著者

Taiki Nishikawa Shinya Shimizu Haruo Kamiya Jun Ueyama Sumio Yamada

出版者

International Heart Journal Association

雑誌

International Heart Journal (ISSN:13492365)

巻号頁・発行日

vol.63, no.6, pp.1107-1114, 2022-11-30 (Released:2022-11-30)

参考文献数

35

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Oxidative stress plays a crucial role in the progression of heart failure (HF). We surveyed the fraction of human mercaptalbumin [f (HMA) ], an indicator of the redox state of human serum albumin (HSA), in patients with HF and examined whether f (HMA) is associated with the severity of HF.We enrolled consecutive elderly patients hospitalized for acute HF or exacerbation of HF. The redox state of HSA was measured by the high-performance liquid chromatography with postcolumn bromocresol green method using serum samples collected close to discharge. First, the distribution of f (HMA) in HF was compared to that in community-dwelling elderly individuals (n = 125; median age, 80 years) as a control group analyzed in a previous study. Overall, 133 patients (median age, 81 years; 75 men) were included. Patients with HF showed a lower level of f (HMA) than those of the control group (55.0% [IQR 47.7-61.3] versus 66.3% [IQR 62.8-70.0], P < 0.001]. Multiple regression analysis showed a negative correlation between f (HMA) and log-transformed B-type natriuretic peptide (standardized beta = −0.19).Patients with HF showed lower f (HMA) than those in the control group. Additionally, f (HMA) was related to HF independently with log-transformed B-type natriuretic peptide in the multivariate regression analysis, suggesting that f (HMA) is a biomarker that reflects the redox state in HF patients.

著者

Masayuki Nadai Miki Kato Kazumasa Yasui Masao Kimura Ying Lan Zhao Jun Ueyama Yoshimi Tsunekawa Hideo Yoshizumi Takaaki Hasegawab

出版者

The Pharmaceutical Society of Japan

雑誌

Biological and Pharmaceutical Bulletin (ISSN:09186158)

巻号頁・発行日

vol.30, no.3, pp.562-568, 2007 (Released:2007-03-01)

参考文献数

49

被引用文献数

1 2 3

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There is an interesting clinical report indicating that aciclovir, which is mainly excreted into urine, decreases the systemic clearance of theophylline by inhibiting cytochrome P450 (CYP) 1A2-mediated metabolism. In this study, we investigated the effect of aciclovir on the metabolism of theophylline, and on the activity and expression of hepatic CYP1A2 in rats. Theophylline (10 mg/kg) was injected intravenously into rats treated with two different dosages of aciclovir. When theophylline was simultaneously administered with aciclovir (50 mg/kg), the systemic clearance of theophylline and metabolic clearance of its major metabolites, 1-methyluric acid and 1,3-dimethyluric acid, were unchanged. In place of theophylline, when 1-methyl-3-propylxanthine (2.5 mg/kg), which is almost metabolized by CYP1A2 in rats, was coadministered intravenously with aciclovir (50 mg/kg), the pharmacokinetics of 1-methyl-3-propylxanthine was also unchanged. When theophylline was administered to rats pretreated with repeated intraperitoneal injections of aciclovir (25 mg/kg twice daily for 3 d), no significant differences in the systemic clearance of theophylline and its metabolic clearance to 1-methyluric acid and 1,3-dimethyluric acid were observed between the control and aciclovir-treated rats. This dosage of aciclovir did not change the activity of 7-ethoxyresorufin O-dealkylation, which is represented as CYP1A2 activity. In Western blot analysis, no significant change in the protein levels of hepatic CYP1A2 was observed between the control and aciclovir-treated rats. The present study suggests that aciclovir has no effect on the pharmacokinetics and metabolism of theophylline and on the activity and expression of hepatic CYP1A2 in rats.