Vladivostok Affiliation of Far-Eastern Research Centre for Physiology and Respiratory Pathology of SB RAMS – Institute of Medical Climatology and Rehabilitative Treatment, Vladivostok, Russian Federation
*Corresponding author: Yulia K. Denisenko, Ph.D, ScDi. Head of Laboratory of biomedicine researches. Vladivostok Affiliation of Far-Eastern Research Centre for Physiology and Respiratory Pathology of SB RAMS – Institute of Medical Climatology and Rehabilitative Treatment. Vladivostok, Russian Federation. E-mail: email@example.com
Published: September 24, 2013
The aim of this study was to determine the effect of a prolonged high-fat (HF) on thiol-disulfide homeostasis via the activity of the glutathione redox-system (GRS) in rat blood and liver.
Methods: The experiment was conducted on male Wistar rats. They were divided into groups and fed on the HF diet for 30, 90 and 180 days, respectively. The HF diet consisted of beef fat and cholesterol (19 % and 2 % of the total diet, respectively). The state of the GRS was assessed in the erythrocytes and liver tissue by the glutathione, glutathione reductase (GR) and glutathione peroxidase (GP) activity. The levels of the initial and final products of lipid peroxidation – lipid hydroperoxides (LOOHs), diene conjugates (DC) and malondialdehydes (MDA) in the blood and liver were investigated.
Results: Within 30 days, the HF diet inhibits the glutathione enzyme activity in the blood (GR: P<0.01; GP: P<0.001) and liver (GR, P<0.01). Within 90 days the HF diet kick-starts the beginning of the GRS compensatory response and restores the thiol-disulfide homeostasis. At 180 days, the HF diet shows failure of the compensatory processes in the glutathione system caused by the redox-imbalance in the thiol-disulfide exchange, which reveals lowered levels of glutathione, GR and GP activity (P<0.001 for all) in the blood and liver.
Conclusion: Our results suggest that the thiol-disulfide status of the cells depends upon the nature of the nutrition, a long-term breach of which triggers a compensatory response and a failure of the compensatory processes in the GRS.
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