Abstract

We intended to determine whether or not dietary canola oil (CO) elevates plasma lipids and oxidative stress, since both of these are, possibly, related to the CO-induced life shortening through exacerbation of hypertension-associated vascular lesions found in stroke-prone spontaneously hypertensive rats (SHRSP). Spontaneously hypertensive rats (SHR) were used in this study to avoid a potential bias in the results due to the irregular death by stroke seen in SHRSP. SHR were fed for 26 weeks on a chow containing either, 10 wt/wt% of CO or soybean oil (SO), i.e., the control. Elevated plasma lipids and glucose-6-phosphate dehydrogenase (G6PD) activation in the liver and erythrocyte were found in SHR fed CO compared to that fed SO, while anti-oxidative enzymes other than G6PD were not activated. The CO diet brought about significant vascular lesions in the kidney, in which abundant cyclooxygenase-2 (COX-2) positive foci were immunochemically located in the juxtaglomerular apparatus. These results suggest that dietary CO induces a hyperlipidemic condition, in which G6PD may serve as an NADPH provider, and aggravates genetic diseases in SHR (also, probably, in SHRSP). The increased COX-2 expression indicates a role of renin-angiotensin-aldosterone system activation in the increased vascular lesions, whereas the effects of oxidative stress remain unclear.

Keywords: Rapeseed (canola) oil; Rats; Lipogenesis; Oxidative stress; cyclooxygenase-2

Abbreviations: CO, canola oil; G6PD, glucose-6-phosphate dehydrogenase; NADPH, nicotinamide adenine dinucleotide phosphate; PBS, phosphate buffered saline; SO, soybean oil; SHR, spontaneously hypertensive rats; SHRSP, stroke-prone spontaneously hypertensive rats; WKY rats, Wistar Kyoto rats

Article Outline

1. Introduction

2. Materials and methods

2.1. Animal husbandry

2.2. Blood biochemistry

2.3. Measurement of enzyme activities in erythrocyte lysate and hepatic cytosol

2.3.1. Erythrocyte lysate

2.3.2. Hepatic cytosol

2.4. Enzyme assay

2.5. Histological examination

2.5.1. Hematoxylin and eosin staining

2.5.2. Immunohistochemical staining for COX-2

2.6. Statistical methods

3. Results

3.1. Plasma levels of lipids and glucose

3.2. Anti-oxidative enzymes and related substances

3.3. Pathology

4. Discussion

Conflict of interest statement

References

A part of this study was presented in ISSFAL 2006 meeting in Cairns on 25 July 2006.