Figure 1.

EGT metabolism in the cell: as an intracellular antioxidant, it may have a protective effect on oxidative damage and inflammation caused by exogenous factors reactive oxygen species (ROS) or UV. When cells are damaged or stressed, OCTN-1 transporters are expressed in large quantities to transport EGT across membranes to cells, and EGT can protect cells in different intracellular subcellular organelles in many ways. After entering the cells, EGT can rapidly chelate metal ions in the cytoplasm to prevent further damage to cells by the Fenton reaction. Simultaneously, EGT potentially regulates the activities of PARPs and sirtuin family enzymes and indirectly affects the transport and circulation of NAD+ in the cytoplasm and mitochondria, directly affecting ROS levels in mitochondria. In the nucleus, EGT protects the normal transcription of DNA and prevents deletions, especially DNA damage caused by copper ions. Additionally, EGT can inhibit the production of tumor necrosis factor-alpha (TNF-α), interleukin (IL)−1β, IL-6, and other inflammatory factors, thereby protecting the cells.