{"id":"1328c84a-4e3f-54af-933a-7fa7cb3da90b","stable_key":"d96b230c-481b-535b-930c-04eb87ec7f02:s-allylcysteine-lung-oxidative-injury","predicate":"increases_tested","statement":"SAC at 20 mM for 72 hours increased lipid oxidative damage in both tested lung cancer lines.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"positive","is_public":true,"mechanism_event_id":"a2060f36-8825-56a6-91f5-827629fbe98b","mechanism_event_label":"Oxidative injury increased under this exposure.","subject":{"id":"8c2c295d-68b3-5e62-b1a7-00fcf915e3cc","slug":"s-allylcysteine","display_name":"S-allyl-L-cysteine / SAC","entity_type_key":"small_molecule"},"object":{"id":"cab08695-1a8e-5ab8-a1d0-e3e10165f418","slug":"human-sac-lung-lipid-damage","display_name":"Lipid oxidative damage in SAC-treated lung cancer cells","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"a2060f36-8825-56a6-91f5-827629fbe98b","stable_key":"d96b230c-481b-535b-930c-04eb87ec7f02:s-allylcysteine-lung-oxidative-injury-event","event_type":"observed_relationship","label":"Oxidative injury increased under this exposure.","description":"SAC at 20 mM for 72 hours increased lipid oxidative damage in both tested lung cancer lines.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"8c2c295d-68b3-5e62-b1a7-00fcf915e3cc","slug":"s-allylcysteine","display_name":"S-allyl-L-cysteine / SAC","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"cab08695-1a8e-5ab8-a1d0-e3e10165f418","slug":"human-sac-lung-lipid-damage","display_name":"Lipid oxidative damage in SAC-treated lung cancer cells","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"acting_entity","value_text":"s-allylcysteine","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"dose","value_text":"10 or 20 mM SAC; mechanistic endpoints 20 mM","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"duration","value_text":"24, 48 or 72 hours; mechanistic endpoints 72 hours","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"evidence_access","value_text":"Primary abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_comparison","value_text":"SAC; BEAS-2B and A549 comparator cell lines also studied","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"HCC827 and NCI-H1975 lung cancer cells","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"interpretation_status","value_text":"Source-derived research curation; not independent primary verification","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Does not establish that usual dietary exposure produces this tissue concentration.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit.","comparator":null,"unit":null,"notes":"","entity":{"slug":"s-allylcysteine","display_name":"S-allyl-L-cysteine / SAC","entity_type_key":"small_molecule"}},{"dimension":"organism","value_text":"Homo sapiens","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Oxidative injury increased under this exposure.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[33136700] S-allylcysteine induces cytotoxic effects in two human lung cancer cell lines via induction of oxidative damage, downregulation of Nrf2 and NF-κB, and apoptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33136700/ · DOI 10.1097/CAD.0000000000001015","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"route","value_text":"Cell culture","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"HCC827 and NCI-H1975 lung cancer cells","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"58075a67-53b4-52cd-aeca-a8d51cab2275","evidence_kind":"source_excerpt","locator":"Lines 320-327","start_line":320,"end_line":327,"excerpt":"## s-allylcysteine-lung-oxidative-injury\nOxidative injury increased under this exposure.\nSAC at 20 mM for 72 hours increased lipid oxidative damage in both tested lung cancer lines.\nModel: HCC827 and NCI-H1975 lung cancer cells\nLimitations: Does not establish that usual dietary exposure produces this tissue concentration.\nEvidence access: Primary abstract\n[33136700] S-allylcysteine induces cytotoxic effects in two human lung cancer cell lines via induction of oxidative damage, downregulation of Nrf2 and NF-κB, and apoptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33136700/ · DOI 10.1097/CAD.0000000000001015\nStructured context: {\"organism\": \"Homo sapiens\", \"tissue_or_cell_type\": \"HCC827 and NCI-H1975 lung cancer cells\", \"dose\": \"10 or 20 mM SAC; mechanistic endpoints 20 mM\", \"duration\": \"24, 48 or 72 hours; mechanistic endpoints 72 hours\", \"route\": \"Cell culture\", \"experimental_comparison\": \"SAC; BEAS-2B and A549 comparator cell lines also studied\", \"acting_entity\": \"s-allylcysteine\", \"interpretation_status\": \"Source-derived research curation; not independent primary verification\"}","model_system":"HCC827 and NCI-H1975 lung cancer cells","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Original curation paraphrase; evidence access and experimental limitations specified.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"3b0d58f9-8a69-579d-9920-518399a9a8bb","stable_key":"import-d96b230c-481b-535b-930c-04eb87ec7f02","title":"S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20)","document_type":"imported_text","citation_label":"AI-assisted research curation; primary references, access levels and experimental limitations individually identified. 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