Differential induction of plant volatile biosynthesis in the lima bean by early and late intermediates of the octadecanoid-signaling pathway. (57/3819)

Plants are able to respond to herbivore damage with de novo biosynthesis of an herbivore-characteristic blend of volatiles. The signal transduction initiating volatile biosynthesis may involve the activation of the octadecanoid pathway, as exemplified by the transient increase of endogenous jasmonic acid (JA) in leaves of lima bean (Phaseolus lunatus) after treatment with the macromolecular elicitor cellulysin. Within this pathway lima bean possesses at least two different biologically active signals that trigger different biosynthetic activities. Early intermediates of the pathway, especially 12-oxo-phytodienoic acid (PDA), are able to induce the biosynthesis of the diterpenoid-derived 4,8, 12-trimethyltrideca-1,3,7,11-tetraene. High concentrations of PDA result in more complex patterns of additional volatiles. JA, the last compound in the sequence, lacks the ability to induce diterpenoid-derived compounds, but is highly effective at triggering the biosynthesis of other volatiles. The phytotoxin coronatine and amino acid conjugates of linolenic acid (e.g. linolenoyl-L-glutamine) mimic the action of PDA, but coronatine does not increase the level of endogenous JA. The structural analog of coronatine, the isoleucine conjugate of 1-oxo-indanoyl-4-carboxylic acid, effectively mimics the action of JA, but does not increase the level of endogenous JA. The differential induction of volatiles resembles previous findings on signal transduction in mechanically stimulated tendrils of Bryonia dioica.  (+info)

Regulation of stearoyl-CoA desaturase by polyunsaturated fatty acids and cholesterol. (58/3819)

The lipid composition of cellular membranes is regulated to maintain membrane fluidity. A key enzyme involved in this process is the membrane-bound stearoyl-CoA desaturase (SCD) which is the rate-limiting enzyme in the cellular synthesis of monounsaturated fatty acids from saturated fatty acids. A proper ratio of saturated to monounsaturated fatty acids contributes to membrane fluidity. Alterations in this ratio have been implicated in various disease states including cardiovascular disease, obesity, non-insulin-dependent diabetes mellitus, hypertension, neurological diseases, immune disorders, and cancer. The regulation of stearoyl-CoA desaturase is therefore of considerable physiological importance and its activity is sensitive to dietary changes, hormonal imbalance, developmental processes, temperature changes, metals, alcohol, peroxisomal proliferators, and phenolic compounds. Two mouse and rat SCD genes (SCD1 and SCD2) and a single human SCD gene have been cloned and characterized. In the past several years we have studied the dietary influences on the genetic expression of the mouse stearoyl-CoA desaturase. The expression of the mouse SCD genes is regulated by polyunsaturated fatty acids and cholesterol at the levels of transcription and mRNA stability. Promoter elements that are responsible for the polyunsaturated fatty acid repression colocalize with the promoter elements for SREBP-mediated regulation of the SCD genes. It is the goal of this review to provide an overview of the genetic regulation of the stearoyl-CoA desaturase in response to dietary polyunsaturated fatty acids and cholesterol.  (+info)

Regulation of RelA subcellular localization by a putative nuclear export signal and p50. (59/3819)

Nuclear factor kappaB (NF-kappaB) represents a family of dimeric DNA binding proteins, the pleotropic form of which is a heterodimer composed of RelA and p50 subunits. The biological activity of NF-kappaB is controlled through its subcellular localization. Inactive NF-kappaB is sequestered in the cytoplasm by physical interaction with an inhibitor, IkappaBalpha. Signal-mediated IkappaBalpha degradation triggers the release and subsequent nuclear translocation of NF-kappaB. It remains unknown whether the NF-kappaB shuttling between the cytoplasm and nucleus is subjected to additional steps of regulation. In this study, we demonstrated that the RelA subunit of NF-kappaB exhibits strong cytoplasmic localization activity even in the absence of IkappaBalpha inhibition. The cytoplasmic distribution of RelA is largely mediated by a leucine-rich sequence homologous to the recently characterized nuclear export signal (NES). This putative NES is both required and sufficient to mediate cytoplasmic localization of RelA as well as that of heterologous proteins. Furthermore, the cytoplasmic distribution of RelA is sensitive to a nuclear export inhibitor, leptomycin B, suggesting that RelA undergoes continuous nuclear export. Interestingly, expression of p50 prevents the cytoplasmic expression of RelA, leading to the nuclear accumulation of both RelA and p50. Together, these results suggest that the nuclear and cytoplasmic shuttling of RelA is regulated by both an intrinsic NES-like sequence and the p50 subunit of NF-kappaB.  (+info)

Incorporation of dietary polyunsaturated fatty acids into pork fatty tissues. (60/3819)

The incorporation and elimination rate of dietary PUFA in pork fat was investigated in this study. Experiment 1 examined the incorporation of dietary PUFA into backfat (BF) and into the triglyceride (TG) and phospholipid (PL) fractions of the i.m. fat of the loin. Experiment 2 examined the elimination of PUFA from BF due to withdrawal of PUFA from the diet. In Exp. 1, Pietrain x Seghers Hybrid pigs (70 barrows and 70 gilts averaging 11 wk of age and 30 kg initially) were assigned to five dietary treatments in a 2 x 5 factorial arrangement during a 16-wk feeding period. Pigs received a diet containing about 2.5% tallow (T) for 8, 10, 12, 14, or 16 wk, followed by a diet containing about 15% full-fat soybeans (FFS) for 8, 6, 4, 2, or 0 wk, respectively. Additionally, BF biopsies were taken every 2 wk from eight pigs on the 8-wk FFS dietary treatment, starting from the time pigs were switched to the FFS diet. Linoleic acid [18:2(n-6)], linolenic acid [18:3(n-3)], eicosadienoic acid [20:2(n-6)], arachidonic acid [20:4(n-6)], and PUFA contents in BF increased (P < .01) with time on the FFS diet, but contents of these fatty acids were similar for pigs fed FFS for 6 or 8 wk. The PUFA content of the biopsies rose throughout the FFS treatment; the greatest increase in PUFA occurred during the first 2 wk of feeding FFS. The PUFA content of the TG and PL fractions in i.m. fat of the longissimus muscle tended to increase with time on the FFS diet. The increase was significant (P < .01) in the TG fraction for 18:3(n-3) and in the PL fraction for 20:4(n-6) and 22:6(n-3). In Exp. 2, 11-wk-old pigs (10 barrows and 10 gilts) were fed a FFS-based diet from 11 to 19 wk of age, followed by the T-diet for an additional 8 wk. During the latter period, biopsies were taken every 2 wk. The elimination of PUFA from BF was greatest during the first 2 wk after the dietary change. The PUFA reached the lowest level at the age of 25 wk. These experiments show that the PUFA: saturated fatty acid ratio of BF can be increased from .34, corresponding with a T-based diet, to .55, by feeding a FFS diet for 6 wk before slaughter.  (+info)

Neonatal dietary zinc deficiency in artificially reared rat pups retards behavioral development and interacts with essential fatty acid deficiency to alter liver and brain fatty acid composition. (61/3819)

The objective of this study was to investigate whether short-term zinc deficiency in the early neonatal period would exacerbate the effects of essential fatty acid (EFA) deficiency on liver and brain long-chain polyunsaturated fatty acid (LCPUFA) composition, as well as on behavioral development in artificially reared rat pups. Using a 2 x 2 factorial design, male Long-Evans rat pups were reared artificially from postnatal d 5 to 16; pups were fed through gastrostomy tubes with rat formula deficient in zinc and/or EFA. As expected, EFA deficiency significantly reduced levels of arachidonic acid [AA, 20:4(n-6)] and docosahexanoic acid [DHA, 22:6(n-3)] in liver phosphatidylcholine (PC) and brain phosphaditylethanolamine (PE), and increased 22:5(n-6) levels in liver and brain PC and PE. There were significant interactions between zinc and EFA in liver such that zinc deficiency reduced AA and DHA in the EFA-adequate groups, but significantly increased AA in the EFA-deficient groups. Contrary to the hypothesis, short-term zinc deficiency did not exacerbate the effects of EFA deficiency in liver phospholipids. In brain PE, a significant interaction between EFA and zinc was observed such that zinc deficiency increased 22:5(n-6) concentrations in EFA-adequate but not in EFA-deficient groups. Regardless of their EFA status, zinc-deficient rats were growth retarded and demonstrated deficits in locomotor skills. Possible effects of long-term zinc and EFA deficiency on brain function should be investigated in future studies.  (+info)

Both (n-3) and (n-6) fatty acids stimulate wound healing in the rat intestinal epithelial cell line, IEC-6. (62/3819)

The control of proliferation and epithelial restitution are processes that are poorly understood. The effects of (n-3), (n-6) and trans fatty acids on proliferation of subconfluent IEC-6 cultures and restitution of wounded IEC-6 monolayers were investigated. Incorporation of supplemented fatty acids into cellular phospholipid was also assessed. Sulforhodamine B protein dye binding assay was utilized to assess the proliferative effects of fatty acids on growth of IEC-6 cultures. Incorporation of supplemental fatty acids into cellular phospholipid was examined by thin-layer chromatography combined with gas chromatography. The modulation of epithelial restitution was examined by razor blade wounding confluent IEC-6 monolayers grown in media supplemented with various fatty acids. Inhibition of eicosanoid synthesis by indomethacin during the wounding assay was also assessed. Both (n-3) and (n-6) fatty acids significantly inhibited growth of this intestinal epithelial cell model at concentrations above 125 micromol/L. The trans fatty acid, linoelaidate 18:2(n-6)trans, inhibited growth of IEC-6 cells at concentrations above 250 micromol/L. Another trans fatty acid, elaidate 18:1(n-9)trans, was well-tolerated at concentrations as high as 500 micromol/L. Eicosapentanoic 20:5(n-3), linoleic 18:2(n-6), alpha-linolenic 18:3(n-3), gamma-linolenic 18:3(n-6) and arachidonic 20:4(n-6) acids all significantly enhanced cellular migration in the IEC-6 model of wound healing. Eicosapentanoate, linoleate, alpha-linolenate, gamma-linolenate and arachidonate are all capable of improving reconstitution of epithelial integrity following mucosal injury. Inhibition of eicosanoid synthesis reduced the enhancement of restitution by n-6 fatty acids back to control levels.  (+info)

Consumption of fish oil leads to prompt incorporation of eicosapentaenoic acid into colonic mucosa of patients prior to surgery for colorectal cancer, but has no detectable effect on epithelial cytokinetics. (63/3819)

Fish oil (FO) was previously reported to partially normalize colorectal crypt cell cytokinetics in patients with colorectal neoplasms. We determined the effect of FO on the fatty acid composition of colonic mucosa and mesenteric adipose tissue and on rectal crypt cell proliferation in patients undergoing surgery for colonic carcinoma. Patients (49-28 males; 21 females) were randomly assigned to consume FO capsules (2 g b.d.; FO group) containing 1.4 g eicosapentaenoic acid (EPA) and 1.0 g docosahexaenoic acid per day, or safflower oil capsules (2 g b.d.; placebo group) for an average of 12.3 +/- 0.5 d prior to surgery. Rectal biopsies were obtained at entry, at surgery, and 8-12 wk postsurgery. Colonic biopsies and samples of mesenteric adipose tissue were analyzed for fatty acids by gas-liquid chromatography. Mitosis was determined in whole crypt mounts. The proportion of EPA (g/100 g total fatty acids) in mucosal lipids was significantly greater in FO patients compared to the placebo group, but there was no effect on mesenteric adipose tissue. However self-reported use of FO supplements prior to surgery was associated with higher levels of EPA in adipose tissue. There was no significant effect of FO on the frequency or spatial distribution of crypt cell mitosis. EPA from marine oil supplements is rapidly incorporated into the colonic mucosal lipids of humans, but the levels achieved in the present study did not modify colorectal cytokinetics.  (+info)

The main fatty acid-binding protein in the liver of the shark (Halaetunus bivius) belongs to the liver basic type. Isolation, amino acid sequence determination and characterization. (64/3819)

Three fatty acid-binding proteins (FABPs) from the liver of the shark Halaetunus bivius were isolated and characterized: one of them belongs to the liver-type FABP family and the other two to the heart-type FABP family. The complete primary structure of the first FABP, and partial primary structures of the two others, were determined. The liver-type FABP constitutes 69% of the total FABPs, and its amino acid sequence presents the highest identity with chicken, catfish, iguana and elephant fish liver basic FABPs. The L-FABP protein has low affinity for palmitic and oleic acids and high affinity for linoleic and arachidonic acids and other hydrophobic ligands, all of them important for the metabolic functions of the liver. In contrast, both heart-type FABPs have the highest affinity for palmitic acid, the principal fatty acid mobilized from fat deposits for beta-oxidation.  (+info)