Iron chelation as a possible mechanism for aspirin-induced malondialdehyde production by mouse liver microsomes and mitochondria.

Schwarz, K B; Arey, B J; Tolman, K; Mahanty, S

Schwarz, K B; Arey, B J; Tolman, K; Mahanty, S.

Affiliation

Schwarz KB; Department of Pediatrics, St. Louis University School of Medicine, Missouri.

J Clin Invest ; 81(1): 165-70, 1988 Jan.

Article in En | MEDLINE | ID: mdl-3335633

Subject(s)

Aspirin/toxicity; Iron Chelating Agents/pharmacology; Malonates/biosynthesis; Malondialdehyde/biosynthesis; Microsomes, Liver/metabolism; Mitochondria, Liver/metabolism; Animals; Deferoxamine/pharmacology; Dose-Response Relationship, Drug; Electric Conductivity; Lipid Peroxides/metabolism; Male; Mice; Mice, Inbred BALB C; Microsomes, Liver/drug effects; Mitochondria, Liver/drug effects

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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Microsomes, Liver / Mitochondria, Liver / Aspirin / Iron Chelating Agents / Malonates / Malondialdehyde Limits: Animals Language: En Journal: J Clin Invest Year: 1988 Document type: Article

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