Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

Lipid peroxidation resulting from increased generation of reactive oxygen species is an important neurodestructive mechanism in stroke. We have investigated nutritional factors that may impact on components of antioxidant defense that are central to peroxide scavenging. The long-term goal is to develop nutritional intervention to reduce brain damage following stroke. Deficiency of sulfur amino acids was studied as these precursors are a major determinant of glutathione (GSH) synthesis in tissues such as liver. Female Long-Evans adult rats were fed a sulfur-deficient diet for 5 days; controls were supplemented with L-cystine and L-methionine (n=6/treatment). GSH concentration was analyzed by reverse-phase high performance liquid chromatography. Liver GSH concentration was depressed by 74% in the sulfur-deficient group. In neocortex, hippocampus, thalamus, and striatum, GSH decreased 10-14% (P < 0.05 in neocortex and thalamus). Selenium status was also studied because of the function of Se in the synthesis and regulation of glutathione peroxidase (GPx). Male, weanling Long-Evans rats were fed for 6 weeks a diet containing either no added selenium (deficient), 0.2 mg Se/kg diet (control) or 0.4 mg Se/kg diet (supplemental) (n=7/treatment). Se deficiency was confirmed by liver cellular GPx activity < 7% of controls. Preliminary analysis suggests that brain GPx activity is unaltered by dietary Se in the absence of increased oxidative stress. The tissue hierarchy for Se partitioning may protect the brain when Se is in limited supply. Future studies will examine the influence of protein and selenium status on peroxide scavenging in the presence of oxidative injury in an animal model of stroke. (Funded by the Heart and Stroke Foundation of Saskatchewan and the University of Saskatchewan President's NSERC Fund)

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Presentation Number SApaterson0526
Keywords: glutathione, selenium, sulfur amino acid, brain, GPX1