Relationship between tissue lipid peroxidation and peroxidizability index after α-linolenic, eicosapentaenoic, or docosahexaenoic acid intake in rats

Abstract

In a previous study, we found that the extent of dietary n-3 docosahexaenoic acid (DHA)-stimulated tissue lipid peroxidation was less than expected from the relative peroxidizability index of the total tissue lipids in rats with adequate vitamin E nutritional status. This suppression of lipid peroxidation was especially prominent in the liver. To elucidate whether this phenomenon was unique to DHA, we compared the peroxidation effects of n-3 a-linolenic acid (a-LN) and n-3 eicosapentaeonic acid (EPA) with those of DHA in rats. Either a-LN (8·6 % of total energy), EPA (8·2 %), or DHA (8·0 %) and one of two levels of dietary vitamin E (7·5 and 54 mg/kg diet) were fed to rats for 22 d. Levels of conjugated diene, chemiluminescence emission and thiobarbituric acid (TBA)-reactive substance in the liver, kidney, and testis were determined as indicators of lipid peroxidation. In rats fed the DHA diet deficient in vitamin E (7·5 mg/ kg diet), TBA values in the liver, kidney, and testis correlated well with the tissues' relative peroxidizability indices. In rats fed the a-LN diet with an adequate level of vitamin E (54 mg/kg diet), a close association between relative peroxidizability indices and lipid peroxide levels was observed in all the tissues analysed. However, in rats fed either the EPA diet or the DHA diet with an adequate level of vitamin E, the extent of lipid peroxidation in each tissue was less than expected from the relative peroxidizability index. This suppression was particularly marked in the liver. We concluded that suppression of lipid peroxidation below the relative peroxidizability index was not unique to DHA, but was also seen with EPA, which has five double bonds, in rats with adequate vitamin E nutritional status, but not with a-LN, which has three double bonds.

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.…”

“…E, AsA and GSH is not enough to suppress the generation of lipid peroxides. Additionally, ingestion of DHA did not increase liver glutathione reductase and glutathione peroxidase activities, even though the tissue lipid peroxide levels in DHA-fed rats were higher [8,9]. These observations suggest that some mechanisms other than antioxidants and antioxidant enzymes are induced in order to suppress the accumulation of lipid peroxides after DHA ingestion.…”

“…In previous studies, we showed that DHA ingestion [7][8][9][10][11], similar to fish oil ingestion [12][13][14][15], enhanced the susceptibility of rat liver and kidney to lipid peroxidation and increased the requirement for vitamin E (Vit. E).…”

“…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.…”

Blood Cell Membrane Omega-3 ( n -3) Fatty Acid Abnormality and Supplementation in Patients with Sickle Cell Anemia

“…The long-chain omega-6 and -3 polyunsaturated fatty acids (LCPUFA) are vital structural and functional components of cells and organelles, and the balance between the two fatty acid families is a determinant of blood cell aggregation and coagulation, adhesion, deformability, and inflammatory response (Mills et al, 1993;Mukherjee et al, 2004;Nishiyama et al, 2000;Saito and Kubo, 2003). Hence, it is postulated that the imbalance of membrane n-6/n-3 LCPUFA is the antecedent of the loss of membrane asymmetry, blood cell adhesion and aggregation, and vasoocclusion in SCD (Ren et al, 2005).…”