Secondary Fish-Odor Syndrome Can be Acquired by Nitric Oxide-mediated Impairment of Flavin-containing Monooxygenase in Hepatitis B Virus-Infected Patients.
- Author:
Hyeon Gyu YI
1
;
Jung Nam LEE
;
Seung Duk RYU
;
Ju Hee KANG
;
Young Nam CHA
;
Chang Shin PARK
Author Information
1. Department of Pharmacology, Medicinal Toxicology Research Center, CDIR, Korea. parkshin@inha.ac.kr
- Publication Type:Original Article
- Keywords:
Fish-odor syndrome;
Flavin-containing monooxygenase;
Trimethylamine;
Chronic viral hepatitis;
Nitric oxide;
Ranitidine
- MeSH:
DNA;
DNA, Viral;
Hepatitis B virus;
Hepatitis B*;
Hepatitis*;
Humans;
Liver Diseases;
Nitric Oxide;
Plasma;
Ranitidine
- From:The Korean Journal of Physiology and Pharmacology
2004;8(4):213-218
- CountryRepublic of Korea
- Language:English
-
Abstract:
Primary fish-odor syndrome (FOS) is a genetic disorder caused by defective flavin-containing monooxygenase 3 gene (FMO3) with deficient N-oxidation of trimethylamine (TMA), causing trimethylaminuria (TMAU). By contrast, secondary FOS can be acquired by decreased FMO activities in patients with chronic liver diseases, but the underlying mechanisms are unknown. In the present study, we examined plasma NOx concentrations and viral DNA contents as well as in vivo FMO activities and their correlations in chronic viral hepatitis (CVH) patients. Plasma concentration of NOx was significantly increased by 2.1 fold (56.2+/-26.5 vs. 26.6+/-5.4micrometer, p< 0.01), and it was positively correlated with plasma hepatitis B virus (HBV) DNA contents (r2=0.2838, p=0.0107). Furthermore, the elevated plasma NOx values were inversely and significantly correlated with in vivo FMO activities detected by ranitidine-challenged test (8.3% vs. 20.0%, r2=0.2109, p=0.0315). TMA N-oxidation activities determined in CVH patients without challenge test were also significantly low (73.6% vs. 95.7%, p< 0.05). In conclusion, these results suggested that secondary FOS could be acquired by the endogenously elevated NO in patients with CVH.
