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Unidentified constituents in fresh pasture increase milk fat cis-9, trans-11 conjugated linoleic acid (CLA) concentration, and prevent milk fat depression, even though ruminal conditions conducive to reducing milk fat synthesis exist. One possible explanation is vitamin E (kappa-tocopherol), a constituent high in fresh pasture, but naturally low in conserved/dried forages and cereal grains. Twenty late-lactating dairy cows previously consuming a total mixed ration (TMR) were randomly allocated to one of two dietary treatments for 21 d: TMR (control; n=10); and TMR plus an additional 10,000 i.u. alpha-tocopherol/d (VIT E; n = 10). These cows were simultaneously compared with 13 late-lactation dairy cows previously grazing fresh pasture (PAS) balanced for age, parity and genetic merit. Average daily alpha-tocopherol intakes were approximately 468, 10,520 and 1,590 i.u./cow for the control, VIT E and PAS treatments, respectively. Dietary alpha-tocopherol supplementation (VIT E v. control) slightly increased milk fat content by 0.23 percentage units, but did not significantly alter milk fatty acid composition. Plasma trans-11 18:1 (VA) content tended to increase and trans-10 18:1 levels numerically declined following alpha-tocopherol supplementation suggesting possible changes in rumen biohydrogenation products. In addition, increased alpha-tocopherol intake in TMR-fed cows decreased serum urea levels and tended to alter milk fat 15:0 suggesting changes in rumen microbial populations. However, when compared with cows grazing pasture, TMR-fed cows supplemented with alpha-tocopherol, still produced milk with lower cis-9, trans-11 CLA and VA, and higher trans-10 18:1 concentrations suggesting alpha-tocopherol is not a primary reason for milk fatty acid profile differences between pasture and TMR-fed cows. Therefore, additional unknown pasture constituents favour production of fatty acids originating from the cis-9, trans-11 instead of the trans-10, cis-12 CLA biohydrogenation pathways.
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PMID:A comparison between feeding systems (pasture and TMR) and the effect of vitamin E supplementation on plasma and milk fatty acid profiles in dairy cows. 1617 64

Six lactating Holstein cows were assigned to a replicated Latin square design to test the effect of dietary vitamin E on milk fat depression and on the increased production of milk trans-10 C18:1 classically observed when feeding high doses of unsaturated fatty acids with low-fiber diets. Two diets (linseed diet and linseed diet + 12,000 IU of vitamin E/d) were compared during 2 periods of 21 d. The linseed diet presented a forage-to-concentrate ratio of 50:50 and contained extruded linseed (1.86 kg/d) and linseed oil (190 g/d). It was conceived to favor the "trans-11 to trans-10 shift" (low structural value and high level of unsaturated fatty acids). Milk yield and protein content were not affected by the diets. Milk of cows fed the linseed diet presented the typical symptoms of milk fat depression associated with a shift in biohydrogenation pathways: low fat content and high level of trans-10 C18:1. However, the high dose of dietary vitamin E provided significantly increased milk fat content (by 17.93%) and yield (by 15.56%) and decreased trans-10 C18:1 content (by 47.06%). In addition, it managed to significantly increase the daily yields of vaccenic (by 102.56%) and rumenic acids (by 56.67%). However, the sequence of administration of vitamin E influenced its effect, as vitamin E seemed to be more active in limiting the "trans-11 to trans-10 shift" when it was incorporated in the diet simultaneously with the fat. Once the shift had occurred, the subsequent addition of vitamin E was no longer able to completely counteract this process.
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PMID:Effect of dietary vitamin E on rumen biohydrogenation pathways and milk fat depression in dairy cows fed high-fat diets. 1642 37

Conjugated linoleic acid (CLA) refers to a mixture of conjugated octadecadienoic acids of predominantly ruminant origin. The main isomer in bovine milk fat is the cis-9, trans-11 CLA. Interest in CLA increased after the discovery of its health-promoting properties, including potent anticarcinogenic activity. Two experiments were conducted to evaluate dietary strategies aimed at increasing the concentration of CLA in bovine milk fat. Both experiments were organized as a randomized complete block design with a repeated measures treatment structure. In Experiment 1, 28 Holstein cows received either a control diet or one of 3 treatments for a period of 2 wk. The control diet consisted of 60% forage (barley silage, alfalfa silage, and alfalfa hay) and 40% concentrate on a dry matter (DM) basis, fed as a total mixed ration (TMR). The concentrate was partially replaced in the treatment groups with 24 ppm of monensin (MON), 6% of DM safflower oil (SAFF), or 6% of DM safflower oil plus 24 ppm of monensin (SAFF/M). Average cis-9, trans-11 CLA levels in milk fat after 2 wk of feeding were 0.45, 0.52, 3.36, and 5.15% of total fatty acids for control, MON, SAFF, and SAFF/M, respectively. In Experiment 2, 62 Holstein cows received either a control diet or one of 5 treatment diets for a period of 9 wk. The control diet consisted of 60% forage (barley silage, alfalfa silage, and alfalfa hay) and 40% concentrate on a DM basis, fed as a TMR. The concentrate was partially replaced in the treatment groups with 6% of DM safflower oil (SAFF), 6% of DM safflower oil plus 150 IU of vitamin E/kg of DM (SAFF/E), 6% of DM safflower oil plus 24 ppm of monensin (SAFF/M), 6% of DM safflower oil plus 24 ppm of monensin plus 150 IU of vitamin E/kg of DM (SAFF/ME), or 6% of DM flaxseed oil plus 150 IU of vitamin E/kg of DM (FLAX/E). Average cis-9, trans-11 CLA levels during the treatment period were 0.68, 4.12, 3.48, 4.55, 4.75, and 2.80% of total fatty acids for control, SAFF, SAFF/E, SAFF/M, SAFF/ME, and FLAX/E, respectively. The combination of safflower oil with monensin was particularly effective at increasing milk fat CLA. The addition of vitamin E to the diet partially prevented the depression in milk fat associated with oilseed feeding, but had no significant effect on the concentration of CLA in milk.
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PMID:Effect of safflower oil, flaxseed oil, monensin, and vitamin E on concentration of conjugated linoleic acid in bovine milk fat. 1642 41

In the present study, the role of pentacyclic triterpenes, lupeol and its ester lupeol linoleate, was studied in relation to hepatic oxidative abnormalities and lipoprotein peroxidation in hypercholesterolemic rats. Hypercholesterolemia was induced in male Wistar rats by feeding them with high cholesterol diet (4% cholesterol + 1% cholic acid; HCD) for 30 days. Pentacyclic triterpenes, lupeol and lupeol linoleate were supplemented (50 mg/kg body wt/day) during the last 15 days. After the experimental period, there was a significant depression in hepatic activities of antioxidant enzymes, SOD (38.39%), CAT (25.03%) and GPx (30.26%) along with a marked fall in the levels of non-enzymic antioxidant molecules GSH (31.39%), vitamin C (46.07%) and vitamin E (42.28%), with a concomitant increase (p<0.001) in lipid peroxidation and in the activities of serum alkaline phosphatase, lactate dehydrogenase and aminotransferases when compared to controls. Treatment with triterpenes decreased lipid peroxidation and reverted the activities of antioxidants (p<0.001 and p<0.01) and marker enzymes to near control. Histopathological findings further confirmed the hepatoprotective nature of triterpenes by showing the normal architecture in treated rats, as against the fatty cellular changes in HCD fed rats. Further, the susceptibility of apo-B containing lipoprotein to oxidation by copper and Fenton's reagent was increased in in vitro condition in HCD fed rats, whereas the lipoproteins were less susceptible to oxidation in triterpenes treated animals. Therefore, it may be concluded that lupeol and its ester afford protection against the hepatic abnormalities and lipoprotein peroxidation in hypercholesterolemic rats.
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PMID:Mitigating role of lupeol and lupeol linoleate on hepatic lipemic-oxidative injury and lipoprotein peroxidation in experimental hypercholesterolemia. 1693 29

The objective of this update is to give an overview of the effects of dietary nutrients on the structure and certain functions of the brain. As any other organ, the brain is elaborated from substances present in the diet (sometimes exclusively, for vitamins, minerals, essential amino-acids and essential fatty acids, including omega- 3 polyunsaturated fatty acids). However, for long it was not fully accepted that food can have an influence on brain structure, and thus on its function, including cognitive and intellectuals. In fact, most micronutrients (vitamins and trace-elements) have been directly evaluated in the setting of cerebral functioning. For instance, to produce energy, the use of glucose by nervous tissue implies the presence of vitamin B1; this vitamin modulates cognitive performance, especially in the elderly. Vitamin B9 preserves brain during its development and memory during ageing. Vitamin B6 is likely to benefit in treating premenstrual depression. Vitamins B6 and B12, among others, are directly involved in the synthesis of some neurotransmitters. Vitamin B12 delays the onset of signs of dementia (and blood abnormalities), provided it is administered in a precise clinical timing window, before the onset of the first symptoms. Supplementation with cobalamin improves cerebral and cognitive functions in the elderly; it frequently improves the functioning of factors related to the frontal lobe, as well as the language function of those with cognitive disorders. Adolescents who have a borderline level of vitamin B12 develop signs of cognitive changes. In the brain, the nerve endings contain the highest concentrations of vitamin C in the human body (after the suprarenal glands). Vitamin D (or certain of its analogues) could be of interest in the prevention of various aspects of neurodegenerative or neuroimmune diseases. Among the various vitamin E components (tocopherols and tocotrienols), only alpha-tocopherol is actively uptaken by the brain and is directly involved in nervous membranes protection. Even vitamin K has been involved in nervous tissue biochemistry. Iron is necessary to ensure oxygenation and to produce energy in the cerebral parenchyma (via cytochrome oxidase), and for the synthesis of neurotransmitters and myelin; iron deficiency is found in children with attention-deficit/hyperactivity disorder. Iron concentrations in the umbilical artery are critical during the development of the foetus, and in relation with the IQ in the child; infantile anaemia with its associated iron deficiency is linked to perturbation of the development of cognitive functions. Iron deficiency anaemia is common, particularly in women, and is associated, for instance, with apathy, depression and rapid fatigue when exercising. Lithium importance, at least in psychiatry, is known for a long time. Magnesium plays important roles in all the major metabolisms: in oxidation-reduction and in ionic regulation, among others. Zinc participates among others in the perception of taste. An unbalanced copper metabolism homeostasis (due to dietary deficiency) could be linked to Alzheimer disease. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells; the dietary reduction of iodine during pregnancy induces severe cerebral dysfunction, actually leading to cretinism. Among many mechanisms, manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals, toxic derivatives of oxygen. More specifically, the full genetic potential of the child for physical growth ad mental development may be compromised due to deficiency (even subclinical) of micronutrients. Children and adolescents with poor nutritional status are exposed to alterations of mental and behavioural functions that can be corrected by dietary measures, but only to certain extend. Indeed, nutrient composition and meal pattern can exert either immediate or long-term effects, beneficial or adverse. Brain diseases during aging can also be due to failure for protective mechanism, due to dietary deficiencies, for instance in anti-oxidants and nutrients (trace elements, vitamins, non essential micronutrients such as polyphenols) related with protection against free radicals. Macronutrients are presented in the accompanying paper.
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PMID:Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. 1706 9

Ceramide, a sphingolipid metabolite, has emerged as a key second messenger molecule that mediates multiple cellular functions. Its de nova synthesis and accumulation in ischemic myocardium, congestive heart failure and diabetic cardiomyopathy is associated with the abnormalities such as abnormal QT prolongation and increased risk of arrhythmias. To investigate how ceramide is involved in modulating cardiac repolarization, we performed whole-cell patch-clamp studies on HERG current (I(HERG)), a critical determinant of cardiac repolarization, expressed in HEK293 cells. Acute application (superfusion for 25 min) of membrane permeable ceramide (C2, 5 microM) did not alter I(HERG). Prolonged incubation with C2 for 10 hrs caused pronounced I(HERG) inhibition in a concentration-dependent and voltage-independent fashion and positive shift of voltage-dependent HERG activation. The IC(50) for I(HERG) suppression was 19.5 microM. C2 did not affect the inactivation property and time-dependent kinetics of I(HERG). Similar effects were observed with production of endogenous ceramide catalyzed by sphingomyelinase. Tyrosine kinase inhibitors failed to reverse C2-induced suppression of HERG function, and PKA and PKC inhibitors only slightly reversed the I(HERG) depression. Western blotting and immunocytochemical analyses indicate that C2 does not alter HERG protein expression on the cytoplasmic membrane. The inhibitory effect of C2 on I(HERG) was reversed by antioxidants vitamin E or MnTBAP. C2 caused considerable production of intracellular reactive oxygen species (ROS), which was prevented by vitamin E or MnTBAP. We conclude that ceramide depresses I(HERG) mainly via ROS overproduction and ceramide-induced I(HERG) impairment may contribute to QT prolongation in prolonged myocardial ischemia, heart failure and diabetic cardiomyopathy.
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PMID:Sphingolipid metabolite ceramide causes metabolic perturbation contributing to HERG K+ channel dysfunction. 1776 70

In addition to cognitive impairment, behavioral changes such as aggressive behavior, depression, and psychosis accompany Alzheimer's Disease. Such symptoms may arise due to imbalances in neurotransmitters rather than overt neurodegeneration. Herein, we demonstrate that combined administration of N-acetyl cysteine (an antioxidant and glutathione precursor that protects against A beta neurotoxicity), acetyl-L-carnitine (which raises ATP levels, protects mitochondria, and buffers A beta neurotoxicity), and S-adenosylmethionine (which facilitates glutathione usage and maintains acetylcholine levels) enhanced or maintain cognitive function, and attenuated or prevented aggression, in mouse models of aging and neurodegeneration. Enhancement of cognitive function was rapidly reversed upon withdrawal of the formulation and restored following additional rounds supplementation. Behavioral abnormalities correlated with a decline in acetylcholine, which was also prevented by this nutriceutical combination, suggesting that neurotransmitter imbalance may contribute to their manifestation. Treatment with this nutriceutical combination was able to compensate for lack of dietary folate and vitamin E, coupled with administration of dietary iron as a pro-oxidant (which collectively increase homocysteine and oxidative damage to brain tissue), indicating that it provided antioxidant neuroprotection. Maintenance of neurotransmitter levels and prevention of oxidative damage underscore the efficacy of a therapeutic approach that utilizes a combination of neuroprotective agents.
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PMID:Effects of dietary supplementation with N-acetyl cysteine, acetyl-L-carnitine and S-adenosyl methionine on cognitive performance and aggression in normal mice and mice expressing human ApoE4. 1791 84

The hypnotic agent propofol has pharmacokinetic characteristics that allow for rapid onset and offset of drug effect and fast elimination from the body. Elderly patients show a greater sensitivity to the hypnotic effect of propofol. The drug is extensively metabolized in the liver through the cytochrome P450 system and glucuronidation, with potential for drug interaction. Propofol does not cause significant inotropic depression at clinically relevant concentrations. But in vitro, propofol impairs isotonic relaxation of the heart and decreases free cytosolic Ca(2+) concentrations in myocardial cells. In animal models, the cardioprotective effects of propofol derive in part from its antioxidant and free radical scavenging properties. Propofol decreases cerebral blood flow and cerebral metabolic rate dose-dependently. The neuroprotective effect of propofol in animal models is attributed to its antioxidant property, the potentiation of gamma-aminobutyric acid type A (GABA(A))-mediated inhibition of synaptic transmission, and the inhibition of glutamate release. Subhypnotic doses of propofol induce sedative, amnestic, and anxiolytic effects in a dose-dependent fashion. Propofol impairs ventilation with a considerable effect on the control of ventilation and central chemoreceptor sensitivity. Propofol reduces the ventilatory response to hypercapnia and the ventilatory adaptation to hypoxia, even at subanesthetic doses. The drug potentiates hypoxic pulmonary vasoconstriction, an effect caused by inhibition of K(+) (ATP)-mediated pulmonary vasodilatation. Most of the pharmacological actions of propofol result from interaction with the GABA(A) receptor or with calcium channels. Propofol prolongs inhibitory postsynaptic currents mediated by GABA(A) receptors, indicating that its effects are associated with enhanced inhibitory synaptic transmission, but propofol also influences presynaptic mechanisms of GABAergic transmission. Propofol modulates various aspects of the host's inflammatory response. It decreases secretion of proinflammatory cytokines, alters the expression of nitric oxide, impairs monocyte and neutrophil functions, and has potent, dose-dependent radical scavenging activity similar to the endogenous antioxidant vitamin E.
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PMID:Propofol. 1817 94

A cross-sectional study was conducted to evaluate the association between dietary intake and depressive symptoms in community-dwelling elderly persons. Five-hundred elderly persons aged 65 to 75 years were randomly selected from the population of O city in Okayama Prefecture, Japan. Among 401 respondents (response rate, 80.0%), data from 279 (133 males, 146 females) who completed the questionnaire concerning dietary intake and depressive state were analyzed using logistic regression. Each of 17 dietary intakes was classified into tertiles:high intake, moderate intake, and low intake. The Center for Epidemiology Studies Depression scale (CES-D) was used. Among males, the observed odds ratios (the 95% confidence intervals) for the depressive state were 0.36 (95% CI:0.13-0.98) in the highest tertile of carotene intake, 0.33 (95% CI:0.12-0.93) in the highest tertile of vitamin C intake, 0.29 (95% CI:0.10-0.85) in the highest tertile of carbohydrate intake, and 0.33 (95% CI:0.12-0.92) in the medium tertile of vitamin E intake. Among females, similar results were observed, but these results were not statistically significant. The results suggested that carbohydrate, carotene, and vitamin C intakes are associated with lowering depressive symptoms among elderly persons dwelling in communities in Japan.
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PMID:Nutrition and depressive symptoms in community-dwelling elderly persons in Japan. 1924 18

Pyridoxal phosphate and pyridoxamine phosphate, the catalytically active forms of vitamin B(6), influence brain function by participating at stages in metabolism of proteins, lipids, carbohydrates, other coenzymes and hormones. Vitamin B(6) participates in the metabolism of amino acids in the form of decarboxylation, transamination, deamination, racemization and desulfhydration reactions. The crucial roles that these coenzymes play in the maintenance of functional integrity of the brain become evident when one realizes that some compounds implicated as neurotransmitters are synthesized and/or metabolized by the aid of the vitamin B(6)-dependent enzymatic reactions. These include dopamine, norepinephrine and serotonin, tyramine, tryptamine, taurine, histamine, gamma aminobutyric acid, and even acetylcholine indirectly. In recent years, the above-mentioned biogenic amines have become of considerable interest to neurobiologists who are investigating the etiology and the pathological manifestations of many disorders of the central nervous system such as Parkinsonism, Huntington's chorea, minimal brain disfunction, schizophrenia, depression, sleep disorders and seizure disorders. Vitamin B(6) deficiency in these cases is characterized by anemia, growth retardation and alteration in neuronal function, including neuropathies, hyperirritability, hyperexcitability and convulsions. The importance of vitamin B(6) in the study of brain function assumes still greater significance when one considers the effects of nutritional deficiencies on growth and development of the brain and mental processes and in the involvement of vitamin B(6) in some inborn errors of metabolism which result in mental retardation. Vitamin B(6) deficiency results in a lowered concentration of Coenzyme A in blood, in reduced absorption and storage of vitamin B(12), and in increased excretion of vitamin C. Furthermore, vitamin B(6) acts synergistically with vitamin E to control metabolism of unsaturated fats, with vitamin C in tyrosine metabolism and with niacin in its action and participates in niacin synthesis. In addition, vitamin B(6) deficiency results in insufficiency of insulin and in alteration of the functions of adrenal and pituitary glands, since it is involved in the synthesis of growth hormone, follicle-stimulating hormone, luteinizing hormone, aldosterone, glucagon, cortisol, estradiol, testosterone and epinephrine. It is hoped that by understanding the factors that regulate the synthesis, binding, storage and degradation of pyridoxal phosphate in the brain, a better insight into the role of vitamin B(6) in neurobiology may be gained.
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PMID:Regulation and function of pyridoxal phosphate in CNS. 1964 63


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