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Palabras clave – provistas por la editorial

toxicity; toll-like receptors; acrolein; hydroxyapatite-based biomaterials; LC-MS/MS; blood–brain barrier; NADPH-oxidase; human neuroblastoma SH-SY5Y cells; NRF2-NQO1 axis; granulocytes; free radicals; antioxidant; plaque vulnerability; bEnd.3; relaxation; Ca2+; keratinocytes; oxidative metabolism of the cells; lipid peroxidation; intermittent hypoxia; osteoblast growth; UV radiation; ROS; bEnd5; cyclopurines; NF?B; glucose deprivation; antimicrobial; endothelial cells; 4-hydroxynonenal (4-HNE); histamine; glutamine deprivation; optical coherence tomography; antioxidants; DNA damage; glutathione; NQO1 transcript variants; xeroderma pigmentosum; cancer cells; VAS2870; reactive oxygen species (ROS); TP53 mutation; DNA and RNA polymerases; viability; oxidative burst; macrophages; inflammation; Nrf2; von Willebrand factor; reactive oxygen species; growth control; intracellular signaling; MFN2; nuclear factor erythroid 2–related factor 2; fusion/fission; IMR-90; calcium; proliferation; mitochondria; pathophysiology of oxidative stress; redox balance; 4-hydroxynonenal; cannabidiol; oxidative homeostasis; rs1800566; neuronal cell death; heme-oxygenase-1; vitamins; cell signaling; TRPM2 channel; aorta; cancer; growth; cancer regression; oxidative stress; nucleotide excision repair