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(2008). https://pubmed.ncbi.nlm.nih.gov/18566994/ DOI: 10.1002/ijc.23696","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Nucleus, antioxidant enzymes and intracellular glutathione","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"6edeacea-86ff-554e-93d3-d5b558a23b2d","evidence_kind":"source_excerpt","locator":"Lines 572-583","start_line":572,"end_line":583,"excerpt":"### lycopene-apo-oxidant-injury\nThe metabolite suppressed endogenous ROS generation and hydrogen-peroxide-induced injury in BEAS-2B cells.\nCondition category: normal\nnutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Cells were less vulnerable to the tested oxidant exposure.\norganism: Human BEAS-2B bronchial epithelial cells\ntissue_or_cell_type: Nucleus, antioxidant enzymes and intracellular glutathione\nexperimental_model: Metabolite exposure and gene/protein/redox measurements\nlimitations: Cell-culture metabolite results do not prove oral lycopene reaches equivalent tissue concentrations or prevents human cancer.\nexposure: Time- and dose-dependent apo-10-prime-lycopenoid exposure\nevidence_span: {\"source_cache\": \"artifacts/lycopene-research/18566994.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534\", \"start_char\": 0, \"end_char\": 1416, \"text_sha256\": \"e34a21bb159c3e48372fd5cb104bfa50572903a5ef168b10100976a718b7b534\"}\n[lycopene-p18566994] Enzymatic metabolites of lycopene induce Nrf2-mediated expression of phase II detoxifying/antioxidant enzymes in human bronchial epithelial cells. 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