linoleic-acid and Stomach-Neoplasms

Polyunsaturated fatty acids (PUFAs) have tumoricidal action, though the exact mechanism of their action is not clear. The results of the present study showed that of all the fatty acids tested, linoleic acid (LA) and α-linolenic acid (ALA) were the most effective in suppressing the growth of normal gastric cells (GES1) at 180 and 200 μM, while gastric carcinoma cells (MGC and SGC) were inhibited at 200 μM. Arachidonic acid (AA) suppressed the growth of GES1, MGC and SGC cells and lower concentrations (120 and 160 μM) of AA were more effective against gastric carcinoma (MGC and SGC) cells compared to normal gastric cells (GES1). Paradoxically, both eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids though are more unsaturated than AA, were less effective compared with LA, ALA and AA in suppressing the growth of both normal and cancer cells. At the concentration used, methotrexate showed much less growth suppressive action compared to all the fatty acids tested. PUFAs-treated cells showed accumulation of lipid droplets. A close association was noted between apoptosis and lipid peroxides formed compared to the ability of normal and tumor cells to generate ROS (reactive oxygen species) and induce SOD (superoxide dismutase activity) in response to fatty acids tested and methotrexate. Both normal and tumor cells generated lipoxin A4 (LXA4) in response to supplementation of fatty acids and methotrexate though no significant correlation was noted between their ability to induce apoptosis and LXA4 formed. These results suggest that PUFAs induced apoptosis of normal gastric and gastric carcinoma cells could, partly, be attributed to lipid peroxidation process.

Topics: alpha-Linolenic Acid; Apoptosis; Cell Line; Cell Line, Tumor; Cell Survival; Fatty Acids; Fatty Acids, Unsaturated; Humans; Linoleic Acid; Lipid Droplets; Lipoxins; Oxidative Stress; Reactive Oxygen Species; Stomach Neoplasms; Superoxide Dismutase

We evaluated the potential of a thermoresponsive hydrogel consisting of conjugated linoleic acid-coupled Pluronic F-127 (Plu-CLA) as a controlled release, intraperitoneal delivery system for docetaxel with the aim of treating peritoneal dissemination of gastric cancer. Previously, we established a peritoneal metastasis model that involves the injection of BALB/c mice with TMK1 human gastric cancer cells. One week after the TMK1 cells were injected, the mice were injected intraperitoneally with docetaxel alone or docetaxel-loaded Plu-CLA. Tumor progression and response to therapy were monitored by micro-positron emission tomography. The total number of peritoneal tumors and the ascites volume were also measured. Compared with docetaxel alone, the combination of docetaxel and Plu-CLA (docetaxel-Plu-CLA) significantly and synergistically reduced tumor cell survival. Docetaxel-Plu-CLA showed excellent anti-tumor activity, inducing apoptosis more potently than docetaxel alone. Docetaxel-Plu-CLA also significantly reduced the number of peritoneal metastatic nodules and increased survival in the peritoneal gastric cancer xenograft model. Our results show that intraperitoneal administration of docetaxel-Plu-CLA synergistically inhibits peritoneal metastasis and prolongs survival in a peritoneal gastric cancer model. Therefore, Plu-CLA is a potential intraperitoneal-route carrier for hydrophobic docetaxel for the effective treatment of peritoneal metastatic gastric cancer.

Topics: Animals; Antineoplastic Agents; Delayed-Action Preparations; Docetaxel; Hot Temperature; Hydrogels; Linoleic Acid; Male; Mice; Mice, Inbred BALB C; Nanocapsules; Peritoneal Neoplasms; Poloxamer; Stomach Neoplasms; Taxoids; Treatment Outcome

The intake of dietary fatty acids is highly correlated with the risk of various cancers. Linoleic acid (LA) is the most abundant polyunsaturated fat in the western diet, but the mechanism(s) by fatty acids such as LA modulate cancer cells is unclear. In this study, we examined the role of LA in various steps in gastric cancer progression.. The difference in gene expression between LA-treated and untreated OCUM-2MD3 gastric carcinoma cells was examined by mRNA differential display. The involvement of candidate genes was examined by oligo- and plasmid-mediated RNA interference. Biological functions of several of these genes were examined using in vitro assays for invasion, angiogenesis, apoptosis, cell viability, and matrix digestion. Angiogenesis in vivo was measured by CD-31 immunohistochemistry and microvessel density scoring.. LA enhanced the plasminogen activator inhibitor 1 (PAI-1) mRNA and protein expression, which are controlled by PAI-1 mRNA-binding protein. LA-stimulated invasion depended on PAI-1. LA also enhanced angiogenesis by suppression of angiostatin, also through PAI-1. LA did not alter cell growth in culture, but increased dietary LA-enhanced tumour growth in an animal model.. Our findings suggest that dietary LA impacts multiple steps in cancer invasion and angiogenesis, and that reducing LA in the diet may help slow cancer progression.

Topics: Angiostatins; Animals; Apoptosis; Cell Survival; Disease Progression; Female; Gene Expression Profiling; Human Umbilical Vein Endothelial Cells; Humans; Linoleic Acid; Mice; Mice, Nude; Microarray Analysis; Neoplasm Invasiveness; Neovascularization, Pathologic; Plasminogen Activator Inhibitor 1; RNA Interference; RNA-Binding Proteins; RNA, Messenger; Stomach Neoplasms; Tumor Cells, Cultured

Dietary (n-6)-polyunsaturated fatty acids influence cancer development, but the mechanisms have not been well characterised in gastric carcinoma.. We used two in vivo models to investigate the effects of these common dietary components on tumour metastasis. In a model of experimental metastasis, immunocompromised mice were fed diets containing linoleic acid (LA) at 2% (LLA), 8% (HLA) or 12% (VHLA) by weight and inoculated intraperitoneally (i.p.) with human gastric carcinoma cells (OCUM-2MD3). To model spontaneous metastasis, OCUM-2MD3 tumours were grafted onto the stomach walls of mice fed with the different diets. In in vitro assays, we investigated invasion and ERK phosphorylation of OCUM-2MD3 cells in the presence or absence of LA. Finally, we tested whether a cyclooxygenase (COX) inhibitor, indomethacin, could block peritoneal metastasis in vivo.. Both the HLA and VHLA groups showed increased incidence of tumour nodules (LA: 53%; HLA: 89%; VHLA: 100%; P<0.03); the VHLA group also displayed increased numbers of tumour nodules and higher total volume relative to LLA group in experimental metastasis model. Both liver invasion (78%) and metastasis to the peritoneal cavity (67%) were more frequent in VHLA group compared with the LLA group (22% and 11%, respectively; P<0.03) in spontaneous metastasis model. We also found that the invasive ability of these cells is greatly enhanced when exposed to LA in vitro. Linoleic acid also increased invasion of other scirrhous gastric carcinoma cells, OCUM-12, NUGC3 and MKN-45. Linoleic acid effect on OCUM-2MD3 cells seems to be dependent on phosphorylation of ERK. The data suggest that invasion and phosphorylation of ERK were dependent on COX. Indomethacin decreased the number of tumours and total tumour volume in both LLA and VHLA groups. Finally, COX-1, which is known to be an important enzyme in the generation of bioactive metabolites from dietary fatty acids, appears to be responsible for the increased metastatic behaviour of OCUM-2MD3 cells in the mouse model.. Dietary LA stimulates invasion and peritoneal metastasis of gastric carcinoma cells through COX-catalysed metabolism and activation of ERK, steps that compose pathway potentially amenable to therapeutic intervention.

Topics: Animals; Carcinoma; Cell Movement; Dietary Fats, Unsaturated; Dose-Response Relationship, Drug; Female; Humans; Linoleic Acid; Mice; Mice, Nude; Neoplasm Invasiveness; Neoplasm Metastasis; Neoplasm Transplantation; Stomach Neoplasms; Transplantation, Heterologous; Tumor Cells, Cultured

We examined the effect of linoleic acid (LA) on tumor formation. Cell growth was suppressed by LA in a dose-dependent manner in MKN28 and Colo320 cells. Continuous treatment with LA provided growth arrest in both cells at 5-7 weeks after the treatment. LA-pretreated MKN28 and Colo320 cells showed higher tumorigenicity (9/10 and 10/10, respectively) than nontreated cells (2/10 and 3/10, respectively; p < 0.01) in nude mice. In contrast, LA-pretreated MKN28 and Colo320 cells showed more suppressed tumor growth than nontreated cells (p < 0.01). LA-pretreated MKN28 and Colo320 cells with LA administration after the inoculation did not form macroscopic tumors. Histological examination revealed small cancer cell aggregations, which showed no proliferative activity. In LA-treated MKN28 and Colo320 cells, protein production of Bcl-2 was increased, whereas Bak, EGFR and VEGF levels were decreased. These findings suggest that LA might induce quiescence and subsequent dormancy in cancer cells.

Topics: Animals; bcl-2 Homologous Antagonist-Killer Protein; Cell Line, Tumor; Cell Proliferation; Colonic Neoplasms; Dose-Response Relationship, Drug; ErbB Receptors; Humans; Linoleic Acid; Mice; Mice, Inbred BALB C; Mice, Nude; Proto-Oncogene Proteins c-bcl-2; Stomach Neoplasms; Vascular Endothelial Growth Factor A; Xenograft Model Antitumor Assays

In this study, we investigated the effects of linoleic acid (LA), a polyunsaturated fatty acid found in most vegetable oils and certain food products, on the growth of AGS human gastric adenocarcinoma cells. LA treatment resulted in a concentration-dependent growth inhibition of AGS cells by inducing apoptosis, as evidenced by the formation of apoptotic bodies, chromatin condensation, and the accumulation cells in the sub-G1 phase. LA treatment induced cyclin-dependent kinase inhibitor p21 in a p53-independent manner; however, this compound did not affect the cell cycle distribution. Reverse transcription-polymerase chain reaction and western blot analyses showed that treating the cells with LA caused the up-regulation of pro-apoptotic Bax expression and the down-regulation of anti-apoptotic Bcl-2 expression. The apoptosis of AGS cells by LA was found to be associated with an elevated Fas and Fas ligand expression in a concentration-dependent manner. Furthermore, a proteolytic activation of caspases (3, 8, and 9), and degradation/cleavage of poly(ADP-ribose) polymerase and phospholipase C-gamma 1 protein were noted in LA-treated AGS cells. The present results indicate that the Fas/Fas ligand pathway might be involved in LA-induced apoptosis of AGS cells.

Topics: Adenocarcinoma; Apoptosis; Caspases; Cell Division; Cell Line, Tumor; Enzyme Activation; Fas Ligand Protein; fas Receptor; Gene Expression; Humans; Linoleic Acid; Poly(ADP-ribose) Polymerases; Proto-Oncogene Proteins c-bcl-2; RNA, Messenger; Stomach Neoplasms; Type C Phospholipases

To study the inhibitory effects of c9, t11-conjugated linoleic acid (c9, t11-CLA) on migration of human gastric carcinoma cell line (SGC-7901) via cyclooxygenase-2 (COX-2) pathway.. After inhibiting COX-2 activity by 100 micromol/L COX-2 inhibitor NS-398 in SGC-7901 cell, we treated SGC-7901 cells with c9, t11-CLA at a concentration of 200,100, 50, 25 micromol/L for 24 h, respectively. Using reconstituted basement membrane invasion, adhesion, chemotaxis assays, we detected the effect of c9, t11-CLA and COX-2 on the cell migration.. Compared to NS-398 group, 200, 100 micromol/L c9, t11-CLA significantly suppressed SGC-7901 cells invading into the reconstituted basement membrane (F = 14.309, P = 0.000; F = 19.005, P = 0.000). 200 micromol/L c9, t11-CLA significantly inhibited SGC-7901 cells adhering to laminin, fibronectin and Matrigel (F = 3.063, P = 0.021; F = 6.692, P = 0.001; F = 11.999, P = 0.000). The chemotaxis of SGC-7901 cells and inhibitory frequency were significantly decreased in the 200 micromol/L c9, t11-CLA group (F = 1.380, P = 0.276).. c9, t11-CLA inhibits invasion, adhesion and chemotaxis of SGC-7901 cells, and the COX-2 plays an important role in the process. [ Key words]

Topics: Cell Movement; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Humans; Linoleic Acid; Neoplasm Invasiveness; Stomach Neoplasms; Tumor Cells, Cultured

The effect on peritoneal metastasis of linoleic acid (LA) was examined using in vitro treatment of cancer cells and mouse peritoneal metastasis models. Firstly, cell growth of MKN28 human gastric cancer cells and Colo320 human colon cancer cells was suppressed by LA in a dose-dependent manner with increment of apoptosis. LA-induced growth inhibition was recovered by the exposure to antisense S-oligodeoxynucleotide for peroxisome proliferator-activated receptor gamma (PPARgamma) or 15-lipoxygenase-1, which converts LA to PPARgamma ligands. LA significantly inhibited invasion into type-IV collagen-coated membrane of MKN28 and Colo320 cells (p<0.05). BALB/c nu/nu mice inoculated with MKN28 and Colo320 cells into their peritoneal cavities were administrated with LA intraperitoneally (weekly, four times). The LA treatment significantly diminished the number of metastatic foci of both cells in the peritoneal cavity (p<0.05). Protein production in MKN28 and Colo320 cells treated with LA showed a decrease of epidermal growth factor receptor and an increase of Bax. These findings suggest that LA inhibits invasion and metastasis of human gastric and colon cancer cells by nondietary administration.

Topics: Animals; Antineoplastic Agents; Apoptosis; Arachidonate 15-Lipoxygenase; bcl-2-Associated X Protein; Cell Line, Tumor; Cell Movement; Colonic Neoplasms; Cricetinae; Dose-Response Relationship, Drug; ErbB Receptors; Humans; Linoleic Acid; Lipoxygenase Inhibitors; Mice; Mice, Inbred BALB C; Mice, Nude; Oligodeoxyribonucleotides, Antisense; Peritoneal Neoplasms; PPAR gamma; Stomach Neoplasms; Xenograft Model Antitumor Assays

To study the effects of c9, t11-conjugated linoleic acid (c9, t11-CLA) on the critical enzyme (COX-2) and its product - prostaglandin E2 (PGE2) of linoleic acid metabolism path in human gastric adenocarcinoma cell line (SGC-7901).. Expression of COX-2 mRNA and protein were measured by reverse transcription polymerase chain reaction (RT-PCR) and Western blot, PGE2 was determined by radioimmunoassay (RIA).. At the concentrations of 25, 50, 100, 200 pmol/L, c9, t11-CLA suppressed the expression of COX-2 mRNA, protein and PGE.. COX-2 is involved anti-cancer action of c9, t11-CLA and is likely to act as an important target.

Topics: Adenocarcinoma; Cell Line, Tumor; Cell Proliferation; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Dinoprostone; Humans; Linoleic Acid; Linoleic Acids, Conjugated; RNA, Messenger; Stomach Neoplasms

To investigate the effect of c9,t11-conjugated linoleic acid (c9,t11-CLA) on the adhesion of human gastric carcinoma cell line (SGC-7901).. SGC-7901 cells were at first treated with different concentrations (25, 50, 100, 200 micromol/L) of c9,t11-CLA and 1 mL/L ethanol (as a negative control) for 24 h. Using adhesion assay and Western blot, we investigated the ability of SGC-7901 cells to adhere to intracellular matrix and examined the expression of E-cadherin (ECD), alpha-catenin, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in these cells.. The attachment rate to laminin of SGC-7901 cells treated with different concentrations of c9,t11-CLA (0, 25, 50, 100, and 200 micromol/L) was 100.0+/-3.3, 95.7+/-4.0, 89.2+/-4.6, 87.9+/-6.1, and 65.9+/-5.8, respectively. The attachment rate to fibronectin was 100.0+/-4.7, 96.8+/-3.8, 94.5+/-4.1, 76.5+/-4.3, and 61.8+/-4.8, respectively. The attachment rate to Matrigel was 99.9+/-6.6, 91.4+/-6.8, 85.5+/-7.4, 79.3+/-5.6, and 69.6+/-5.1, respectively. Besides, c9,t11-CLA could increase the level of ECD and alpha-catenin, and decrease the level of ICAM-1 and VCAM-1 in SGC-7901 cells.. c9,t11-CLA can reduce the adhesion of human gastric carcinoma cells to laminin, fibronectin and Matrigel. c9,t11-CLA can increase the level of ECD and alpha-catenin, and decrease the level of ICAM-1 and VCAM-1 in human gastric carcinoma cells.

Topics: alpha Catenin; Animals; Cadherins; Cell Adhesion; Cell Line, Tumor; Collagen; Cytoskeletal Proteins; Drug Combinations; Fibronectins; Humans; Intercellular Adhesion Molecule-1; Laminin; Linoleic Acid; Proteoglycans; Stomach Neoplasms; Vascular Cell Adhesion Molecule-1

To explore the inhibition of conjugated linoleic acid isomers in different purity (75 % purity c9,t11-, 98 % purity c9,t11- and 98 % purity t10,c12-CLA) on the formation of forestomach neoplasm and chemopreventive mechanisms.. Forestomach neoplasm model induced by B(a)P in KunMing mice was established. The numbers of tumor and diameter of each tumor in forestomach were counted; the mice plasma malondialdehyde (MDA) were measured by TBARS assay; TUNEL assay was used to analyze the apoptosis in forestomach neoplasia and the expression of MEK-1, ERK-1, MKP-1 protein in forestomach neoplasm were studied by Western Blotting assay.. The incidence of neoplasm in B(a)P group, 75 % purity c9, t11-CLA group, 98 % purity c9,t11-CLA group and 98 % purity t10, c12-CLA group was 100 %, 75.0 %(P>0.05), 69.2 % (P<0.05) and 53.8 % (P<0.05) respectively and the effect of two CLA isomers in 98 % purity on forestomach neoplasia was significant; CLA showed no influence on the average tumor numbers in tumor-bearing mouse, but significantly decreased the tumor size, the tumor average diameter of mice in 75 % purity c9,t11-CLA group, 98 % purity c9,t11-CLA group and 98 % purity t10, c12-CLA group was 0.157+/-0.047 cm, 0.127+/-0.038 cm and 0.128+/-0.077 cm (P<0.05) and 0.216+/-0.088 cm in B(a)P group; CLA could also significantly increase the apoptosis cell numbers by 144.00+/-20.31, 153.75+/-23.25, 157.25+/-15.95(P<0.05) in 75 % purity c9,t11-CLA group, 98 % purity c9,t11-CLA group and 98 % purity t10,c12-CLA group (30.88+/-3.72 in BP group); but there were no significant differences between the effects of 75 % purity c9,t11-CLA and two isomers in 98 % purity on tumor size and apoptotic cell numbers; the plasma levels of MDA in were increased by 75 % purity c9,t11-CLA, 98 % purity c9,t11-CLA and 98 % purity t10,c12-CLA. The 75 % purity c9,t11-CLA showed stronger inhibition; CLA could also inhibit the expression of ERK-1 protein and promote the expression of MKP-1 protein, however no influence of CLA on MEK-1 protein was observed.. Two isomers in 98 % purity show stronger inhibition on carcinogenesis. However, the inhibitory mechanisms of CLA on carcinogenesis is complicated, which may be due to the increased mice plasma MDA, the inducing apoptosis in tumor tissues. And the effect of CLA on the expression of ERK-1 and MKP-1 may be one of the mechanisms of the inhibition of CLA on the tumor.

Topics: Animals; Apoptosis; Benzo(a)pyrene; Cell Cycle Proteins; Dietary Fats, Unsaturated; Dual Specificity Phosphatase 1; Immediate-Early Proteins; In Situ Nick-End Labeling; Linoleic Acid; Lipid Peroxidation; MAP Kinase Kinase 1; Mice; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinase Kinases; Mitogen-Activated Protein Kinases; Phosphoprotein Phosphatases; Protein Phosphatase 1; Protein Serine-Threonine Kinases; Protein Tyrosine Phosphatases; Random Allocation; Stomach; Stomach Neoplasms; Thiobarbituric Acid Reactive Substances

To study the effects of c9,t11-conjugated linoleic acid (c9,t11-CLA) on invasive ability of human gastric carcinoma cell line (SGC-7901) and to explore its possible mechanism.. Reconstituted basement membrane invasion assay was used to evaluate invasive ability of cancer cells. Expression of TIMP-1, TIMP-2 and nm23-H(1) mRNA was measured by reverse transcription polymerase chain reaction (RT-PCR) in SGC-7901 cells.. At the concentrations of 200 micromol/L, 100 micromol/L and 50 micromol/L, c9,t11-CLA suppressed their reconstituted basement membrane invasion of SGC-7901 by 53.7%, 40.9% and 29.3%, respectively. c9,t11-CLA could induce the expression of TIMP-1, TIMP-2 and nm23-H(1) mRNA in SGC-7901 cells.. The invasion of SGC-7901 cells could be inhibited by c9,t11-CLA through reconstituted basement membrane. Anti-invasion action of c9,t11-CLA might be associated with induction of expression of TIMP-1, TIMP-2 and nm23-H(1) mRNA in tumor cells.

Topics: Adenocarcinoma; Gene Expression; Humans; Linoleic Acid; Monomeric GTP-Binding Proteins; Neoplasm Invasiveness; NM23 Nucleoside Diphosphate Kinases; Nucleoside-Diphosphate Kinase; RNA, Messenger; Stomach Neoplasms; Tissue Inhibitor of Metalloproteinase-1; Tissue Inhibitor of Metalloproteinase-2; Transcription Factors; Tumor Cells, Cultured

To study the inhibitory effect of CLA on the postinitiation phase of forestomach neoplasia formation induced by B(a)P and explore its possible mechanism of anticarcinogenesis.. Kunming mice were divided into five groups, i.e. salad oil control group, CLA control group, B(a)P group, B(a)P + high dose CLA group and B(a)P + low dose CLA group. The experimental period was 23 weeks, and the endpoints included cell proliferation, expression of Pan-ras P21 and some enzymes.. Short term CLA treated significantly inhibited the forestomach neoplasia formation induced by B(a)P at postinitiation phase. The incidence of tumor in the groups of B(a)P, B(a)P + high dose CLA and B(a)P + low dose CLA was 100%, 60% and 69% respectively (P < 0.05). The possible mechanism of this anticarcinogenic effect may be related to the inhibition of cell proliferation and the induction of the activities of GSH-Px, GST and SOD, irrespective of the regulation of expression of Pan-ras P21.. CLA is a promising chemopreventive agent, and its anticarcinogenic effect may involve its effects on the redox system.

Topics: Animals; Anticarcinogenic Agents; Benzo(a)pyrene; Female; Glutathione Peroxidase; Linoleic Acid; Liver; Mice; Oncogene Protein p21(ras); Stomach Neoplasms; Superoxide Dismutase

HGT cells are a human gastric tumor cell line. Preliminary data have shown that HGT cells incorporate exogenous arachidonic acid (AA) in their membrane lipids. However, we found that HGT cells are unable to produce significant amounts of AA metabolites after stimulation with calcium ionophore A23187. Furthermore, no lipoxygenase activity was detected in crude HGT cell extracts by employing an assay monitoring the in vitro utilization of linoleic acid. The meaning of these results is discussed in respect of the role of eicosanoids during cell proliferation.

Topics: Calcimycin; Eicosanoids; Humans; Linoleic Acid; Linoleic Acids; Stomach Neoplasms; Tumor Cells, Cultured

Grilled ground beef contains factors that inhibit the initiation of mouse epidermal carcinogenesis by 7,12-dimethylbenz(a)anthracene. Previously we isolated an active principal and characterized it as an isomeric mixture of conjugated dienoic derivatives of linoleic acid (CLA). We now show that synthetic CLA inhibits the initiation of mouse forestomach tumorigenesis by benzo(a)pyrene. Four and 2 days prior to p.o. treatment with benzo(a)pyrene, female ICR mice were given (a) CLA in olive oil, (b) linoleic acid in olive oil, or (c) olive oil alone or plus 0.85% saline (control groups). Three days later the cycle was repeated for a total of 4 times. At 30 wk of age, the mice were sacrificed. In three independent experiments, mice treated with CLA developed only about half as many neoplasms/animal as mice in the control groups (P less than 0.025); in two of the experiments tumor incidence was also reduced (P less than 0.05). There were no significant differences in food intake or body weight among the groups. High-performance liquid chromatography/gas chromatography analysis established that, following intubation, only the c-9, t-11 CLA isomer was incorporated into forestomach phospholipids. In studies aimed at elucidating the mechanism of action, we found that CLA is an effective antioxidant. Under the conditions of the test CLA was more potent than alpha-tocopherol and almost as effective as butylated hydroxytoluene. These observations indicate that CLA might serve as an in situ defense mechanism against membrane attack by free radicals and may, at least in part, explain the anticarcinogenic properties of CLA.

Topics: Animals; Antioxidants; Benzo(a)pyrene; Female; Gastric Mucosa; Linoleic Acid; Linoleic Acids; Mice; Mice, Inbred ICR; Oxidation-Reduction; Spectrophotometry, Ultraviolet; Stomach Neoplasms

To examine changes in fatty acid composition of serum lipids, sixteen patients with gastric cancer were maintained on total parenteral nutrition (TPN) or intravenous feeding immediately after total gastrectomy. Subjects receiving no fat showed decreases in linoleic acid, linolenic acid and arachidonic acid and increases in palmitoleic acid and oleic acid, whereas those receiving fat emulsion showed no detectable changes. Decrease in the linoleic acid content was greater in subjects on a higher carbohydrate intake, but less in those on a higher fat intake. Multiple regression analysis of the relationships among carbohydrate intake (X1) and fat intake (X2) and changes in the linoleic acid percentage of total serum fatty acids (Y) in each case yielded an equation: Y =-4.75 X1 + 69.0 X2 - 27.9 (R = 0.885, p less than 0.05). Approximately 1 g/kg/day of fat provided in 40-50 kcal/kg/day of nonprotein energy intake was estimated to prevent decrease in the linoleic acid content in the serum fatty acid pattern during the postoperative catabolic stage.

Topics: Adult; Aged; Fat Emulsions, Intravenous; Fatty Acids; Fatty Acids, Essential; Female; Gastrectomy; Humans; Linoleic Acid; Linoleic Acids; Male; Middle Aged; Parenteral Nutrition, Total; Postoperative Care; Postoperative Complications; Stomach Neoplasms