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Nutritional n-3 polyunsaturated fatty acids deficiency alters cannabinoid receptor signaling pathway in the brain.

cb1 mood evolution

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#1 Ruth

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Posted 05 June 2018 - 12:42 AM


https://www.research...ehavior_in_mice

Nutritional n-3 polyunsaturated fatty acids deficiency alters cannabinoid receptor signaling pathway in the brain and associated anxiety-like behavior in mice

"Altogether, our results suggest a lack of activation of CB1 in response to WIN55,212-2 in the PFC of n-3 deficient mice. This is in agreement with our previous results showing that a nutritional n-3 deficiency throughout life alters the CB1 system in the PFC [16]. ThestimulationofCB1receptorsbyCBagonists(THC, WIN55,212-2 and CP-55940) has been previously reported to activate MAPK signaling pathway both in vitro and in vivo [3, 9]. It is surprising that in our experiments, p44/p42 phosphorylation decreases in responsetoWIN55,212-2treatmentinthebrainofthen-3 control diet mice. However, because we analyzed MAPK phosphorylation only at one time point (15 min), it could be that the phosphorylation occurs at an earlier time point. The CB agonist acts rapidly, as demonstrated by Bouaboula and coworkers showing an increase in MAPK phosphorylation in vitro as early as 1minaftertheCBagonisttreatment[3].IntheHTofthe n-3deficientmice,WIN55,212-2inducesthephosphorylation of p44/p42 MAPK but does not increase the expression of Egr1. This suggests a deregulation of the
eCBsystembyn-3deficiencyinthePFCandintheHT. The decrease in the levels of brain DHA could explain such discrepancies because DHA and eCB are closely linked [33]. In support of this, n-3 deficiency differentially affects the magnitude of the decrease in DHA levels in the PFC and the HT, with the PFC displaying a higher decrease in DHA levels [17]. In summary, we showed that nutritional n-3 deficiency throughout life leads to the development of anxiety/depressive-like behavior and eCB system alteration in the PFC and the HT as revealed by the alteration of WIN55,212-2-induced MAPK pathway activation. Our results illustrate a potential mechanism by which the consumption of n-3 PUFAs works against the risk for altered emotional behavior linked with endocannabinoids."

#2 Ruth

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Posted 05 June 2018 - 12:53 AM

https://www.aimedjou...0157-X/abstract Use of fish-oil: Docosahexaenoic acid (DHA) or eicosapentaenoic acid (EPA) for chronic psychological stress
https://www.nature.c...1538-017-0002-4 The processes that define mammalian physiology evolved millions of years ago in response to ancient signaling molecules, most of which were acquired by ingestion and digestion. In this way, evolution inextricably linked diet to all major physiological systems including the nervous system. The importance of diet in neurological development is well documented, although the mechanisms by which diet-derived signaling molecules (DSMs) affect cognition are poorly understood. Studies on the positive impact of nutritive and non-nutritive bioactive molecules on brain function are encouraging but lack the statistical power needed to demonstrate strong positive associations. Establishing associations between DSMs and cognitive functions like mood, memory and learning are made even more difficult by the lack of robust phenotypic markers that can be used to accurately and reproducibly measure the effects of DSMs.

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#3 Ruth

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Posted 05 June 2018 - 12:56 AM

https://www.metaboli...0142-1/abstract N-3 PUFA (n-3) polyunsaturated fatty acids (PUFA) are a family of fatty acids mainly found in oily fish and fish oil supplements. The effects of n-3 PUFA on health are mainly derived from its anti-inflammatory proprieties and its influence on immune function. Lately an increased interest in n-3 PUFA supplementation has reached the world of sport nutrition, where the majority of athletes rely on nutrition strategies to improve their training and performance. A vast amount of attention is paid in increasing metabolic capacity, delaying the onset of fatigue, and improving muscle hypertrophy and neuromuscular function. Nutritional strategies are also frequently considered for enhancing recovery, improving immune function and decreasing oxidative stress. The current review of the literature shows that data regarding the effects of n-3PUFA supplementation are conflicting and we conclude that there is, therefore, not enough evidence supporting a beneficial role on the aforementioned aspects of exercise performance.

#4 Ruth

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Posted 05 June 2018 - 12:59 AM

Mitochondrial Production of Perhydroxyl Radical (HO2•) as Inducer of Aging and Age-Related Pathologies Panov A* Institute of Molecular Biology and Biophysics, Siberian Division of the Russian Academy of Sciences, Novosibirsk, Russia *Corresponding author: Panov A, 3647 N. Kimberly Drive, Atlanta, GA, USA, Tel: 81-404-210-7031, E-mail: alexander.panov55@gmail.com Citation: Panov A (2017) Mitochondrial Production of Perhydroxyl Radical (HO2•) as Inducer of Aging and Age-Related Pathologies. J Biochem Biophy 1(1): 105
All organisms age, in the search of the universal mechanisms of aging Barja analyzed results obtained with various species of mammals and birds and concluded that only two known factors correlate in the right sense (inversely) with animal longevity in vertebrates: the long life span is associated with (a) low rates of mitochondrial reactive oxygen species production, and (b) low degree of fatty acid polyunsaturation of cellular membranes including the mitochondrial ones [Barja (2014) Prog Mol Biol Transl Sci. 127:1-27]. 20 years ago it was established that polyunsaturated fatty acids (PUFA), when still being esterified with the membrane phospholipids, undergo autoxidation with formation of products with large isomerism [Morrow et al. (1990). PNAS USA. 87: 9383-9387]. This process is known as the Isoprostane pathway of lipid peroxidation (IPLP), but the mechanism of IPLP initiation remained obscure. We propose that perhydroxyl radical (HO2•), which is a protonated form of the superoxide radical (O2•), initiates within the membrane a chain of reactions with formation of first H2O2, which in the hydrophobic environment undergoes homolytic fission producing two •OH radicals, thus very rapidly abstracting three H atoms from a PUFA. As a result, the HO2• molecule is converted to two molecules of water, and the molecule of a PUFA loses two double bonds, becomes highly unstable and undergoes peroxidation and random intramolecular re-arrangements causing a very large isomerism of the final products. Formation of O2•, and thus of HO2• radical, are inevitable consequences of the mitochondrial aerobic respiration, and because HO2• has very high affinity to PUFA, even the smallest amounts of this radical will cause damages to lipids, proteins and mtDNA. Our hypothesis is fully compatible with the conclusions made by Barja, and provides reasonable explanation for one of the important aging mechanisms. Abstract Keywords: Aging; Mitochondria; Oxidative stress; Superoxide radical; Perhydroxyl radical; Polyunsaturated fatty acids; Fatty acids autoxidation; Lipid peroxidation
Aging is the process of growing older or changing over time [1]. In other words, aging is the entire sequence of changes during ontogenesis of an individual organism during its lifetime. The major difference in the meanings of “ontogenesis” and “aging” is that the latter term, from the medical point of view, bears a strongly negative hint. Harman [2] defined aging as “progressive accumulation of diverse, deleterious changes with time that increase the chance of disease and death”. Knight [3] observed that “although the specific biologic basis of aging remains obscure, there is general agreement that its elucidation will be at the molecular
List of abbreviations: AA: Arachidonic Acid (C20:4 ω6); ANT: Aadenine Nucleotide Translocase; CL: Cardiolipin; СОХ1 and COX2: Cyclooxygenases; DHA: Docosahexaenoic acid (C22:6 ω3); DNA: Deoxyribonucleic acid; EPA: Eicosapentaenoic acid; FRTA: Free Radical Theory of Aging; GSH: Reduced Glutathione, HO2•: Perhydroxyl radical; IMM: Inner Mitochondrial Membrane; IsoPs: Isoprostanes; IPLP: Isoprostane pathway of lipid peroxidation, LOX: Lipoxygenases; LP: Lipid Peroxidation; MFRTA: Mitochondrial Free Radical Theory of Aging; mtDNA: mitochondrial deoxyribonucleic acid; mtROS: mitochondrial reactive oxygen species; •NO: nitric oxide radical; •NO2: Nitric dioxide radical; O2•: superoxide radical; •OH: hydroxyl radical; OMM: Outer mitochondrial membrane; •OONO: peroxynitrite radical; O2NOO•: peroxynitrate radical; PEA: Phosphatidylethanolamine; PGF2: Isoprostanes containing F-type prostane rings; PGs: Prostaglandins; PLA2: Ca-independent phospholipases A2; PUFA: Polyunsaturated Fatty Acids; RET: Reverse Electron Transport; ROS: Reactive Oxygen Species; SOD: Superoxide Dismutase; SOD1 (Cu,Zn-SOD1): Cytoplasmic SOD, SOD2 (MnSOD2) mitochondrial SOD

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#5 Ruth

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Posted 05 June 2018 - 01:01 AM

https://europepmc.or...ct/med/29679203 Mouse-sized naked mole-rats (Heterocephalus glaber), unlike other mammals, do not conform to Gompertzian laws of age-related mortality; adults show no age-related change in mortality risk. Moreover, we observe negligible hallmarks of aging with well-maintained physiological and molecular functions, commonly altered with age in other species. We questioned whether naked mole-rats, living an order of magnitude longer than laboratory mice, exhibit different plasma metabolite profiles, which could then highlight novel mechanisms or targets involved in disease and longevity. Using a comprehensive, unbiased metabolomics screen, we observe striking inter-species differences in amino acid, peptide, and lipid metabolites. Low circulating levels of specific amino acids, particularly those linked to the methionine pathway, resemble those observed during the fasting period at late torpor in hibernating ground squirrels and those seen in longer-lived methionine-restricted rats. These data also concur with metabolome reports on long-lived mutant mice, including the Ames dwarf mice and calorically restricted mice, as well as fruit flies, and even show similarities to circulating metabolite differences observed in young human adults when compared to older humans. During evolution, some of these beneficial nutrient/stress response pathways may have been positively selected in the naked mole-rat. These observations suggest that interventions that modify the aging metabolomic profile to a more youthful one may enable people to lead healthier and longer lives.





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