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PubMed2003

Inhibition of conjugated linoleic acid on mouse forestomach neoplasia induced by benzo (a) pyrene and chemopreventive mechanisms.

AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Animals↗
PubMed2006

The natural concentration of the conjugated linoleic acid, cis-9,trans-11, in milk fat has antiatherogenic effects in hyperlipidemic hamsters.

Milk fat is usually considered to be proatherogenic, although its fatty acid composition can vary, due mainly to farming conditions. No study has evaluated whether such variation can modify the atherogenic properties of dairy fat. Aortic lipid deposition and related risk factors were examined in Syrian hamsters fed diets for 12 wk containing 200 g/kg of 2 commercial milk fats [high content of saturated fatty acids (HSF) and low content of saturated fatty acids (LSF)] contrasting, respectively, in total saturated fatty acids (72 vs. 67 g/100 g), 18:1, trans (4.24 vs. 7.26 g/100g), and conjugated linoleic acid (mainly cis-9,trans-11 or rumenic acid; 0.39 vs. 2.59 g/100 g). Hamsters fed the LSF-diet had 25% less aortic cholesteryl-ester deposition than those fed the HSF-diet; this was accompanied by an improved plasma cholesterol profile (lower LDL cholesterol and LDL:HDL cholesterol ratio), a lower local inflammatory status (aortic gene expression of cyclooxygenase-2), and lower aortic gene expression of vascular cell adhesion molecule-1 (all P < 0.05). Supplementation of the LSF-diet with rumenic acid (up to 9 g/kg) amplified the antiatherogenic effect of the original LSF-diet compared with the HSF-diet, i.e., less aortic cholesterol loading, increased reverse cholesterol transport potential (higher plasma HDL cholesterol concentration and ATP-binding cassette, subfamily A, transporter 1 gene expression in aorta), and decreased LDL-peroxidability index and gene expression of proinflammatory IL-1beta in the aorta (all P < 0.05). In conclusion, our results suggest that the atherogenic potential of milk fat can be greatly reduced in products with a naturally high abundance of rumenic acid, and argue for increasing this fatty acid in milk.

Adipose Tissue↗
PubMed2003

Inhibition of linoleic acid hydroperoxide-induced toxicity in cultured human fibroblasts by anthocyanidins.

The protective effect of anthocyanidins against the toxicity induced by linoleic acid hydroperoxide (LOOH) was examined in cultured human fetal lung fibroblasts, TIG-7. Cyanidin was more effective than pelargonidin or delphinidin in inhibiting LOOH-induced cytotoxicity. The presence of a catechol moiety in the B ring is shown to be important for the protective activities against the cytotoxicity of LOOH.

Anthocyanins↗
PubMed1999

Conjugated linoleic acid activates peroxisome proliferator-activated receptor alpha and beta subtypes but does not induce hepatic peroxisome proliferation in Sprague-Dawley rats.

Since conjugated linoleic acid (CLA) has structural and physiological characteristics similar to peroxisome proliferators, we hypothesized that CLA would activate peroxisome proliferator-activated receptor (PPAR). We compared the effects of dietary CLA (0.0, 0.5, 1.0 and 1.5% by weight) with a peroxisome proliferator (0.01% Wy-14,643) in female and male Sprague-Dawley (SD) rats. Dietary CLA had little effect on body weight, liver weight, and hepatic peroxisome proliferation, compared to male rats fed Wy-14,643 diet. Lipid content in livers from rats fed 1.5% CLA and Wy-14,643 diets was increased (P < 0.01) when compared to rats fed control diets regardless of gender. Hepatic acyl-CoA oxidase (ACO) mRNA levels were increased 3-fold in male rats fed 1.5% CLA diet compared to rats fed control diets while Wy-14,643 supported approximately 30-fold ACO mRNA accumulation. A similar response was observed for liver fatty acid-binding protein (L-FABP) mRNA. The effect of dietary treatments on hepatic PPAR-responsive genes in female rats was weaker than in male rats. The (9Z,11E)-CLA isomer activated PPAR alpha in transfected cells to a similar extent as Wy-14,643, whereas the furan-CLA metabolite was comparable to bezafibrate on activating PPAR beta. These data suggest that while CLA was able to activate PPARs it is not a peroxisome proliferator in SD rats.

Acyl-CoA Oxidase↗
PubMed1975

Relationship between lipids in plasma and skin secretions of neonatal calf with particular reference to linoleic acid.

A study has been made on the lipid composition of the skin secretions and plasma of the neonatal calf. A significant proportion of the skin surface lipids was comprised of triglycerides. Saturated fatty acids comprised the major proportion of the fatty acids of the skin surface triglycerides at birth. Immediately after birth, the proportion of the saturated fatty acids decreased, and there was a concomittant increase in the proportion of 18:1. Some 3-4 weeks after birth, the proportion of 18:2 delta cis-9, cis-12 in the skin surface triglycerides increased to ca. 14 percent, and there was a decrease in the proportion of 18:1. The 18:2 was shown to be confined almost entirely to the 2 position of the triglycerides. During the first 5 weeks after birth, the concentrations of the cholesteryl esters and phospholipids in the plasma increased markedly and were accompanied by a rapid increase in the proportion of 18:2 within these 2 fractions. The results are discussed in relation to the known role of 18:2 in the metabolism of biological systems.

Animals↗
PubMed2003

Isolation of unsaturated diols after oxidation of conjugated linoleic acid with peroxygenase.

Oat seeds are a rich source of peroxygenase, an iron heme enzyme that participates in oxylipin metabolism in plants. An isomer of CLA, 9(Z),11 (E)-octadecadienoic acid (1), believed to have anticarcinogenic activity, was used as a substrate for peroxygenase in an aqueous medium using t-butyl hydroperoxide as the oxidant. After acidification of the reaction medium, the products were extracted with ethyl ether, converted to their methyl esters, and characterized using HPLC. Major products after reaction for 24 h showed resonances from 1H NMR spectroscopy that were further downfield than the expected epoxides and were thought to be diol hydrolysis products. However, analyses by HPLC with atmospheric pressure chemical ionization MS (APCI-MS) of the putative allylic diols or their bis-trimethylsilyl ether derivatives gave incorrect M.W. The M.W. of the diols could be obtained by APCI-MS after removal of unsaturation by hydrogenation or by EI-MS after conversion of the allylic 1,2-diols to cyclic methyl boronic esters. Data from MS in conjunction with analyses using 1H and 13C NMR showed that the methylated products from 1 were methyl 9,10(threo)-dihydroxy-11 (E)-octadecenoate, methyl 9,10(erythro)-dihydroxy-11(E)-octadecenoate, methyl 9,12(erythro)-dihydroxy-10(E)-octadecenoate, and methyl 9,12(threo)-dihydroxy-10(E)-octadecenoate. Solid-phase extraction without prior acidification and conversion of the products to methyl esters allowed identification of the following epoxides: methyl 9,10(Z)-epoxy-11 (E)-octadecenoate (6M), methyl 9,10(E)-epoxy-11 (E)-octadecenoate, and methyl 11,12(E)-epoxy-9(Z)-octadecenoate. At times of up to at least 6 h, 6M accounted for approximately 90% of the epoxide product. Product analysis after the hydrolysis of isolated epoxide 6M showed that hydrolysis of epoxide 6 could largely account for the diol products obtained from the acidified reaction mixtures.

Biochemistry↗
PubMed2004

Contrasting effects of t10,c12- and c9,t11-conjugated linoleic acid isomers on the fatty acid profiles of mouse liver lipids.

The purpose of this study was to examine the effects of two purified isomers of CLA (c9,t11-CLA and t10,c12-CLA) on the weights and FA compositions of hepatic TG, phospholipids, cholesterol esters, and FFA. Eight-week-old female mice (n = 6/group) were fed either a control diet or diets supplemented with 0.5% c9,t11-CLA or t10,c12-CLA isomers for 8 wk. Weights of liver total lipids and those of individual lipid fractions did not differ between the control and the c9,t11-CLA groups. Livers from animals fed the t10, c12-CLA diet contained four times more lipids than those of the control group; this was mainly due to an increase in the TG fractions (fivefold), but cholesterol (threefold), cholesterol esters (threefold), and FFA (twofold) were also significantly increased. Although c9,t11-CLA did not significantly alter the weights of liver lipids when compared with the control group, its intake was associated with significant reductions in the weight percentage (wt% of total FAME) of 18:1n-9 and 18:1n-7 in the TG fraction and with significant increases in the weight percentage of 18:2n-6 in the TG, cholesterol ester, and phospholipid fractions. On the other hand, t10,c12-CLA intake was linked with a significant increase in the weight percentage of 18:1n-9 and a decrease in that of 18:2n-6 in all lipid fractions. These changes may be the result of alterations in the activity of delta9-desaturase (stearoyl CoA desaturase) and the enzymes involved in the metabolism of 18:2n-6. Thus, the two isomers differed not only in their effects on the weights of total liver lipids and lipid fractions but also on the FA profile of the lipid fractions.

Animals↗
PubMed2005

Culture age and carbamoylcholine increase the incorporation of endogenously synthesized linoleic acid in lipids of Trypanosoma cruzi epimastigotes.

Physiological and cellular adaptations to environmental changes are known to be related to modifications in membrane lipids. This work provides metabolic and compositional evidence that Trypanosoma cruzi epimastigotes are able to synthesize and desaturate fatty acids, to incorporate them into their lipids, and to modify this incorporation when carbamoylcholine is present in the medium. The fatty acids formed from [2-(14)C]acetate in the period from 2 to 9 days were mostly (70%) incorporated in phospholipids, the remainder 30% being recovered in neutral lipids, such as triacylglycerols (TAG) and diacylglycerols (DAG). The main fatty acids formed from [2-(14)C]acetate were saturates (16:0, 18:0), monoenes (16:1, 18:1) and dienes (mostly 18:2). The ratios between labelled unsaturated and saturated fatty acids increased continuously with growth, consistent with a precursor-product relationship between the main fatty acids, and with the occurrence in T. cruzi of Delta(9)- and Delta(12)-desaturases. From days 2 to 5, [(14)C]18:2 was the main fatty acid produced. Accordingly, the fatty acid profiles showed a significant increase in the percentage of 18:2 in all lipids in the period under study, especially in the first 2 to 5 days. In the presence of carbamoylcholine, the labelling of DAG and TAG with [(14)C]18:2 augmented. The results indicate that T cruzi is able to synthesize the main types of fatty acids required to form its membrane lipids, and to exchange them actively in response to environmental stimuli.

Acetates↗
PubMed2003

Alleviation of the cytotoxic activity induced by trans10, cis12-conjugated linoleic acid in rat hepatoma dRLh-84 cells by oleic or palmitoleic acid.

We showed the inhibitory effect of oleic and palmitoleic acids (OA and POA) on this trans10, cis12 (10t, 12c)-CLA induced cytotoxic activity. When cells were cultured in the presence of 10t, 12c-CLA, this potent cytotoxic effect on dRLh-84 cells was clearly obvious when compared to the control vehicle group. It was revealed that the levels of cellular OA and POA levels decreased upon cis9, trans11 (9c,11t) or 10t, 12c-CLA treatment in a time course dependent manner. OA or POA demonstrates a dose dependent inhibition of the 10t, 12c-CLA induced cytotoxicity. Notable nuclear fragmentation or activation of caspase-3 and 9 by 10t, 12c-CLA in dRLh-84 was counteracted by treatment with OA or POA. Results also suggest that 10t, 12c-CLA induced apoptosis can be inhibited by treatment with OA or POA.

Animals↗