Changes in susceptibility of tissues to lipid peroxidation after ingestion of various levels of docosahexaenoic acid and vitamin E

Abstract

To examine the effects of dietary docosahexaenoic acid (DHA) on the potential changes in endogenous lipid peroxidation in the liver and kidney, diets containing a fixed amount of vitamin E (VE; RRR-a-tocopherol equivalent; 134 mg/kg diet) and a graded amount of DHA at the levels of 0, 1.0, 3.4 and 8.7 % of total dietary energy were fed to rats for 14 d (Expt 1). In Expt 2, diets containing a fixed amount of DHA (8-7 % of total dietary energy) and a graded amount of VE at the levels of 54,134 and 402 mg/kg were fed to rats for 15 d. In Expt 1 it was found that endogenous lipid peroxide contents of the liver and kidney, as measured by thiobarbituric acid value and chemiluminescence intensity, were higher, and their or-tocopherol contents lower than those of the controls, with a gradual increase and decrease in values respectively as the dietary DHA level increased (Expt 1). However, the contents of water-soluble antioxidants, i.e. ascorbic acid and nonprotein-SH (glutathione), increased with increases in the dietary DHA level, while the Se-dependent glutathione peroxidase (EC 1.11.1.9) activities did not change or tended to be lower. When the graded level of VE was given to rats in Expt 2, lipid peroxide contents in the liver and kidney did not change significantly in response to the increasing levels of dietary VE, although their or-tocopherol contents were higher than control values, increasing with increases in the dietary VE levels. The lipid peroxide scavengers other than a-tocopherol changed similarly to those in Expt 1. The results obtained in Expts 1 and 2 indicate that DHA enhances the susceptibility of the liver and kidney to lipid peroxidation concomitant with higher levels of DHA in these tissues, as shown by the fatty acid composition. In addition, VE is unable to protect membranes of the liver and kidney rich in DHA from lipid peroxidation, even after ingestion of the highest level of VE. However, the liver lipid peroxide content of the group given the highest level of DHA was not as high as expected, based on the peroxidizability index which was calculated from the fatty acid composition of the liver lipid.Vitamin E: Docosahexaenoic acid: Lipid peroxidation Fish oils are rich in polyunsaturated fatty acids (PUFA) of n-3 type, such as eicosapentaenoic acid (20:5n-3; EPA), and docosahexaenoic acid (22:6n-3; DHA). Consumption of fish oils is particularly associated with a low incidence of atherosclerosis and cardiovascular diseases, and this prophylactic effect of fish oil ingestion is attributed to n-3 polyunsaturated fatty acids

Docosahexaenoic Acid-Induced Lipid Peroxidation and Urinary Excretion of Mercapturic Acid in Rats

“…Furthermore, although the Vit. E level in the kidney becomes lower with DHA intake, the extent of the decrease is small compared with that in the liver, as already observed [7,8,9,16]. Hence, the requirement for Vit.…”

“…One is an antioxidative mechanism that suppresses the generation of lipid peroxides, and the other is a detoxification and/or excretion mechanism that suppresses the accumulation of lipid peroxides. The former mechanism is thought to be exerted through increases in ascorbic acid (AsA) and glutathione (GSH) induced by DHA intake [8,9,16], which potentiates reductive recycling of Vit. E, thus maintaining antioxidative potency.…”

Induction of Multidrug Resistance-Associated Protein MRP3 in the Liver of Rats Fed with Docosahexaenoic Acid

“…Peroxidation of lipids is associated with oxygen toxicity and causes degeneration of cell membranes and other lipid-containing structures, and thus is closely associated with pathologies. 5) We have shown in previous studies that the ingestion of DHA, [6][7][8][9][10] as with the ingestion of fish oil, [11][12][13][14] enhanced the susceptibility of rat liver and kidney to lipid peroxidation and increased the requirement for vitamin E (VE). This enhanced lipid peroxidation was a function of the dietary DHA level and was thought to be attributable to the replacement of membrane fatty acids with highly unsaturated DHA.…”

Antioxidative mechanism involved in the preventive efficacy ofBergenia ciliatarhizomes against experimental nephrolithiasis in rats

“…Oxalate increases the production of free radicals, which can induce a cell death process, crystal deposition in the renal tubules, which further leads to growth of calcium oxalate stones. The human, animal, explants and in vitro studies indicate that raised oxidative stress is often present in urolithiasis and oxalate promotes oxidative stress, which is substantially retarded by antioxidants (Kubo et al, 1997). A well-known antioxidant, vitamin E along with mannitol, has been reported to prevent the deposition of CaC 2 O 4 crystals in the kidneys of rats injected with sodium oxalate (Thamilselvan & Menon, 2005).…”