of the superoxide anion (O₂•–) into hydrogen peroxide and oxygen.
Oxidative stress plays a dual role in cancer: while moderate levels of ROS can promote cell proliferation and survival signaling, excessive ROS can cause cellular damage and trigger apoptosis.
Alterations in SOD expression may therefore contribute to either tumor suppression or promotion depending on the context:
• Upregulation of SOD can protect normal and cancer cells against oxidative damage, sometimes supporting tumor cell survival under stress.
• Conversely, low SOD activity may lead to increased ROS, DNA damage, and mutagenesis, thereby contributing to tumor initiation.
– The specific impact of changes in T‐SOD levels often depends on the isoform in question, the type of cancer, and the balance with other oxidative stress regulators.
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