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(2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Plasma","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"a7a2c826-536d-5232-9946-8a896bcf0f7f","evidence_kind":"source_excerpt","locator":"Lines 156-167","start_line":156,"end_line":167,"excerpt":"### vc-transport-svct1-plasma\nPlasma ascorbate was approximately 50–70% lower in Slc23a1-null mice than wild-type mice.\nCondition category: machinery_impairment\nnutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Renal vitamin C wasting lowered circulating vitamin C in these mice.\norganism: Mus musculus\ntissue_or_cell_type: Plasma\nexperimental_model: Slc23a1 knockout mice and wild-type controls\nlimitations: Mouse concentration phenotype; do not use as a human deficiency threshold.\nexposure: Slc23a1 knockout versus wild type\ncross_nutrient: false\n[corpe2010] Vitamin C transporter Slc23a1 links renal   reabsorption, vitamin C tissue accumulation,   and perinatal survival in mice. 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