The effect of fatty acid composition of rapeseed oil on plasma lipids and oxidative stability of low‐density lipoproteins in cholesterol‐fed hamsters

We studied the effect of four rapeseed oils with different fatty acid profiles on parameters implicated in the pathogenesis of atherosclerosis in humans in a model experiment with hamsters. The hamsters were divided into seven groups and fed a semi‐synthetic, cholesterol‐enriched diet (5 g/kg diet) containing 15% of the fat in question for a period of six weeks. The following rapeseed oils were used: (1) conventional rapeseed oil (6% saturated fatty acids [SFA], 64% monounsaturated fatty acids [MUFA], 18% linoleic acid [LA], 9% α‐linolenic acid [ALA]), (2) linoleic acid‐rich rapeseed oil (6% SFA, 61% MUFA, 28% LA, 2% ALA), (3) oleic acid‐rich rapeseed oil (6% SFA, 74% MUFA, 11% LA, 5% ALA), (4) myristic acid‐rich rapeseed oil (11% myristic acid, 35% SFA, 44% MUFA, 14% LA, 5% ALA). Sunflower oil, olive oil and lard were used as control fats. The concentrations of the lipids in the plasma, in the lipoprotein fractions and in the liver, the fatty acid composition of various tissues, the tocopherol status and the susceptibility of low‐density lipoproteins (LDL) to in vitro‐oxidation were determined. The concentrations of total cholesterol found in the plasma and in the LDL fraction and the ratios of LDL to HDL were similar after feeding the four different types of rapeseed oil, sunflower oil and olive oil. Lard produced the highest concentrations of cholesterol in plasma and the LDL fraction and the highest ratio of LDL to HDL. Feeding conventional, oleic acid‐ and myristic acid‐rich rapeseed oils resulted in markedly lower ratios of arachidonic to eicosapentaenoic acid in the lipids of the liver and the erythrocytes. This is considered beneficial for the formation of eicosanoids. The lag‐time before the onset of peroxidation of the LDL lipids, induced by copper ions, was not statistically significant between the seven hamster groups suggesting that the susceptibility of LDL to lipid peroxidation was similar after feeding all types of fat. Considering all parameters obtained in the used hamster model it is obvious that all four rapeseed oils are at least as favourable as olive oil or sunflower oil.     

Dietary fish oil and vitamin E enhance doxorubicin effects in P388 tumor-bearing mice

In this study, four kinds of rodent diets, CO, FO, CVe, and FVe, were sued by addition of canola oil, oil mixture (fish oil + canola oil), canola oil plus vitamin E, and oil mixture plus vitamin E, respectively, to a basic diet, AIN-93G, to investigate the influence of dietary fish oil and vitamin E on doxorubicin (DOX) treatment in P388 ascitic mice. Animal life span (LS) and heart damage were recorded in mice fed the four different diets and treated with different doses of DOX. The optimal doses of DOX for antitumor effect as manifested by increased LS were 6.0 and 9.0 mg/kg. Both fish oil and vitamin E significantly enhanced this effect. On the other hand, DOX at 12.0 mg/kg induced severe heart damage, which was also significantly aggravated by both fish oil and vitamin E, as shown by both decreased LS and increased serum creatine phosphokinase activity. Fish oil and vitamin E appeared to enhance the antitumor effect of optimal doses of DOX but to aggravate cardiotoxicity owing to DOX overdose.     

The effect of clofibrate on heart and plasma lipids in rats fed a diet containing rapeseed oil

The effect of clofibrate on heart and plasma lipids in rats fed a diet containing 30% of the calories as peanut oil (PO) or rapeseed oil (RSO) (42.7% erucic acid and 0.5% eicosenoic acid) was studied. A decrease of erucic acid content to one-third and concomitant increase in the content of 18∶1, 16∶1 and 16∶0 fatty acids in plasma triacylglycerols were observed after administration of clofibrate to rats fed the RSO-diet. It is suggested that these changes reflect the increased capacity of the liver to chainshorten very long chain length fatty acids. The extent of lipidosis in the heart of rats fed the RSO-diet was decreased by 50% by clofibrate. However, the concentration of erucic acid in heart triacylglycerols decreased much less (30%) than the concentration of all other fatty acids (50–65%). It is concluded that the clofibrate administration increased the oxidative capacity of the heart mitochondria and that the heart cell does not have an efficient system to handle very long chain length monounsaturated fatty acids as does the liver.     

Metabolic effects of selenium as related to vitamin E

Trace amounts of dietary selenium, which prevent certain vitamin E deficiency symptoms, have been found to affect the composition of chick tissues. Both selenium and vitamin E increased liver coenzyme A levels to normal when cystine was omitted from the diet. Liver and plasma total fatty acids were unaltered by selenium but vitamin E increased the arachidonic acid content slightly. There was no effect of either selenium or vitamin E on total lipid, cholesterol, phopholipid or coenzyme Q in liver. Low dietary levels of either selenium or vitamin E, which were insufficient in preventing deficiency symptoms, completely eliminated mortality from toxic amounts of a dietary antioxidant. The ability of dietary selenium to reducein vitro lipid peroxidation in chick liver homogenates was not demonstrable with rat liver. Presented at the AOCS meeting in Toronto, Canada, 1962.     

Solubilization of vitamin C in fish oil and synergistic effect with vitamin E in retarding oxidation

Antioxidative effects of ascorbic acid and δ-tocopherol on the oxidation of sardine oil stored at 30°C in the dark has been investigated. It was found from phase diagrams and peroxide values of fish oil/lecithin/water systems that the desirable levels of lecithin and water to solubilize ascorbic acid in the oil were 0.3% (w/w) and 0.1% (w/w), respectively. When ascorbic acid (0.02%) and δ-tocopherol (0.4%) were used together, the induction period of fish oil could be lengthened 22-fold, due to their synergism. They could inhibit the production of carbonyl and volatile compounds and oxidative polymerization.     

Sparing effects of selenium and ascorbic acid on vitamin C and E in guinea pig tissues

Background

Selenium (Se), vitamin C and vitamin E function as antioxidants within the body. In this study, we investigated the effects of reduced dietary Se and L-ascorbic acid (AA) on vitamin C and α-tocopherol (AT) status in guinea pig tissues.

Methods

Male Hartley guinea pigs were orally dosed with a marginal amount of AA and fed a diet deficient (Se-D/MC), marginal (Se-M/MC) or normal (Se-N/MC) in Se. An additional diet group (Se-N/NC) was fed normal Se and dosed with a normal amount of AA. Guinea pigs were killed after 5 or 12 weeks on the experimental diets at 24 and 48 hours post AA dosing.

Results

Liver Se-dependent glutathione peroxidase activity was decreased (P < 0.05) in guinea pigs fed Se or AA restricted diets. Plasma total glutathione concentrations were unaffected (P > 0.05) by reduction in dietary Se or AA. All tissues examined showed a decrease (P < 0.05) in AA content in Se-N/MC compared to Se-N/NC guinea pigs. Kidney, testis, muscle and spleen showed a decreasing trend (P < 0.05) in AA content with decreasing Se in the diet. Dehydroascorbic acid concentrations were decreased (P < 0.05) in several tissues with reduction in dietary Se (heart and spleen) or AA (liver, heart, kidney, muscle and spleen). At week 12, combined dietary restriction of Se and AA decreased AT concentrations in most tissues. In addition, restriction of Se (liver, heart and spleen) and AA (liver, kidney and spleen) separately also reduced AT in tissues.

Conclusion

Together, these data demonstrate sparing effects of Se and AA on vitamin C and AT in guinea pig tissues.     

Effect of selenium and vitamin E supplements on tissue lipids, peroxides, and fatty acid distribution in experimental diabetes

The protective role of selenium (Se), given as a Se-rich yeast, selenomethionine or selenomethionine+vitamin E supplement, toward changes in lipid, peroxide, and fatty acid distribution in tissues of streptozotocin-induced diabetic rats, was investigated, after 24 wk of disease. Diabetes increased liver thiobarbituric acid-reactive substances and conjugated dienes; Se supplement completely corrected these changes. In kidney, as in heart, the peroxide levels were not significantly changed by diabetes. In diabetic rat liver, a significant drop in triglycerides and phospholipids (P<0.05) was observed; this was modulated by Se+vitamin F supplementation. Se+vitamin E supplementation also inhibited the decrease in 18∶2n-6 and the increase in 22∶6n-3 observed in liver of diabetic rats, changes which reflect altered glycemic control. In kidney, heart, and aorta, diabetes produced some changes in lipid content and fatty acid distribution, especially an increase in heart triglycerides which was also corrected by the Se supplement. Se supplementation to diabetic rats also increased 18∶0 etherlinked alcohol, 20∶4 n-6, and 22∶5 n-3 in cardiac lipids. In aorta, Se + vitamin E significanlty increased 20∶5 n-3. These polyunsaturated fatty acids are precursors, in situ, of prostaglandin l₂ (PGl₂) and PGl₃ which may protect against cardiovascular dysfunction. In kidney, converrely, Se decreased 20∶4 n-6, the precursor of thromboxane A₁ implicated in diabetic glomerular injury. thus Se, and more efficiently Se + vitamin E supplementation, in experimental diabetes could play a role in controlling oxidative status and altered lipid metabolism in liver, thereby maintaining favorable fatty acid distribution in the major tissues affected by diabetic complications.     

Lipoprotein lipase in rats fed fish oil: Apparent relationship to plasma insulin levels

To investigate the role of lipoprotein lipase (LPL) and hepatic lipase in the triacylglycerol lowering effects of fish oil, rats were fed lard (L), corn oil (CO) or menhaden oil (MO) as the primary fat source in otherwise identical diets. After 2 weeks, soleus muscle LPL differed between groups (MO>CO>L). Hepatic lipase did not differ between CO- and MO-fed rats but was elevated in L-fed rats. Adipose LPL did not differ between diet groups. Total epididymal fat weight was reduced in MO-fed rats. There was a significant positive correlation between adipose tissue weight and plasma free fatty acids. MO-fed rats had lower plasma insulin levels. Insulin was directly correlated with plasma triacylglycerol and glucose, consistent with a hyperinsulinemic, insulin-resistant state in CO-and L-fed rats, and a protective effect with MO feeding. In addition, insulin was directly correlated with adipose LPL. A negative relationship between soleus muscle LPL and insulin approached significance. Soleus muscle LPL was significantly inversely correlated with triacylglycerol. The data indicate that increased skeletal muscle LPL, in response to MO or a MO-induced decrease in insulin, may contribute to the triacylglycerol-lowering effects of fish oil. Decreased fat weight and adipose LPL and increased soleus muscle LPL and decreased plasma triacylglycerol suggest a shift from fat deposition to oxidation with MO feeding. The lack of response of hepatic lipase to MO feeding suggests that this enzyme does not contribute to the fish oil-stimulated lowering of plasma triacyglycerolvia hepatic reuptake of very low density lipoproteins or other triacylglycerol-rich lipoproteins.     

Myocardial lipids and nucleotides of rats fed olive oil or rapeseed oil

After 1 week, the level of myocardial fatty acids was 4 times greater in young rats fed high erucic rapessed oil than in those fed olive oil. The proportion of erucic acid was 5.6% in the mitochondrial fraction, 15.1% in the microsomal fraction, and 34.8% in the floating fat fraction. This incorporation of erucic acid into triglycerides of the floating fat was evidence of esterification. The changes in the mitochondrial lipids did not alter the content of adenine nucleotides of the myocardium nor its apparent capacity to oxidize substrates.     

Fish oil fatty acid esters of phytosterols alter plasma lipids but not red blood cell fragility in hamsters

In an attempt to combine the hypocholesterolemic properties of plant sterols with the hypotriglyceridemic action of fish oil FA, plant sterols have recently been esterified to fish oil n−3 PUFA. The objective of this study was to determine the effects of plant sterols esterified to n−3 PUFA on plasma lipid levels and erythrocyte fragility. For 5 wk, male Golden Syrian hamsters were fed diets varying in cholesterol and plant sterol content: (i) Noncholesterol (semipurified diet with no added cholesterol or plant sterols) (ii), Cholesterol (0.25% cholesterol) (iii), Sterols (0.25% cholesterol plus 1% nonesterified plant sterols), or (iv) Fish oil esters of plant sterols (0.25% cholesterol plus 1.76% EPA and DHA sterol esters, providing 1% plant sterols). The addition of fish oil esters of plant sterols to the cholesterol diet decreased (P=0.001) plasma total cholesterol levels by 20%, but nonesterified plant sterols did not have such a beneficial impact. In addition, non-HDL cholesterol concentrations were 29% lower in hamsters fed fish oil esters of plant sterols than in hamsters fed nonesterified plant sterols (P<0.0001). Despite higher (P<0.0001) plant sterol levels in whole erythrocytes of hamsters fed nonesterified plant sterols and fish oil esters of plant sterols compared with hamsters fed no plant sterols, no difference was observed in erythrocyte fragility. The present results show that EPA and DHA esters of plant sterols have a hypocholesterolemic effect in hamsters, and that these new esters of plant sterols exert no detrimental effect on erythrocyte fragility.     

Lactose-induced diarrhea increases oxidative stress and it is more severe in rats deficient in vitamin E

Diarrhea is the disease with high incidence in the world and causes infant mortality and malnutrition in the developing world. This justifies the study of nutrition and diarrhea. Due to ethical and financial considerations it is difficult to study nutrition and diarrhea in children thus animal models have become a convenient alternative. In previous studies it was shown that lactose induced diarrhea in rats was associated with a reduction in tissue levels of vitamin E and also with evidence of an inflammatory response of the intestine. Accordingly, in this study, in order to determine the effect of this type of diarrhea on the level of oxidative stress, diarrhea was induced in vitamin E sufficient and deficient rats. The results showed that after 23 days the tissue concentration of vitamin E decreased in all the rats with diarrhea but this reduction was substantially greater in the vitamin E deficient group. Moreover, diarrhea was 60% more severe in the vitamin E deficient rats than in the vitamin E sufficient group that also had diarrhea. Both diarrhea and vitamin E deficiency altered malonaldehyde and superoxide dismutase levels in various tissues. However, the most outstanding changes associated with diarrhea were a 100% increment in plasma malonaldehyde and erythrocyte superoxide dismutase activities which were 8 to 11 times higher than those seen in the rats without diarrhea. These non-invasive changes correlated well with the severity of diarrhea. The study shows that vitamin E deficiency results in diarrheas which are more severe and that lactose induced diarrhea is associated with higher levels of oxidative stress.     

Effect of cold stress on rapeseed oil fed rats

No mortality was observed in 6 week old male Sprague-Dawley rats subjected to cold at 4 C for 3 weeks and fed either a control diet (Chow) or a semisynthetic diet containing 20% by wt rapeseed oil high in erucic acid (23.6%). All rats fed the Chow diet and 17 of 20 rats fed the rapeseed oil-containing diet survived 4 weeks in the same environment. Three rats on the latter diet died of self-mutilation. Marked myocardial lipidosis as well as a large accumulation of 20∶1 and 22∶1 was observed in the hearts of rats fed the rapeseed oil-containing diet. Five of 20 rats on the Chow diet and 2 of 20 rats on the rapeseed oil-containing diet had focal necrotic areas in the myocardium.     

Effect of sesaminol on plasma and tissue alpha-tocopherol and alpha-tocotrienol concentrations in rats fed a vitamin E concentrate rich in tocotrienols

We have shown that sesame lignans added to rat diet resulted in significantly greater plasma and tissue concentrations of α- and γ-tocopherol concentrations in supplemented rats than in rats without supplementation. In the present studies we examined whether sesaminol, a sesame lignan, enhances tocotrienol concentrations in plasma and tissues of rats fed diets containing a tocotrienol-rich fraction of palm oil (T-mix). In Ex-periment 1, effects of sesaminol on tocotrienol concentrations in plasma, liver, and kidney were evaluated in rats fed diets containing 20 mg/kg of T-mix (20T) and 50 mg/kg of T-mix (50T) with or without 0.1% sesaminol. Although the T-mix contained 23% α-tocopherol, 22% α-tocotrienol, and 34% γ-tocotrienol, α-tocopherol constituted most or all of the vitamin E in plasma and tissue (from 97% in kidney to 100% in plasma), with no or very little α-tocotrienol and no γ-tocotrienol at all. Addition of sesaminol to the T-mix resulted in significantly higher plasma, liver, and kidney α-tocopherol concentrations compared to values for T-mix alone. Further, T-mix with sesaminol resulted in significantly higher α-tocotrienol concentrations in kidney, although the concentration was very low. In Experiment 2, we examined whether sesaminol caused enhanced absorption of α-tocopherol and α-tocotrienol in a dosage regimen supplying T-mix and sesaminol on alternating days and observed significantly higher levels of α-tocopherol and α-tocotrienol in rats fed sesaminol, even without simultaneous intake, compared to those in rats without sesaminol. In Experiment 3, α-tocopherol was supplied to the stomach with and without sesaminol, and α-tocopherol concentrations in the lymph fluid were measured, α-Tocopherol concentrations were not different between groups. These results indicated that sesaminol produced markedly higher α-tocopherol concentrations in plasma and tissue and significantly greater α-tocotrienol concentrations in kidney and various other tissues, but the concentrations of α-tocotrienol were extremely low compared to those of α-tocopherol (Exps. 1 and 2). However, the sesaminol-induced increases of α-tocopherol and α-tocotrienol concentrations in plasma and tissue were not caused by their enhanced absorption since sesaminol did not enhance their absorption.     

Identification and quantification of prostaglandin E3 in renal medullary tissue of three strains of rats fed fish oil

Three strains of rats were fed a fish oil diet to verify their ability to incorporate and convert dietary eicosapentaenoic acid (20∶5ω3) into trienoic prostaglandins. Our results show that such conversion indeed occurs in kidney medullae homogenates. Specifically, the presence of prostaglandin E₃ (PGE₃) was established by gas chromatographic-mass spectrometric (GC-MS) analysis. That compound was conclusively identified by comparison of fragment ions and their relative intensities with those obtained from authentic PGE₃. Further evidence was provided by studying the recovery of exogenously added PGE₃. The crude ethyl acetate extracts of the medullary homogenates were methylated and cleaned up by liquid-gel chromatography with Lipidex-5000 prior to conversion to PGB₃ for GC-MS analysis. The PGE₃ was quantified by selected ion monitoring (SIM) with [3,3,4,4-²H₄PGE₂ as internal standard. The levels of PGE₃ were similar, about 3 ng/mg of wet tissue, in the 3 strains of rats. Identical in vivo conversion of the 20∶5ω3 fatty acid to PGE₃ could not be positively established by analysis of pooled urine specimens.     

Serum lipids in spontaneously hypertensive rats and sprague-dawley rats fed menhaden oil

Dietary n-3 fatty acids, abundant in fish oil, exert a variety of effects that attenuate cardiovascular disease. In this study, we assessed the effect of fish oil (menhaden oil) on the serum lipid profile in hypertensive and normotensive rats. Spontaneously hypertensive rats (SHR) or Sprague-Dawley rats (SD) were fed either standard powdered diet (L-485), or L-485+5% menhaden oil (MO) or L-485+5% corn oil (CO) from weaning through eight months of age. Systolic blood pressure (BP) was periodically determined on SHR. Serum lipid profiles were performed at eight months on sample taken from the exposed hearts of anesthetized, fasted rats. SHR, compared with SD (diets combined) had significantly lower triaclyglycerols (TG), higher cholesterol (CHOL), higher high density lipoprotein cholesterol (HDL CHOL), higher low density lipoprotein cholesterol (LDL CHOL), and a higher LDL:HDL ratio. Comparison among diets (strains combined) revealed that rats fed MO had the lowest values for TG, CHOL, LDL and LDL:HDL; HDL did no vary with diet. SHR were less responsive to diet-induced changes than were SD; no decrease in TG, LDL or LDL:HDL was observed in SHR, nor was degree of hypertension altered in SHR by the MO or CO diet. In summary, MO is more effective than CO in shifting the lipid profile of rats toward one that is less atherogenic. However, the SD rat is more susceptible to diet-induced lipid modification than is the SHR.     

Lipid peroxidation and antioxidant status is affected by different vitamin E levels when feeding fish oil

The protective role of vitamin E and changes in the status of several physiological antioxidants after feeding rats a fish oil diet were investigated. Six-week-old male Sprague-Dawley rats were divided into four groups and fed experimental diets for 8 wk. Three fish oil (FO) groups were fed a menhaden fish oil and soybean oil (SO) (9∶1) mixture as 10% (w/w) of the diet. These groups were provided with ≤3, 45 or 209 IU of vitamin E/kg diet. One SO group was used as control and was fed ≤45 IU of vitamin E/kg diet. Plasma vitamin E levels, when expressed as vitamin E per mL plasma, were extremely low in the group fed FO and ≤3 IU of vitamin E, and were lower in the groups fed FO than in the group fed SO. However, plasma vitamin E levels when expressed per mg plasma lipid were higher in the FO groups provided with ≤45 and 209 IU of vitamin E than in the SO group. Compared with the SO group, plasma levels of thiobarbituric acid reactive substances (TBARS), when expressed per mg lipid, were higher in the three FO groups, plasma retinol levels were lower in the FO groups provided with ≤3 and 45 IU of vitamin E, and ascorbic acid levels were lower only in the FO group provided with ≤3 IU of vitamin E. Blood glutathione (GSH) levels were lower in all three FO groups than in the SO group. Liver vitamin E levels increased as the dietary level of vitamin E increased, but all FO groups had higher liver levels of TBARS than the SO group. The dietary vitamin E levels were correlated positively with plasma vitamin E (r=0.71) and negatively with TBARS in both the plasma and liver of rats fed FO. Among the antioxidants measured, correlations were found between plasma retinol and vitamin C (r=0.64), and plasma vitamin C, uric acid (r=0.72) and blood GSH (r=0.60). Weaker correlations were found between plasma retinol, uric acid and blood GSH. It is concluded that vitamin E requirements are higher when feeding fish oil. Vitamin E seems necessary to prevent enhanced lipid peroxidation and to maintain appropriate levels of other physiological antioxidants.     

Vitamin E inhibits fish oil-induced hyperlipidemia and tissue lipid peroxidation in hamsters

Previous research has linked hyperlipidemia with increased serum concentrations of lipid peroxidation products; however, a specific association between diet-induced oxidative stress and hyperlipidemia has not been studied. In the present study, the relationship between tissue lipid peroxidation and hyperlipidemia induced by ingestion of fish oil was examined. In Experiment 1, male Golden Syrian hamsters were fed semipurified diets composed of 1.6 wt% safflower oil plus 15.0 wt% of either butterfat (BF), safflower oil (SAFF), or high-cholesterol menhaden oil [MHO(H-CHOL)] semipurified diets for 27 d. The cholesterol contents of the diets were adjusted to 0.088%. The MHO(H-CHOL)-fed hamsters exhibited higher serum concentrations of total cholesterol, triglycerides, apolipoprotein B, and lipid peroxides when compared to the BF and SAFF diet groups. In a further study (Experiment 2), hamsters were fed for 27 d three dietary treatments: (i) MHO(H-CHOL) with no vitamin E content; (ii) a low-cholesterol menhaden oil containing high concentrations of vitamin E (2.5 mg tocopherol/g oil or dietary concentrations of 375 mg/kg) [MHO(L-CHOL)+E]; and (iii) the MHO(L-CHOL+E) with added cholesterol (595 mg/kg) [MHO(L-CHOL)+CHOL+E] to match the cholesterol content of the MHO(H-CHOL). The MHO(L-CHOL)+E and MHO(L-CHOL)+CHOL+E diet groups showed lower concentrations of serum cholesterol, triglycerides, and hepatic lipid peroxides than the MHO(H-CHOL)-treated group. Moreover, in contrast to the hypercholesterolemia caused by the MHO(H-CHOL) feeding, the MHO(L-CHOL)+E and MHO(L-CHOL)+CHOL+ E diets did not show a serum cholesterol-elevating action. This study supports the hypothesis that oxidative stress in the Syrian hamster could play a causal role in dietary-induced hyperlipidemia which can be inhibited by high vitamin E intake.     

Monoethylenic isomers in cardiac lipids of rats fed partially hydrogenated herring oil

Compositional studies have been carried out to compare the monoethylenic fatty acid isomers of a partially hydrogenated herring oil with those found in the cardiac lipid of young rats fed this oil for 1 or 16 weeks. In general, all geometrical and positional isomers with chain lengths C₁₆, C₁₈, C₂₀ and C₂₂ found in the hydrogenated oil were also observed in cardiac lipid. Evidence was also obtained for the occurrence of β-oxidation in the catabolism of thecis andtrans isomers of these long chain acids. Presented at the AOCS Meeting, Ottawa, September 1972.     

The influence of vitamin E and selenium on lipid peroxidation and aldehyde dehydrogenase activity in rat liver and tissue

Malondialdehyde (MDA) production and cytosolic aldehyde dehydrogenase (ALDH) response were examined in rat liver tissues after feeding different levels of dietary vitamin E and/or selenium and polyunsaturated fat for 12–38 wk. MDA production was significantly increased by vitamin E deficiency or by high levels of polyunsaturated fat intake, but not by selenium deficiency. The activity of cytosolic ALDH increased upon increased production of MDA after 12–16 wk of feeding the lipid peroxidation-inducing diets. However, ALDH activity was suppressed after 38 wk of feeding the vitamin E-deficient diet. The results indicate that the hepatic cytosolic ALDH may be involved in the metabolism of MDA during a relatively short-term increase inin vivo lipid peroxidation, but that ALDH activity becomes suppressed after more severein vivo lipid peroxidation has been produced. Hepatic and plasma α-tocopherol levels and lipid peroxidation products were measured for the various dietary groups.