Lipid peroxidation in mice fed a choline-deficient diet as evaluated by total hydroxyoctadecadienoic acid

Yoshida, Yasukazu; Itoh, Nanako; Hayakawa, Mieko; Habuchi, Yoko; Inoue, Ruriko; Chen, Zhi-Hua; Cao, Jiaofei; Cynshi, Osamu; Niki, Etsuo

doi:10.1016/j.nut.2005.07.020

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Volume 22, Issue 3 , Pages 303-311, March 2006

Lipid peroxidation in mice fed a choline-deficient diet as evaluated by total hydroxyoctadecadienoic acid

Yasukazu Yoshida, Ph.D.
- Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Osaka, Japan
- Corresponding author. Tel.: +81-72-751-8183; fax: +81-72-751-9964.
Nanako Itoh, B.Sc.
- Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Osaka, Japan
Mieko Hayakawa, B.Sc.
- Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Osaka, Japan
Yoko Habuchi, B.Sc.
- Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Osaka, Japan
Ruriko Inoue, B.Sc.
- Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Osaka, Japan
Zhi-Hua Chen, Ph.D.
- Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Osaka, Japan
Jiaofei Cao, M.D.
- Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Osaka, Japan
Osamu Cynshi, Ph.D.
- Fujigotemba Research Laboratories, Chugai Pharmaceutical Co. Ltd., Shizuoka, Japan
Etsuo Niki, Ph.D.
- Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Osaka, Japan

Received 31 May 2005; accepted 28 July 2005.

Abstract

Objective

The relevance of oxidative stress in mice fed a choline-deficient diet (CDD) was investigated in relation to the oxidative stress marker, hydroxyoctadecadienoic acid (HODE) in comparison with F2-isoprostanes. Further, the protective effects of antioxidants against oxidative damage were assessed by using HODE.

Methods

We recently proposed total HODE as a biomarker for oxidative stress in vivo. Biological samples such as plasma, urine, and tissues were first reduced and then saponified to convert various oxidation products of linoleates to HODE. In the present study, this method was applied to measure oxidative damage in mice induced by CDD for 1 mo.

Results

CDD, when compared with choline-controlled diet (CCD), increased liver weight and fatty acid accumulation but the increase in body weight was less significant. Remarkable increases in HODE and 8-iso-prostaglandin F_2α in liver and plasma were observed when mice were fed with the CDD for 1 mo compared with the CCD. The HODE level was about two to three orders higher than the F2-isoprostane level. This increase was decreased to the level of the CCD when α-tocopherol or 2,3-dihydro-5-hydroxy-4,6-di-tert-butyl-2,2-dipentylbenzofuran, a potent synthetic antioxidant, was mixed with the CDD. The stereoisomer ratio of HODE (9-and-13 (Z,E)-HODE/9-and-13 (E,E)-HODE) was decreased by CDD compared with CCD, which was spared by the addition of α-tocopherol and 2,3-dihydro-5-hydroxy-4,6-di-tert-butyl-2,2-dipentylbenzofuran. However, the increase in plasma glutamic-pyruvic transaminase and fatty acids in liver induced by the CDD was not recovered by any antioxidant.

Conclusions

This study clearly demonstrated that oxidative stress was involved in fatty liver formation induced by the CDD and that HODE was a good biomarker for an oxidative stress in vivo.

Keywords: Choline deficient , Antioxidant , Hydroxyoctadecadienoic acid: Isoprostanes , Vitamin E , 2,3-dihydro-5-hydroxy-4,6-di-tert-butyl-2,2-dipentylbenzofuran