Metabolism and disposition of luminol in the rat.

Xenobiotica

Laboratory of Pharmacology and Chemistry, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.

Published: March 2000

AI Article Synopsis

  • Luminol (LMN) is a forensic reagent that emits light when oxidized; its metabolism and excretion were studied to assess its toxicity.
  • Most of the administered LMN (about 90%) was eliminated through urine within 24 hours, primarily as two metabolites, while the expected oxidative product did not form in the body.
  • The absorption of LMN via injection or ingestion was similar, with minimal retention in tissues, and its poor dermal absorption suggests low risk for chronic toxicity in humans.

Article Abstract

1. The metabolism and disposition of Luminol (LMN, 3-aminophthalhydrazide), a widely used forensic and laboratory reagent that chemiluminesses upon oxidation, was determined as part of its overall toxicological characterization. 2. Radiolabelled LMN was well absorbed, metabolized and excreted following p.o. administration of a range of doses. About 90% of the total dose was recovered within 24 h of administration in urine in the form of two metabolites identified as LMN N8-glucuronide and LMN N8-sulphamic acid. 3-Aminophthalic acid, the oxidative product of LMN in the light-emitting reaction, was apparently not formed in vivo. 3. Metabolism and disposition of an i.v. administered dose was similar to that following gavage. Little or no LMN-derived radioactivity was present in tissue within 12 h post-dosing. Excretion of radioactivity in bile following i.v. injection was minimal (approximately 8% of the total dose in 6 h) and consisted of the same urinary-excreted glucuronide and sulphate conjugates. 4. LMN was not absorbed dermally in rat, potentially a major route of exposure to human. If the fate of LMN is similar between species, this compound should have little potential for either dermal absorption, bioaccumulation in tissues following other routes of exposure or chronic toxicity in humans.

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http://dx.doi.org/10.1080/004982500237659DOI Listing

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