Biomedical subjects

O S Kwon

Publications and source records attributed to O S Kwon.

57 records · Page 4Linked to original sources

PubMedDate not supplied

Quantitative determination of stanozolol and its metabolite in urine by gas chromatography/mass spectrometry.

The amount of stanozolol and 3'-hydroxystanozolol in urine was determined after oral administration of stanozolol. A gas chromatograph/mass selective detector equipped with a capillary column was used for these determinations. The GC/MS was operated in the SIM mode, and m/z 581, 669, and 315 were monitored for stanozolol, 3'-hydroxystanozolol, and calusterone (internal standard), respectively. The detection limit was approximately 1 ng/mL for both steroids. The maximum excretion rate of stanozolol was reached in 8 h and the maximum of 3'-hydroxystanozolol in 19 h. However, only 3% of the administered amount was recovered in urine.

Administration, Oral↗

PubMedDate not supplied

Analysis of anabolic steroids using GC/MS with selected ion monitoring.

This study describes the use of gas chromatography/mass spectrometry with selected ion monitoring to screen 18 anabolic steroids banned by the International Olympic Committee. These anabolic steroids are analyzed in two fractions depending on their excretion pattern: nonconjugated (free) or conjugated fraction. The wet procedure of extracting steroids from urine consists of an initial isolation of lipophilic compounds on a column packed with Amberlite XAD-2 resin, followed by enzymatic hydrolysis with beta-glucuronidase from Escherichia coli. After extraction, the hydrolyzed steroids are derivatized to the corresponding trimethylsilyl ethers. The derivatized steroids are analyzed by gas chromatography/mass spectrometry with selected ion monitoring of their characteristic ions. It takes 12 and 26 min to run GC/MS and edit the raw data for nonconjugated and conjugated fractions respectively.

Anabolic Agents↗

PubMedDate not supplied

Nicotine-enhanced epithelial differentiation in reconstructed human oral mucosa in vitro.

Oral mucosal keratinocytes represent the cells that first encounter tobacco components. Therefore, tobacco-induced abnormal alteration of the mucosal keratinocytes may contribute to the development of oral white lesions. Nicotine is an ingredient of all tobacco products and pharmacologically the most active component of tobacco smoke. To clarify the effects of nicotine on the keratinization of oral mucosal and epidermal keratinocytes, we reconstructed artificial buccal mucosal and skin equivalents using keratinocytes and fibroblasts from noncornifying buccal mucosa and adult foreskin, respectively. The effect of nicotine on keratinization was assessed with morphology, immunohistochemistry and immunoblotting. Long-term treatment with nicotine for 2 weeks enhanced in a dose-dependent manner the expression of differentiation-specific proteins of oral mucosal keratinocytes on living oral mucosal equivalent and epidermal keratinocytes on living skin equivalent, respectively. The effect of nicotine on the cell viability was measured by the 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay. Oral mucosal keratinocytes showed a higher resistance to nicotine toxicity than epidermal keratinocytes. Our results suggest that nicotine stimulates differentiation of both mucosal and epidermal keratinocytes, and this nicotine-induced abnormal differentiation may be associated with the development of oral white lesions.

Adult↗