{"id":"e9c61550-48ff-59c5-8355-4f4ff7bf5014","stable_key":"d96b230c-481b-535b-930c-04eb87ec7f02:s-allylcysteine-pag-response","predicate":"changes_tested","statement":"PAG coadministration lowered the SAC-associated CSE activity and eliminated the favorable infarct-size pattern; PAG alone also worsened injury.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"915d61dc-50c7-58ab-8f82-dda1e7944739","mechanism_event_label":"Blocking the proposed pathway altered the outcome, with an important inhibitor control.","subject":{"id":"9dce0a0c-da29-5652-b5f2-7a7671bb964b","slug":"dl-propargylglycine","display_name":"DL-propargylglycine, experimental CSE inhibitor","entity_type_key":"small_molecule"},"object":{"id":"6a78956b-7b54-5c81-b8de-7cdb55df8542","slug":"rat-sac-cardioprotection","display_name":"Cardiac injury response to SAC in infarcted rats","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"915d61dc-50c7-58ab-8f82-dda1e7944739","stable_key":"d96b230c-481b-535b-930c-04eb87ec7f02:s-allylcysteine-pag-response-event","event_type":"observed_relationship","label":"Blocking the proposed pathway altered the outcome, with an important inhibitor control.","description":"PAG coadministration lowered the SAC-associated CSE activity and eliminated the favorable infarct-size pattern; 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PAG-alone injury complicates attribution.","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":"Rattus norvegicus","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Blocking the proposed pathway altered the outcome, with an important inhibitor control.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[17766469] S-allylcysteine mediates cardioprotection in an acute myocardial infarction rat model via a hydrogen sulfide-mediated pathway. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17766469/ · DOI 10.1152/ajpheart.00853.2007","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"route","value_text":"Administration route not specified in accessed abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Acute myocardial infarction; 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left ventricular and plasma measurements\", \"dose\": \"SAC 50 mg/kg/day; PAG 10 mg/kg/day\", \"duration\": \"Seven-day pretreatment; assessed 48 hours after infarction\", \"route\": \"Administration route not specified in accessed abstract\", \"experimental_comparison\": \"Saline, SAC, SAC plus PAG, and PAG-alone groups\", \"acting_entity\": \"dl-propargylglycine\", \"interpretation_status\": \"Source-derived research curation; not independent primary verification\"}","model_system":"Acute myocardial infarction; left ventricular and plasma measurements","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; 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