Rat vitamin E status and heart lipid peroxidation: Effect of dietary α‐Linolenic acid and marine n−3 fatty acids

Abstract

Three groups of sixteen male rats each were fed semi-purified diets containing 15% by weight of lipid for a period of 4 wk. The diets contained the same amount of polyunsaturated fatty acids (PUFA) (20% of total fatty acids) and saturated fatty acids (19% of total fatty acids). Dietary PUFA were represented exclusively by linoleic acid (18:2 diet), or 10% linoleic acid and 10% linolenic acid (18:3 diet), or 10% linoleic acid and 10% long-chain n-3 fatty acids (LCn-3 diet). The overall amount of vitamin E was similar in the three diets, i.e., 140, 133 and 129 mg/kg diet, respectively. Following appropriate extraction, tocopherol levels in heart, liver, brain, adipose tissue (AT) and plasma were measured by high-performance liquid chromatography. The level of vitamin E in the heart decreased with n-3 PUFA diets, most markedly with LCn-3 PUFA. Liver and AT vitamin E contents also decreased with n-3 PUFA diets when expressed as micrograms/mg total lipids and micrograms/mg phospholipids, respectively. Total plasma vitamin E was lower in rats fed the LCn-3 diet, but there was no significant difference when expressed as microgram/mg total lipids. Brain vitamin E was not affected by the various diets. In vitro cardiac lipid peroxidation was quantified by the thiobarbituric acid reactive substances (TBARS) test. Heart homogenates were incubated at 37 degrees C for 15 and 30 min in both the absence (uninduced) or presence (induced) of a free radical generating system (1 mM xanthine, 0.1 IU per mL xanthine oxidase, 0.2 mM/0.4 mM Fe/ethylenediaminetetraacetic acid). TBARS release was time-independent but significantly higher when LCn-3 fatty acids were fed to rats in either the uninduced or induced system. The study demonstrated that n-3 PUFA diets can influence vitamin E status of rats even in short-term experiments and can change the susceptibility of the heart to in vitro lipid peroxidation.

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“…This is in agreement with earlier studies [10][11] . Cyanogenic glycosides, which are physiologically important but quantitatively at minor levels, are present in flaxseed.…”

“…Therefore, use of flaxseed based diet at higher dosage for a longer period might causes an increased oxidative stress and a reduced antioxidant vitamins. There are reports on use of flaxseed fed to rats at 20% caused a reduction in plasma and liver vitamin E levels [10][11] . The major antinutritional factors present in flaxseed are phytic acid, cyanogenic glycosides and linatine.…”

“…SDG of flaxseed is well known for antioxidant, antibacterial, antitumor, antiviral and cytotoxic properties [8][9] . Earlier reports have demonstrated a reduction in vitamin E levels in plasma and liver of rats fed with 20% flaxseed [10][11] . There is growing awareness about the use of flaxseed as a source of food and also for several therapeutic principles.…”

Lipid peroxidation during n−3 fatty acid and vitamin E supplementation in humans

“…Peroxide values of both oils remain similar during storage, suggesting that lipid peroxidation occurred in vivo. Other studies in animals showed an increase in lipid peroxidation along with a reduction in antioxidant defense systems (32)(33)(34)(35). Possible effects from lipid peroxidation products within the food cannot be completely ruled out (29,36).…”

Long-Chain n-3 Fatty Acids Specifically Affect Rat Coagulation Factors Dependent on Vitamin K

“…Thus, it was demonstrated that more tissue ␣-tocopherol was required to protect rat liver membranes when they were enriched in n-3 fatty acids 45 and that the antioxidant efficiency was lower for n-3 than for n-6 fatty acids in monkey liver. 16 In our in vivo experiments, production of tocopherolquinone was likewise strongly correlated only with the sum of liver long-chain n-3 fatty acids, not only in each dietary group but also in all pooled animals (rϭ0.57, Pϭ0.001, nϭ32).…”