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Biomedical subjects

K L Fritsche

Publications and source records attributed to K L Fritsche.

At least 19 recordsLinked to original sources
PubMed1997

An esterification protocol for cis-parinaric acid-determined lipid peroxidation in immune cells.

Loss of fluorescence from cis-parinaric acid (cPnA) is a sensitive indicator of lipid peroxidation. The purpose of this study was to utilize cPnA to determine, at the level of the intact immune cell, whether enrichment of membranes with polyunsaturated fatty acids (PUFA) increased lipid peroxidation. P388D1 macrophages were labeled by addition of cPnA as an ethanolic solution. Within two minutes of addition, in the absence-of serum, cPnA rapidly intercalated into the plasma membrane. Lipid peroxidation was initiated by addition of Fe(2+)-EDTA resulting in a dose-dependent decrease in fluorescence with increased oxidant concentration. Cells previously enriched with PUFA and labeled by intercalation showed no differences in spontaneous or Fe(2+)-induced lipid peroxidation. In separate experiments, 20 microM cPnA in ethanolic solution was injected into cell culture media containing 0.1% essentially fatty acid free bovine serum albumin (BSA). Cells were resuspended and incubated for 90 min at 37 degrees C. After washing with BSA to remove cPnA which had not incorporated, 0.5% (0.1 microM) of the added cPnA was found esterified within cellular lipids. This level of cPnA provided a 100-fold increase over basal autofluorescence levels. Cells labeled in this manner also lost fluorescence in a dose-dependent manner as levels of oxidant stress increased. Cells enriched with PUFA and labeled by esterification had significantly increased rates and total amounts of lipid peroxidation. Co-incubation with alpha-tocopherol and PUFA resulted in a decrease in lipid peroxidation which was not significantly different from control cells. In conclusion, esterification of cPnA into membrane phospholipids can sensitively detect changes in lipid peroxidation induced by alteration of membrane PUFA and/or vitamin E content.

Cells, Cultured↗
PubMed1997

Dietary fish oil reduces survival and impairs bacterial clearance in C3H/Hen mice challenged with Listeria monocytogenes.

1. To investigate the effect of dietary fat source on host resistance to intracellular pathogens, weanling female C3H/Hen mice were fed one of three experimental diets containing, 20% by weight, lard, soybean oil or 17% menhaden fish oil plus 3% corn oil. After 4 weeks, survival of mice (n = 12/treatment group) injected intraperitoneally with 2 x 10(6) colony forming units of live Listeria monocytogenes was determined. In a second study, bacterial clearance from the liver and spleen at 2, 4 and 7 days post-challenge was determined (n = 8/treatment group). 2. We found that the survival of mice fed the diets with soybean oil or menhaden fish oil was significantly lower than those fed lard (P < 0.05). Survival rates were 58% (7/12), 33% (4/12) and 100% (12/12), respectively, for mice fed soybean oil, menhaden fish oil and lard. In the second study, mice fed menhaden fish oil had approximately 1 log10 greater bacteria in their spleens at day 4 than mice fed lard or soybean oil (P < 0.001). There were no significant treatment differences in the number of bacteria recovered from liver samples. 3. In summary, dietary fat source significantly affects murine resistance to Listeria, with diets rich in n-3 polyunsaturated fatty acids, such as from fish oil, having the most detrimental effect.

Animals↗
PubMed1997

Dietary fish oil enhances circulating interferon-gamma in mice during listeriosis without altering in vitro production of this cytokine.

The objective of this study was to investigate the impact of feeding mice a diet rich in n-3 polyunsaturated fatty acids (PUFA) from fish oil on the interferon-gamma (IFN-gamma) response during an active infection with Listeria monocytogenes. Weanling female C3H/Hen mice were fed experimental diets containing 20% by weight one of the following fats: soybean oil, lard, or a mixture of menhaden fish oil and corn oil (17:3, w/w). After 4 weeks, mice were injected with 10(5) live L. monocytogenes, and the concentration of IFN-gamma in serum and spleen was determined 0, 2, 4, and 7 days postinfection by enzyme-linked immunosorbent assay (ELISA). Fish oil-fed mice showed significantly higher IFN-gamma in their blood at 2 and 4 days postchallenge compared with mice fed the soybean oil-containing or lard-containing diets (p < 0.001). A higher concentration of IFN-gamma was also found in the spleen homogenate of fish oil-fed mice on day 4 postchallenge (p < 0.005). To examine in vitro IFN-gamma production, splenocytes were isolated from fish oil-fed and soybean oil-fed mice on day 4 postchallenge and cultured with concanavalin A (1 microgram/ml and 10 micrograms/ml) for 24 and 48 h. There were no significant differences in the IFN-gamma concentration in cell culture supernatants between these diet treatments. This study demonstrated that the elevation in the concentration of IFN-gamma in blood and spleen during murine listeriosis is accentuated and prolonged by dietary n-3 PUFA, and these effects may not be due to changes in IFN-gamma production.

Animals↗
PubMed1997

Fish oil source differentially affects rat immune cell alpha-tocopherol concentration.

We have previously reported that both the source of dietary fish oil and the chemical form of vitamin E supplied in the diet affect the vitamin E status of immune cells in rats. The purpose of this study was to investigate further the effect of fish oil source on immune cell vitamin E status using free alpha-tocopherol (alpha-T) at the AIN recommended level as the sole source of vitamin E. Sixty weanling female rats were fed semipurified, high fat (20 g/100 g) diets containing either tocopherol-stripped lard (LRD), menhaden fish oil (MFO), sardine fish oil (SRD) or cod liver oil (CLO) as the primary lipid source. Endogenous alpha-T concentration was measured and equalized to 150 mg/kg oil by addition of free RRR-alpha-T to each lipid source, allowing for a final concentration of alpha-T in the mixed diet of 30 mg/kg. An additional group of rats was fed LRD without supplemental vitamin E (LRD-) as a negative control. After feeding experimental diets for 5 or 10 wk, tissues were collected for alpha-T analysis by HPLC. After 5 wk, plasma and liver alpha-T (micromol alpha-T/g lipid) were significantly lower in SRD- and CLO-fed rats compared with LRD-fed rats. At 10 wk, only plasma alpha-T in CLO-fed rats remained significantly depressed. Plasma and liver alpha-T concentrations (micromol alpha-T/g lipid) were not significantly lower in MFO-fed rats than LRD-fed rats at either time point. Compared with LRD, feeding MFO to rats for 5 or 10 wk resulted in significantly greater alpha-T content of immune cells. In similar fashion, SRD-fed rats, compared with LRD-fed rats, also had significantly greater alpha-T content in splenocytes at both time points and greater thymocyte alpha-T at 10 wk. In all instances, the alpha-T status of rats fed CLO was indistinguishable from that of rats fed the vitamin E-free diet (LRD-). These data further demonstrate the complexity of the relationship between vitamin E status and dietary (n-3) polyunsaturated fatty acids (PUFA).

Animals↗
PubMed1997

Effects of thermal environment on response to acute peripheral lipopolysaccharide challenge exposure in neonatal pigs.

OBJECTIVE: To evaluate effects of thermal environment on response to acute peripheral lipopolysaccharide (LPS) challenge exposure in neonatal pigs. ANIMALS: 26 neonatal pigs. PROCEDURE: Pigs were assigned to the following treatment groups: 1 warm environment/LPS; 2 warm environment/saline solution; 3 cool environment/LPS; and 4 cool environment/saline solution. For each pig given LPS, 1 littermate of the same sex was given saline solution. Sows with baby pigs were housed in a warm (32 C) or cool (21 C) thermal environment. At 28 days of age, pigs were given 150 micrograms/kg of body weight of Escherichia coli LPS or saline solution intraperitonealy as a control. Rectal temperature and signs of sickness were monitored for 3 hours after LPS administration, when pigs were euthanatized and blood samples were collected to determine serum concentrations of tumor necrosis factor (TNF) alpha and cortisol. To determine in vitro production of TNF alpha, alveolar macrophages were collected by tracheal lavage and incubated for 24 hours at 37 or 41 C, with or without LPS (10 micrograms/ml). RESULTS: Thermal environment had a significant (P = 0.0004) effect on rectal temperature; LPS administration induced a febrile response (P = 0.0007) only in pigs in the warm environment. All LPS-injected pigs developed signs of endotoxemia; serum TNF alpha and cortisol concentrations were significantly increased (TNF alpha, P = 0.003; cortisol, P = 0.0001); there was no significant in vivo thermal effect on serum TNF alpha and cortisol concentrations. LPS-stimulated alveolar macrophages produced significantly less (P = 0.0086) TNF alpha when incubated at 41 C. CONCLUSIONS: Thermal environment can have a significant impact on the response of neonatal pigs exposed to bacterial endotoxins.

Acute-Phase Reaction↗
PubMed1996

Metabolism of [3H]arachidonic acid by n-3 polyunsaturated fatty acid-enriched piglet alveolar macrophages.

The metabolism of [3H]arachidonic acid (3H-AA) by control and omega-3 polyunsaturated fatty acid (n-3 PUFA)-enriched piglet alveolar macrophages (AM) was studied after a 4 and 24 h labeling period. 3H-AA metabolites were separated by gradient HPLC. Incorporation of exogenous 3H-AA for either 4 or 24 h was similar for n-3 PUFA-enriched AM compared with control AM. Calcium ionophore (A23187, 10 microM) stimulated a greater release of 3H-AA from n-3 PUFA-enriched AM compared with control AM. Furthermore, AM labeled for 24 h had a lower spontaneous release and higher stimulated release than those labeled for only 4 h. The major 3H-AA metabolites detected in AM supernatants were PGF2 alpha, LTB4, and 5-HETE. Significant amounts of 3H-PGE2 were observed in the supernatants of those cells labeled for 24 h, but not 4 h. The absence of 3H-TXB2 was notable, since enzyme immunoassay detected significant quantities of this AA metabolite in all of the stimulated cell supernatants. From these data we conclude that n-3 PUFA enrichment of piglet AM alters the metabolism of recently incorporated 3H-AA and that the metabolism of labeled AA may not parallel endogenous AA.

Animals↗
PubMed1995

Fish oils lower rat plasma and hepatic, but not immune cell alpha-tocopherol concentration.

These studies were designed to measure the impact of different fish oil sources of dietary (n-3) polyunsaturated fatty acid on the alpha-tocopherol content of rat immune cells. In the first experiment, rats were fed diets containing either lard, corn oil, menhaden fish oil or cod liver oil. In the second study, sardine fish oil replaced corn oil. Dietary fat source did not significantly influence body weights or the yield of immune cells in either study. In both studies, plasma and liver alpha-tocopherol concentrations were significantly lower in (n-3) polyunsaturated fatty acid-fed rats than in rats fed lard. In the first study, immune cell alpha-tocopherol concentrations followed those observed in the plasma and liver. These concentrations closely paralleled the amount of RRR-alpha-tocopheryl acetate added to diets and not the total vitamin E present, which was the same for all treatment groups. However, in the second study, alpha-tocopherol concentration of immune cells was not significantly different among rats fed lard, menhaden fish oil, and sardine fish oil. In that study both the amount and form of vitamin E were carefully balanced across dietary treatment groups. In conclusion, despite having similar amounts of (n-3) polyunsaturated fatty acids, two out of three fish oils tested did not lower immune cell alpha-tocopherol concentration even in the face of significantly reduced plasma and liver alpha-tocopherol concentrations.

Animals↗
PubMed1993

Maternally-supplied fish oil alters piglet immune cell fatty acid profile and eicosanoid production.

This study was designed to examine the incorporation of omega-3 (n-3) fatty acids into the immune tissues of pigs nursing fish oil-fed sows and to determine the effect of maternal dietary n-3 consumption on in vitro immune cell eicosanoid production. On day 107 of gestation, 12 sows were randomly allotted to a diet containing either 7% menhaden fish oil (MFO) or lard (LRD). The fatty acid profile of serum, liver, thymus, splenocytes and alveolar macrophages (AM) of 18-21-day-old pigs was significantly affected by the fat source provided to the sow. Arachidonic acid (20:4n-6) content was typically reduced by more than 50% in MFO as compared with LRD pigs. In MFO pigs, eicosapentaenoic acid (20:5n-3) was the major n-3 polyunsaturated fatty acid, and its levels matched or exceeded those of arachidonic acid. Basal release of prostaglandin E, thromboxane B and leukotriene B by AM was 60-70% lower in MFO vs. LRD pigs. However, when these immune cells were stimulated with calcium ionophore A23187, release of leukotriene B was similar in MFO and LRD pigs. In conclusion, substituting MFO for LRD in a sow's late-gestation and lactation diet greatly elevated the content of n-3 fatty acids in the nursing pig immune cells and generally reduced in vitro eicosanoid release by pig immune cells.

Animals↗
PubMed1993

Enrichment of omega-3 fatty acids in suckling pigs by maternal dietary fish oil supplementation.

This study was designed to determine whether substituting menhaden fish oil (FO) for lard (LA) in a practical sow diet was a suitable method for enriching newborn pigs with omega-3 polyunsaturated fatty acids (n-3 PUFA). On d 107 of gestation, 18 crossbred sows were randomly allotted to one of three experimental diets, in which FO was substituted for LA at 0, 3.5, and 7% of the diet. On d 1, 7, 14, and 21 after farrowing samples of milk and serum from the sows and pig serum were collected for fatty acid analysis. The content of n-3 PUFA in the serum of sows fed FO increased six-fold over that in serum of LA-fed sows P < .0001). Feeding FO decreased the levels of arachidonic acid in maternal serum by approximately 50% (P < .0001). Similar changes were reflected in the fatty acid profiles of sow's milk. Pig serum n-3 PUFA levels were elevated over 5- and 10-fold within 24 h of birth in those litters born to sows fed 3.5 and 7% fish oil, respectively. Eicosapentaenoic acid levels in pig serum increased linearly (P < .01) during the first 2 wk postnatally in pigs suckling FO-feds sows and accounted for as much as 12% of the total fatty acids present on d 21. In conclusion, we have demonstrated that feeding FO to sows during late gestation and lactation enriches the newborn pig with n-3 PUFA.

Animal Feed↗
PubMed1992

Alteration in mouse splenic phospholipid fatty acid composition and lymphoid cell populations by dietary fat.

The fatty acid composition of diacyl- and alkylacylglycerophosphocholine (PC), phosphatidylinositol (PI), phosphatidylserine (PS), alkenylacyl-glycerophosphoethanolamine (aPE), and diacyl- and alkylacyl-glycerophosphoethanolamine (dPE) was assessed in isolated splenocytes from C3H/Hen mice fed one of four purified isocaloric diets for six weeks. Diets contained 20% by weight of either a high-linoleate sunflower oil (Hi 18:2), a high-oleate sunflower oil (Hi 18:1), a mixture of 17% menhaden fish oil and 3% high-linoleate sunflower oil (Hi n-3), or a mixture of 17% coconut oil and 3% high-linoleate sunflower oil (Hi SFA). Spleen weight and immune cell yield were significantly higher (P less than 0.05) in mice fed the Hi 18:1 or the Hi n-3 diets compared with those fed the Hi 18:2 and Hi SFA diets. Distinctive patterns of fatty acids were observed for each phospholipid in response to dietary fatty acids. Dietary fat significantly affected (P less than 0.05) total polyunsaturated fatty acids (PUFA) in PC and dPE, total saturated fatty acids (SFA) in PC, total monounsaturated fatty acids (MUFA), and n-3 PUFA in all phospholipid classes examined. In mice fed the Hi n-3 diet, n-3 PUFA were significantly elevated, whereas n-6 PUFA decreased in all of the phospholipids. In these mice, eicosapentaenoic acid (EPA) was the predominant n-3 PUFA in PC and PI, whereas docosahexaenoic acid (DHA) was the major n-3 PUFA in aPE and PS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Dietary (n-3) fatty acid and vitamin E interactions in rats: effects on vitamin E status, immune cell prostaglandin E production and primary antibody response.

To examine the interaction between dietary fat and vitamin E at the level of the rat immune system, a 2 x 3 factorial study was designed. Weanling female Sprague Dawley rats were fed for 8-9 wk diets that contained either corn oil (CO diet) or fish oil (FO diet) and one of three levels (30, 300, 900 mg/kg) of all-rac-alpha-tocopheryl acetate. At the lowest level of dietary vitamin E, alpha-tocopherol content of splenocytes from FO-fed rats was approximately 40% lower (P less than 0.05) than in those from CO-fed rats. Supplementation with all-rac-alpha-tocopheryl acetate elevated alpha-tocopherol in splenocytes from FO-fed rats but not in those from CO-fed rats, and reduced the relative proportion of arachidonic acid and eicosapentaenoic acid in the serum of CO-fed and FO-fed rats, respectively. Prostaglandin E production by isolated immune cells was not affected by all-rac-alpha-tocopheryl acetate supplementation. However, feeding the FO diet consistently reduced prostaglandin E synthesis by 70-80% as compared with the CO diet. Antibody production against sheep RBC was highest in rats fed the FO diet supplemented with 900 mg all-rac-alpha-tocopheryl acetate/kg of diet. However, antibody response was not directly correlated to diet-induced changes in immune cell prostaglandin E production or alpha-tocopherol content. Our data suggest that there are significant interactions between vitamin E and (n-3) fatty acids that affect the immune system and that further research in this area is warranted.

Animals↗
PubMed1992

Dietary fat influences Ia antigen expression and immune cell populations in the murine peritoneum and spleen.

Peritoneal cells (PEC) and splenocytes were obtained from Listeria monocytogene (LM)-infected or noninfected mice fed a 20% fat diet rich in either (n-3) polyunsaturated fatty acids [(n-3) PUFA diet], linoleate [(n-6) PUFA diet], oleate (MONO diet), or saturated fatty acids (SAT diet) for 6 wk and were assessed for T cells, B cells, macrophages and Ia expression by flow cytometric analysis. In the peritoneum of noninfected mice, dietary fat did not affect total cell yield or the percentage of B cells, macrophages or Ia+ cells, but the (n-3) PUFA-fed group had a greater percentage of T cells than did the other groups. Among the LM-infected mice, the (n-3) PUFA-fed group generally had the highest percentage of B cells and the lowest percentages of T cells, macrophages and Ia+ cells in the peritoneum. Listeria monocytogene infection elevated peritoneal T cell numbers in all mice except the (n-3) PUFA-fed group. The density of Ia molecules on PEC was 40% lower in mice fed the (n-3) PUFA diet. In the spleen, dietary fat also influenced the immune cell populations and Ia+ cells. Two-color staining of spleen cells revealed that Ia+ splenocytes were predominately B cells. These data demonstrate that dietary fats influence Ia expression and immune cell populations and that the effects observed in one immune tissue or cell type may not be readily extrapolated to others.

Animals↗
PubMed1992

Dietary n-3 fatty acids reduce antibody-dependent cell cytotoxicity and alter eicosanoid release by chicken immune cells.

The overall goal of the present study was to determine whether the incorporation of n-3 fatty acids into poultry rations would alter the immune response of broiler chickens. Female broiler chicks were fed a corn and soybean meal-based diet to which one of four dietary fats were added: lard (LA), corn oil (CO), flaxseed oil (SO), or menhaden fish oil (FO). The latter two fat sources are rich in n-3 polyunsaturated fatty acids (PUFA). Enriching the diet with n-3 PUFA did not alter the primary or secondary antibody response of broiler chickens to sheep red blood cells. Dietary fat source had no effect on antibody-dependent cell cytotoxicity (ADCC) by peripheral blood leukocytes, but ADCC by splenocytes was 50% lower in chickens fed SO and FO compared with LA and CO (P less than .005). As expected, the fatty acid profile of the isolated immune cells reflected the fatty acid composition of the dietary fats fed. Basal release and calcium ionophore (A23187)-stimulated (10 microM) release of thromboxane B were significantly lower (P less than .05) in the SO and FO groups compared with the LA and CO groups. Total leukotriene B release was not significantly altered by dietary fat source. In conclusion, feeding broiler chickens diets rich in n-3 PUFA reduced ADCC of splenocytes and altered eicosanoid production by isolated immune cells.

Animals↗
PubMed1991

Essential fatty acid sufficiency does not preclude fat-soluble-vitamin deficiency in short-bowel syndrome.

Patients with extensive small-bowel resection may experience malabsorption and nutrient deficiencies. We evaluated the ability to absorb fat and fat-soluble vitamins in a short-gut patient. For 18 wk after stopping intravenous lipid, while consuming a low-lactose, low-fat diet, he exhibited no clinical manifestations of essential fatty acid deficiency (EFAD). Serum 20:4n-6 (20:4 omega-6) and 18:2n-6 fatty acid concentrations were normal, whereas the concentration of 20:3n-9 remained less than or equal to 0.1% of total serum fatty acids. Although serum vitamin A was normal, beta-carotene was undetectable despite oral supplementation. Prothrombin time was elevated until parenteral vitamin K was given. This patient has fat absorption adequate to prevent EFAD but inadequate absorption of fat-soluble vitamins. In patients with short bowel, the requirements for parenteral lipids and fat-soluble vitamins should be determined independently.

Absorption↗
PubMed1991

Effect of dietary fat source on antibody production and lymphocyte proliferation in chickens.

The purpose of the present study was to assess the effect of fat source on the immune response of chickens. One-day-old pullets were fed corn and soybean meal-based diets containing 7% by weight one of the following fat sources: lard, corn oil, canola oil, linseed oil (LO), or fish oil (FO). After being fed experimental diets for 3 wk, humoral and cellular immune responses were assessed. Chicks were injected with SRBC and antibody titers were measured, 7 days later, by hemagglutination. Concanavalin A (Con A), pokeweed mitogen (PWM), or lipopolysaccharide (LPS)-stimulated proliferation of splenocytes was assessed by [3H]thymidine incorporation. Results demonstrated that antibody titers in FO-fed chicks were higher (P less than .005) compared with titers in chicks fed the other fat sources. The proliferative response to Con A and PWM were 30 to 50% lower (P less than .13 and P less than .05, respectively) in chicks fed the oils rich in omega-3 fatty acids, LO and FO. The response to LPS was poor. The effect of dietary fats source on lymphocyte proliferation was completely abrogated when autologous chicken serum was excluded from the culture medium. Fat source also seemed to affect growth and feed intake of the chickens. In conclusion, dietary fat source has a significant impact on the immune response of chickens.

Animal Feed↗
PubMed1991

Effect of dietary fats on the fatty acid compositions of serum and immune tissues in chickens.

The purpose of the present study was to measure the effect of dietary fat source on the fatty acid composition of immune cells in chickens. One-day-old female chicks were fed corn and soybean meal-based diets containing 7% of either lard, corn oil, canola oil, linseed oil (LO), or menhaden fish oil (FO). After being fed experimental diets for 3 to 4 wk, samples of serum, thymus glands, bursa of Fabricius glands, and splenocytes were collected. All samples were frozen and stored at -80 C until lipid analysis. Results indicate that the fatty acid composition of the sera and immune tissues of chickens reflected the fat in the diet. The relative content of long-chain polyunsaturated fatty acids varied considerably among immune tissues, with, from greatest to least, spleen, bursa, and thymus. The young chick demonstrated a substantial capacity to elongate and desaturate linoleic (C18:2n-6) and alpha-linolenic acids (C18:3n-3). Feeding chicks fats rich in n-3 fatty acids (e.g., LO or FO) decreased significantly (P less than .05) the level of arachidonic acid (C20:4n-6) present in the serum and immune tissues by 50 to 75%. The levels of eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C20:6n-3) were substantially increased (P less than .05) by FO and LO feeding. However, LO, which is rich in C18:3n-3, was generally only one-half to one-quarter as effective as FO in elevating EPA and DHA levels in immune tissues. The implications for these changes in serum and immune tissue fatty acid profiles are discussed briefly.

Animals↗
PubMed1990

Effect of dietary alpha-linolenic acid on growth, metastasis, fatty acid profile and prostaglandin production of two murine mammary adenocarcinomas.

The purpose of this study was to determine whether dietary (n-3) fatty acids would affect mammary tumor growth and metastasis. Weanling female BALB/c mice were fed diets that contained 10% corn oil (CO), linseed oil (LO) or a fish oil-corn oil mix (FO) for 3-8 wk prior to receiving subcutaneous injections of one of two syngeneic mammary tumor cell types (410 and 410.4). Tumor growth was assessed by monitoring mean tumor diameter and tumor weight upon removal. Feeding LO, but not FO, reduced the growth (p less than 0.05) of 410.4 mammary tumors compared with growth in those fed CO. Metastasis data paralleled the tumor growth rate. Feeding LO and FO enhanced (p less than 0.005) incorporation of (n-3) fatty acids into tumors. Tumor prostaglandin E (PGE) production was reduced (p less than 0.005) by LO and FO, compared with CO. FO feeding reduced 410.4 tumor PGE synthesis more (p less than 0.05) than LO feeding, yet tumor growth was only inhibited by LO. These data suggest an inhibitory effect of dietary linolenic acid [i.e., 18:3 (n-3)] on mammary tumor growth and metastasis. However, this effect did not directly correlate with diet-induced changes in PGE synthesis.

Adenocarcinoma↗