Menhaden Oil Diet Research Articles

Influence of dietary n-3 fatty acids on myocardial ischemia and reperfusion

We have investigated the effect of elevated n-3 (omega-3) fatty acid content in the diet on arrhythmias, ischemic damage, and inflammatory cell infiltration into the reperfused left ventricular free wall (LVFW). Weanling rats were fed purified diets in which the lipid was replaced with either corn oil (CO) or menhaden oil (MO). After 4 wk, MO feeding resulted in significant elevations in both the ratio of n-3 to n-6 fatty acids and the unsaturation index in myocardial phospholipids. Rats were subjected to 15 min of ischemia followed by reperfusion. After 6 h of reperfusion of the left coronary artery there was significantly less creatine kinase (CK) lost from the LVFW of rats fed MO. Leukocyte infiltration into the LVFW, as measured by myeloperoxidase (MPO) activity, was also significantly reduced with MO feeding at 6 h. Arrhythmias were studied in a separate group of 17 rats; both the incidence and severity of ventricular tachycardia and ventricular fibrillation were significantly reduced during the ischemic and reperfusion periods with MO feeding. After 24 h of reperfusion there was also significantly less CK lost from the LVFW of MO-fed rats; however, there was no significant difference in tissue MPO activity in ventricular homogenates. Survival after 24 h of reperfusion was 76% (16/21) for MO- and 41% (9/22) for CO-fed rats. The data suggest a protective effect for dietary MO in myocardial ischemia-reperfusion, which may involve both an early reduction in leukocyte infiltration and a reduction in the incidence of fatal arrhythmias.

Transglutaminase activity in mouse liver is unaffected by dietary menhaden oil

In order to determine the effect of dietary fats on hepatic transglutaminase activity, male CD-1 mice were fed diets containing 10 wt% menhaden oil (MO) or 10 wt% corn oil (CO) for 4 weeks. Dietary fatty acids significantly altered the fatty acid composition of liver phospholipids. Arachidonic and linoleic acids were replaced by eicosapentaenoic acid and docosahexaenoic acid in mice consuming the MO diet. PGE 2 synthesis decreased by 32% in the livers from mice consuming MO compared to that observed in CO fed mice. Liver transglutaminase activity was unchanged by MO indicating that n-3 polyunsaturated fatty acids do not affect its synthesis or activity.

Enrichment of (n-3) Fatty Acids of Suckling Rats by Maternal Dietary Menhaden Oil

The study was undertaken to determine whether the content of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in neonatal rats can be increased through milk provided by lactating mothers fed a diet containing 20% menhaden oil (experimental group), in comparison with a group fed a 20% corn oil diet (control group). The test diets were isocaloric and provided 41% of total energy as fat. Coinciding with 3-9% higher maternal body weight gain throughout the lactation period with the menhaden oil diet, the suckling rats in the experimental group at the ages of 3-9 d gained 5-10% more weight than did their control counterparts. When compared with corn oil, maternal dietary menhaden oil induced not only a higher weight percentage but also higher concentrations (microgram/mL) of EPA, DHA and total (n-3) fatty acids in milk, plasma, platelets and erythrocytes of neonates. These changes were accompanied by lower arachidonic and linoleic acid levels. EPA and DHA were detected in all three blood components of the control group, whose corn oil diet contained linolenic acid but not longer chain (n-3) fatty acids. This finding, together with the higher DHA to EPA ratios found in the three blood components than in the milk of the experimental group, suggests that neonatal rats possess the enzymes necessary for producing DHA from EPA and linolenate by desaturation and elongation mechanisms.

Effect of dietary menhaden oil and vitamin E onin vivo lipid peroxidation induced by iron

Weanling rats were fed diets containing 10% menhaden oil (MO) or 10% corn oil-lard (1:1, COL) with low (less than or equal to 5 IU/kg) or supplementary (35 IU/kg) vitamin E for six weeks. The rats were killed 30 min after injection with 24 mg iron/kg as ferrous chloride because thiobarbituric acid-reactive substances (TBARS) in liver homogenates were highest at 30 min after injection of iron into rats fed a standard diet. Tissue homogenates were used either without incubation (zero-time) or after incubation at 37 degrees C for 1 hr. In addition to TBARS and conjugated dienes, headspace hexanal and total volatiles (TOV) determined by capillary gas chromatography were useful indices of lipid peroxidation since they were decreased by vitamin E supplementation and were increased with increasing iron dose. Regardless of the dietary lipid used, vitamin E supplementation decreased headspace hexanal, TOV, TBARS and conjugated dienes in both zero-time and incubated homogenates of liver and kidney. Dietary MO increased TBARS in both zero-time and incubated homogenates of tissue from rats injected with iron. In contrast, dietary MO decreased hexanal and TOV in incubated tissue homogenates. The study demonstrated the usefulness and limitations of using hexanal and TOV as indices of lipid peroxidation.

Influence of menhaden oil on mitochondrial respiration in BHE rats.

The effects of corn or menhaden oil and thyroxine treatment on hepatic mitochondrial respiration was studied. BHE rats were fed a 64% sucrose, 6% corn, or menhaden oil diet until they were 60-70 days of age. Succinate-supported mitochondrial respiration was studied at 3 degrees C intervals from 4 to 40 degrees C. Upper and lower activation energies and transition temperatures were determined through the calculation of Arrhenius plot. Menhaden oil plus daily thyroxine injection resulted in higher and lower activation energies than the other treatments. This combined treatment also resulted in lower state 3 and higher state 4 respiration rates and tighter coupling of respiration to ATP synthesis. These effects were thought to be due to the effect this treatment combination had on membrane fluidity.

Effect of Dietary Lipids and Vitamin E on in Vitro Lipid Peroxidation in Rat Liver and Kidney Homogenates

Rats were fed for 5 wk 10% (wt/wt) menhaden oil (MO) or a 10% corn oil-lard (COL) mixture (1:1) in diets with a low vitamin E content (less than or equal to 5 mg/kg) or supplemented with d-alpha-tocopheryl succinate to a total of 30 or 150 mg per kg. Thiobarbituric acid-reactive substances (TBARS), conjugated dienes (CD), hexanal and total volatiles (TOV) were measured in tissue homogenates incubated at 37 degrees C for 1 h in the absence (uninduced) and presence of 15 microM ferrous sulfate (induced). The fatty acid composition of liver and kidney reflected that of dietary lipids. For uninduced peroxidation, there was in general a significant inverse correlation of TBARS, CD and TOV with the log of dietary vitamin E content for liver and kidney from rats fed either lipid. For induced peroxidation, the inverse correlation was significant for liver, but not for kidney, from rats fed either lipid. The correlation was generally higher for liver and kidney from rats fed COL than for tissues from rats fed MO. Vitamin E was thus a more effective antioxidant for liver than for kidney regardless of the dietary lipid, and for liver and kidney from rats fed COL than from rats fed MO. Dietary MO enhanced tissue susceptibility to both peroxidation systems. A simulation model developed to mimic the experiments showed good correlations between experimental data and simulated values.

Interacting effects of menhaden oil and sucrose on the lipogenic response to starvation-refeeding

The interacting effects of fat type and carbohydrate source on the hepatic lipogenic response to starvation-refeeding were studied. Three experiments were conducted using male rats fed ad libitum or starved for 48 hours and refed one of four diets. The diets contained corn or menhaden oil and glucose or sucrose. The activities of NADP-linked glucose 6-phosphate dehydrogenase and malic enzyme were determined as were liver lipid (Experiments 1 and 2) and de novo fatty acid synthesis (Experiment 3). Experiment 1 used Sprague-Dawley rats while experiments 2 and 3 used BHE rats. Rats refed the menhaden oil diets had less of a lipogenic response to starvation-refeeding compared to rats refed the corn oil diets. Sucrose-refed rats had more of an enzyme response and a greater fatty acid synthesis response to refeeding than BHE rats refed either of the menhaden oil diets or the corn oil-glucose diet. The percent increment in these parameters was strain dependent. We conclude that the effectiveness of menhaden oil in decreasing fatty acid synthesis is dependent on the type of carbohydrate in the diet and the genetic character of the animal used.

Effects of dietary fats on fatty acid composition and delta 5 desaturase in normal and diabetic rats.

We have studied the effect of various diets on the phospholipid fatty acid composition and in vitro delta 5 desaturase activity of hepatic microsomes derived either from the normal or streptozotocin-induced diabetic rat. The diets studied were the standard rat chow diet and a basal fat-free diet supplemented either with 20 percent saturated fat, 20 percent unsaturated fat, or 20 percent menhaden oil. Phospholipid fatty acid composition analysis revealed that the normal rat fed the saturated fat or menhaden oil diet had significantly decreased arachidonate levels, consistent with decreased delta 5 desaturase activities and decreased 18:2n-6 intake. On the contrary, the unsaturated fat diet decreased dihomo-gamma-linolenate and increased arachidonate levels, without increased delta 5 desaturase activity. Streptozotocin-induced diabetes resulted in decreased arachidonate and delta 5 desaturase activity. The unsaturated fat diet fed to the diabetic rat also failed to correct this decreased delta 5 desaturase activity. The unsaturated fatty acids in this diet also displaced a substantial amount of n-3 fatty acids in both normal and diabetic microsomes, due to the competition between these two fatty acid families for incorporation into the membrane phospholipids. Conversely, the menhaden oil diet fed to the normal and diabetic rats displaced n-6 fatty acids, reduced delta 5 desaturase activity, and enhanced 22:6n-3 incorporation into diabetic microsomes.

Dyslipoproteinemia in murine systemic lupus erythematosus.

Dyslipoproteinemia, a feature of systemic lupus erythematosus may contribute to premature atherosclerosis. In order to develop an experimental model for this dyslipoproteinemia we measured plasma concentrations of lipoproteins in juvenile NZB/W (lupus) and NZB/B (control) mice. Additionally to evaluate the effects of a diet rich in n - 3 fatty acids we measured lipoprotein concentrations in mice on normal or menhaden oil-enriched diets. The lupus mice had elevated triglycerides compared to the controls, similar to that seen in human SLE patients (161 +/- 31 vs 113 +/- 13 mg/dl, P less than 0.003). In contrast, the menhaden oil diet fed NZB/W mice had triglycerides similar to the NZB/B control fed group. In the NZB/W murine SLE model, dyslipoproteinemia is an early sign of disease as has been shown in man, therefore this model will be useful in elucidating the mechanism of dyslipoproteinemia in SLE.

Modulation of Kupffer cell membrane phospholipid function by n-3 polyunsaturated fatty acids

Dietary n-3 polyunsaturated fatty acids (PUFAs) have been reported to improve clinical outcome in a number of inflammatory diseases including burns and sepsis. One mechanism contributing to the anti-inflammatory effect is the incorporation of n-3 PUFAs into membrane phospholipids which decreases macrophage eicosanoid production. We hypothesize that an additional mechanism for their effects is an alteration of membrane signal transduction that decreases macrophage responsiveness to inflammatory stimuli. Kupffer cells, the fixed macrophages of the liver, were obtained from rats pair fed diets for 6 weeks with 15% of calories supplied as menhaden (high n-3), corn (control), or safflower (high n-6) oils. The effects of the dietary oils on Kupffer cell membrane signal transduction and eicosanoid production were assessed by measuring inositol phospholipid (PI) metabolism, intracellular calcium responses, and prostaglandin E 2 (PGE 2) production to the inflammatory signals endotoxin (LPS) and platelet activating factor (PAF). The menhaden oil diet resulted in significant incorporation of n-3 PUFAs into total cellular PUFAs compared to corn and safflower oil. (total n-3 PUFAs, 28.1% menhaden vs 2.1% corn vs 1.2% safflower, P < 0.03) This incorporation altered signal transduction of PAF as both PI turnover (65% ± 10% of corn oil) and calcium response (0.6-fold vs 5.0-fold for corn oil) were significantly reduced in the menhaden oil group. ( P < 0.05) The menhaden oil diet also reduced significantly PGE 2 production in response to PAF and LPS (corn, 348 ± 23 pg/ml; menhaden, 48 ± 6 pg/ml, P < 0.01). We conclude that, in addition to modulating eicosanoid production, n-3 PUFAs can also alter macrophage membrane signal transduction. These mechanisms may contribute to observed anti-inflammatory effects and offer the potential ability to down-regulate macrophage-mediated hypermetabolism in critically ill surgical patients.

Effect of menhaden oil and various seedoils on serum lipids and lipoproteins in rabbits

Four groups of New Zealand White rabbits (n=8) were fed semi-synthetic diets containing 7.6% fat (w/w) for 20 weeks. The fats were: 1. hydrogenated soybean oil (HSBO), 80% stearic acid, with 2% safflower oil (SO), 2. safflower oil, 78% linoleic acid, 3. linseed oil (LO), 54% linolenic acid, and 4. menhaden oil (MO), 21% palmitic acid, 13% eicosapentaenoic acid (EPA), and 8% docosahexaenoic acid (DHA). The diets contained 20% of calories from protein, 56% from carbohydrate, and 24% from fat. The MO diet also contained 0.06% cholesterol while the other diets were cholesterol free. Before assignment to experimental diets, the animals had serum cholesterol values of 62.1±20.3 mg/dl and triglyceride concentration of 40.3±14.3 mg/dl (mean±S.D.). After 4 weeks on the diets, the cholesterol values in the four groups were: HSBO, 70.9±21.2 mg/dl; SO, 59.1±15.9 mg/dl; LO, 65.1±50.7 mg/dl; and MO, 141.7±67.2 mg/dl. Only the MO value differed significantly from the pre-diet value (P<0.01). For the remainder of the study serum cholesterol value in the MO group did not change significantly while in the HSBO group the cholesterol and triglyceride concentrations rose significantly to 127.8±82.2 mg/dl, and 130.6±60.3 mg/dl, respectively, at the end of the study (P<0.05). The MO group's serum triglycerides trended higher but the change did not reach statistical significance. Low density lipoproteins (LDL) were significantly elevated (P<0.01) in the HSBO and MO groups but not in the SO and LO groups. It remains to be determined if the twenty and twenty-two carbon n-3 fatty acids (EPA and DHA) in menhaden oil will elevate serum cholesterol in rabbits in the absence of dietary cholesterol.

Endotoxin challenge after menhaden oil diet: effects on survival of guinea pigs

Improvement in survival to endotoxin has been seen after pretreatment with cyclooxygenase inhibitors. Because eicosapentaenoic acid (EPA), found in menhaden oil, competitively inhibits cyclooxygenase, we fed two groups of guinea pigs diets, in which the fat source was either menhaden or safflower oil, for 6 wk. A third group was allowed the safflower oil diet ad libitum. Menhaden oil-fed animals showed enhanced survival compared with safflower oil control animals 20 h after endotoxin (87 vs 63%, p less than 0.05). Ad libitum-fed safflower oil animals survived least well, with 47% alive at 20 h (p less than 0.005 vs menhaden oil group). We conclude that feeding animals a diet whose predominant lipid source is fish oil significantly improves survival after endotoxin. Dietary fat should be viewed not only as a caloric source but as a pharmacologically active substance that can have profound effects on the host's response to toxic insults.

Dietary Fish Oil Inhibits Bleomycin-Induced Pulmonary Fibrosis in the Rat

Intratracheal bleomycin induces pulmonary fibrosis in experimental animals, but the mechanisms involved are poorly understood. Since altered levels of fatty acid metabolites are associated with bleomycin-induced lung injury, we examined the effects of a change in dietary fat on bleomycin-induced fibrosis. Previously we have shown that an essential fatty acid-deficient diet can reduce the severity of bleomycin-induced pulmonary fibrosis. The present study examined the effect of replacement of usual dietary fat with menhaden oil, rich in eicosapentaenoic acid, on the development of pulmonary fibrosis. Weanling rats were raised on a standard laboratory diet or a diet consisting of a fat-free powder to which was added 25% (w/w) of menhaden oil. After 8 weeks of feeding, the animals received either 1.5 units of bleomycin or an equivalent volume of saline intratracheally. In animals receiving the laboratory diet, bleomycin treatment produced a 44% increase in total lung protein content when compared to saline-treated controls (p less than 0.001) and a 77% increase in total lung hydroxyproline content (p less than 0.01). In contrast, bleomycin-treated animals receiving the menhaden oil diet had only small increases, which did not reach statistical significance, in protein and hydroxyproline content in the lung. Bronchoalveolar lavage cellularity did not differ among the treatment groups, but the percentage of lavage macrophages was slightly diminished in bleomycin-treated animals receiving the laboratory diet. Cellular differentials of lavage fluid did not differ significantly between bleomycin- and saline-treated animals receiving the menhaden oil diet. Bleomycin-induced histologic changes, quantitated by morphometric analysis, were significantly reduced with the menhaden oil diet. We conclude that a diet rich in eicosapentaenoic acid can significantly ameliorate bleomycin-induced pulmonary fibrosis, possibly via alterations in eicosanoid metabolism.

Eicosanoid synthesis in 7,12-dimethylbenz(a)anthracene-induced mammary carcinomas in Sprague-Dawley rats fed primrose oil, menhaden oil or corn oil diet.

The comparative effects of high-fat diets (20%, w/w) on eicosanoid synthesis during mammary tumor promotion in 7,12-dimethylbenz(a)anthracene (DMBA)-induced rats were studied using diets containing 20% primrose oil (PO), 20% menhaden oil (MO) or 20% corn oil (CO). Sprague-Dawley rats fed the PO or MO diet had 21% of 24% fewer adenocarcinomas, respectively, than rats fed the CO diet. Histologically (i.e., mitotic figures, inflammatory cell infiltration and necrosis), the CO-fed rats exhibited the highest frequency of changes within tumors. Plasma fatty acid composition was significantly altered by diet, reflecting the composition of the oils which were being fed. Only the plasma of PO-fed rats contained detectable levels of gamma-linolenic acid (GLA). Arachidonic acid (AA) levels were significantly higher (p less than 0.05) in PO-fed than in CO- or MO-fed rats. MO-fed rats had significantly higher levels of plasma palmitic acid, while palmitoleic, eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids were detected only in MO-fed rats. As expected, linoleic acid (LA) and AA levels were lower (p less than 0.05) in the MO-fed rats than in PO- or CO-fed groups. The plasma of the CO-fed rats contained significantly higher levels of oleic acid. Eicosanoid synthesis in mammary carcinomas of rats fed the 20%-fat diets was 2-10 times higher than in mammary fat pads of control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of dietary fish oils on eicosanoid biosynthesis in peritoneal macrophages is influenced by both dietary n-6 polyunsaturated fats and total dietary fat

Recent research has implicated dietary fish oils in the reduction of eicosanoids formed from arachidonic acid and amelioration of chronic diseases such as coronary heart disease, atherosclerosis and inflammation. Feeding studies were conducted to determine if the efficacy of dietary n-3 polyunsaturated fatty acids (PUFA) from fish oils was influenced by the quantity of n-6 polyunsaturated fatty acids and the total level of fat in the diet. Groups of mice were fed diets composed of 5 and 20% total fat with varying proportions of linoleic acid as a source of n-6 PUFA. Menhaden oil as a source of n-3 PUFA was fed at two levels of n-6 at each level of total fat. Eicosanoid biosynthesis was stimulated and assayed in the mouse peritoneum using zymosan as an inflammatory stimulus. Production of LTE 4 and PGE 2 was enhanced by increasing n-6 PUFA in the diet at both levels of total fat. High dietary fat significantly suppressed leukotriene (LT) synthesis. Dietary menhaden oil reduced LTE 4 and PGE 2 synthesis at both levels of dietary n-6 in the low fat study. In animals on 20% dietary fat menhaden oil significantly reduced LT synthesis only at a relatively low dietary n-6 PUFA. On a high n-6 PUFA high fat diets, menhaden oil did not significant affect LTE 4 synthesis in response to zymosan stimulation. The results suggest that the effectiveness of fish oils in reducing eicosanoids in response to specific stimulation is influenced by the level of n-6 and the total quantity of fat in the diet.

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 samples taken from the exposed hearts of anesthetized, fasted rats. SHR, compared with SD (diets combined) had significantly lower triacylglycerols (TG), higher cholesterol (CHOL), higher high density lipoprotein cholesterol (HDL CHOL), higher low density lipoprotein cholesterol (LDL CHOL), and a higher LDL:HDL ratio. Comparisons among diets (strains combined) revealed that rats fed MO had the lowest values for TG, CHOL, LDL and LDL:HDL; HDL did not 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.

Dietary menhaden oil: effects on the rate and magnitude of modification of phospholipid fatty acid composition of mouse heart and brain.

1. Male CD-1 white mice, 18-20 g body-weight, were given semi-purified diets containing 100 g menhaden oil (MO) or hydrogenated coconut oil (HCO)/kg for 23 d. Mice were killed on days 0, 3, 5, 7, 14, 23. After 23 d of MO supplementation the remaining mice were switched to the HCO diet for an additional 10 d. 2. The progressive change(s) in the polyunsaturated fatty acid (PUFA) composition of cardiac and brain phospholipid classes were followed during the MO supplementation and depletion periods. 3. The content of fatty acids 20:5n-3, 22:5n-3 and 22:6n-3 increased immediately following ingestion of the MO diet and continued to increase at a steady rate in both heart and brain phospholipid classes. 4. In general, the period required to reach steady-state was 1 week for n-3 PUFA and 18:2n-6, and 2 weeks for 20:4n-6. 5. Cessation of MO consumption for 10 d resulted in marked decreases in the content of n-3 PUFA and increases in n-6 PUFA in cardiac phospholipids in particular. Brain phospholipids were less responsive. 6. The results suggest that dietary fish oil must be consumed for at least 1 week before maximum changes in PUFA composition are observed, and fish oil ingestion must be continuous to maintain elevated n-3 PUFA levels in heart and brain phospholipids.

Fetal growth and fetal lung phospholipid content in rats fed safflower oil, menhaden oil, or hydrogenated coconut oil

The objective was to determine if dietary fish oil decreased the degree of fatty acid saturation in rat lung phosphatidylcholine (PC). A diet containing 12% of its energy as fat was fed for 3 wk to growing male Sprague-Dawley rats (trial I) or to pregnant rats for days 8-21 of gestation (trial II). The dietary fat treatments in trial I were safflower oil (SO), menhaden oil (MO), or hydrogenated coconut oil (HCO) and in trial II were SO, MO, HCO, or SO-MO (75%:25%). Polyunsaturated fatty acids reduced (p less than 0.05) hepatic fatty acid synthetase (MO greater than SO) in growing rats but the dietary lipids had no effect on lung palmitate content. Maternal consumption of MO vs SO reduced (p less than 0.05) fetal body weight and lung weight but not lung:body wt ratio. Dietary MO and SO-MO increased (p less than 0.05) disaturated PC content of fetal lungs. The fetal lung data indicate that maternal ingestion of fish oil improve fetal lung maturation.

Effects of dietary menhaden oil and retinyl acetate on the growth of DU 145 human prostatic adenocarcinoma cells transplanted into athymic nude mice.

The effects of feeding menhaden oil (MO), rich in omega-3 fatty acids, or supplemental vitamin A [as retinyl acetate (RA)], on the growth of DU 145 human prostate cancer cells were studied in athymic nude mice. The mice were fed AIN-76A diets containing either 23% corn oil (CO), a mixture of 17% MO and 6% CO, or 23% CO plus RA. After irradiation sterilization, the RA-supplemented diet was found to contain approximately 15 times the amount of vitamin A present in the control diet. There were 24 mice in each dietary group. Three weeks after commencement of feeding the experimental diets, 1 x 10(6) or 5 x 10(6) DU 145 cells were inoculated into subgroups of 12 animals, and the appearance and growth of solid tumors followed over a 6-week period. There was no significant difference in tumor latency between mice fed MO plus CO, and those fed CO alone, regardless of the inoculum size. However, the appearance of palpable tumors was more rapid in mice inoculated with 5 x 10(6) cells and fed the RA-supplemented CO diet (91% after 17 days) compared with mice receiving the same tumor cell load but fed the unsupplemented CO diet (55% after 17 days). Growth of the solid tumors was retarded significantly in mice inoculated with 1 x 10(6) cells and fed the MO-containing diet compared with the CO controls; this effect was not evident in animals who received 5 x 10(6) cells. RA supplementation caused accelerated tumor growth, which, again, only achieved statistical significance in the group inoculated with 1 x 10(6) cells.

Dietary n-3 Polyunsaturated Fatty Acids: Rate and Extent of Modification of Fatty Acyl Composition of Lipid Classes of Mouse Lung and Kidney

The rate and extent of modification of fatty acid composition of mice lung and kidney by dietary menhaden oil (MO) was investigated. White mice were fed 2 wt% safflower oil and either 10 wt% MO or 10 wt% hydrogenated coconut oil (HCO) for 23 d. The stability of dietary MO-induced fatty acid modifications was assessed by replacing the MO diet of a group of mice after 23 d with the HCO diet for an additional 10 d. Mice were sacrificed on d 0, 1, 3, 5, 7, 14, 23 and 33. The n-3 polyunsaturated fatty acid (PUFA), 20:5n-3 and 22:6n-3 were rapidly incorporated into lung and kidney phosphoglyceride (PL) classes during the first 7 d of MO ingestion relative to the controls. After 1 wk of MO consumption, the rate of incorporation either plateaued at an elevated level or continued to increase at a much more gradual rate. A marked increase in the content of 22:5n-3 in lung and kidney was observed. A concomitant and rapid decrease was observed in the n-6 PUFA, 20:4n-6, 22:5n-6 and 18:2n-6. The minimum content of 20:4n-6 was reached between 1 and 2 wk, whereas the minimum levels of 18:2n-6 and 22:5n-6 occurred within 72 h. The n-6/n-3 PUFA ratio in lung and kidney and PL classes Increased in mice fed HCO and decreased in mice fed dietary MO. When dietary MO was removed, the n-3 PUFA levels decreased with a concomitant increase in n-6 PUFA after 10 d of HCO consumption. These data are useful in defining the rates and extent of change of organ fatty acid composition in response to fish oil consumption and suggest that a continual ingestion is necessary to maintain the modifications in organ fatty acid composition.