Development of acute and subacute toxicity with the serotonin transporter radiopharmaceutical, ADAM

Kang Wei Chang, Chia Chieh Chen, Shih Ying Lee, Lie Hang Shen, Hsin Ell Wang

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

It is predicted that depression will become the most common neurological disease in the new millennium. Its incidence is currently about 3% of diseases worldwide. Serotonin is an essential neurotransmitter for the central and peripheral nervous systems and plays a crucial role in neuropsychiatric disorders. 123I-labeled ADAM was developed to facilitate an early diagnosis of serotonin transporter (SERT) abnormalities in the brain. Many studies have confirmed that the binding of this radiotracer to SERTs is associated with depression. The aim of this study was to evaluate the acute and subacute toxicity of ADAM and to determine its no observed adverse effect level (NOAEL) by administering it via intravenous injection to Sprague-Dawley rats for 14 consecutive days. None of the animals died, and no treatment-related clinical signs were observed. Urinalysis, hematology, and clinical chemistry analysis revealed that daily administration of ADAM (2-2- dimethylaminomethylphenylthio-5-iodophenylamine) for 2 weeks had no toxicological effects. It is concluded that ADAM exerts no adverse toxic effects on this animal model. The NOAEL was 155μg/kg/day.

Original languageEnglish
Pages (from-to)393-402
Number of pages10
JournalDrug and Chemical Toxicology
Volume33
Issue number4
DOIs
Publication statusPublished - Oct 1 2010
Externally publishedYes

Keywords

  • ADAM
  • Depression
  • Toxicity

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology
  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis
  • Chemical Health and Safety

Fingerprint

Dive into the research topics of 'Development of acute and subacute toxicity with the serotonin transporter radiopharmaceutical, ADAM'. Together they form a unique fingerprint.

Cite this