1. ¹Department of Pharmacology & Toxicology Atlanta, Georgia, USA
2. ²Department of Space Medicine and Life Sciences Research Center Atlanta, Georgia, USA
3. ³Department of Clinical Research Center, Morehouse School of Medicine, Atlanta, Georgia, USA

Correspondence: Dr. Mohamed A. Bayorh, Department of Pharmacology/Toxicology, Morehouse School of Medicine, 720 Westview Drive, SW, Atlanta, Georgia 30310-1495, USA. E-mail: bayorh@msm.edu

^*This work was supported in part by National Institutes of Health grants S06GM08248-12 (MAB) and P20RR11104-07 (IKA), and PORIM.

Received 5 October 2001; Accepted 22 March 2002.

Abstract

Background: Oxidative stress, associated with increased plasma isoprostane (ISO) and reductions in plasma glutathione (GSH), has been shown to cause severe hypertension in normal rats. Palm oil (PO), with an unsaturated-to-saturated fatty acid ratio close to one and rich in antioxidant vitamins, has been investigated for its beneficial effects on arterial thrombosis and atherosclerosis. In this study, the effect of PO on oxidative stress induced by inhibition of GSH synthesis (using buthionine sulfoximine [BSO]) was examined.

Methods: Sprague-Dawley rats were separated into two groups and received either natural vitamin-rich PO (Carotino, 5 g/kg daily) or water by gavage. After 4 weeks, they were further divided between receiving either BSO (30 mmol/L/day in the drinking water) or drug-free water for an additional week. Mean arterial pressure (MAP), heart rate (HR), and body weight (BW) were measured before and weekly during the experiment. The levels of plasma ISO, nitric oxide (NO), prostacyclin (PGI₂), and thromboxane A₂ (TXA₂) were determined by enzyme immunoassay, and plasma, heart, and kidney GSH by high-performance liquid chromatography.

Results: The PO reduced the age-dependent increase in MAP, and the pressor response to BSO, without changing the HR or BW compared to the BSO and control groups. It also elevated PGI₂, NO, and aortic cGMP, but decreased TXA₂ and aortic cAMP. In addition, the BSO-induced increase in ISO and TXA₂, and the reduction in kidney GSH were attenuated by PO. However, the PO effect on NO, PGI₂, cGMP, and TXA₂ was partly counteracted by BSO.

Conclusions: Palm oil reduces BSO-induced oxidative stress and attenuates hypertension by mechanisms involving changes in endothelium-derived factors.