Componentes biológicamente activos y beneficios para la salud del aceite de semilla de ortiga

The biologically active components of nettle seed oil and important lipid indices, which are criteria for the health benefits of the oil, have been examined. Linoleic acid predominates in triacylglycerols (77.7%), followed by oleic (16.2%). Sterols in the lipids are present at 1.1% and β-sitosterol is the main component (90.1%). The oil contains 711 mg/kg tocopherols and γ-tocopherol predominates (36.1%), followed by α-tocopherol (28.9%) and δ-tocopherol (26.9%). Atherogenicity and thrombogenicity index values are significantly low, which determine the best anti-atherogenic and anti-thrombogenic properties of the oil. The cholesterolemic index and the ratio of polyunsaturated and saturated fatty acids are considerably higher than 1.0 and reveal good hypocholesterolemic potential and nutritional value. The content of biologically active components of nettle seed oil indicates that it is a rich source of essential fatty acids, sterols and tocopherols and this oil can be used in food, cosmetics, and pharmaceutical products.Se han determinado los componentes biológicamente activos del aceite de semilla de ortiga y los índices lipídicos más importantes, como criterios sobre los beneficios para la salud del aceite. El ácido linoleico predomina en los triacilgliceroles (77,7%), seguido por oleico (16,2%). Los esteroles son el 1,1% siendo el β-sitosterol el componente mayoritario (90,1%). Los tocoferoles son 711 mg/kg y predomina el γ-tocoferol (36,1%), seguido por α-tocoferol (28,9%) y δ-tocoferol (26,9%). Los valores de los índices de aterogenicidad y trombogenicidad son significativamente bajos, lo que determina las buenas propiedades antiaterogénicas y antitrombogénicas del aceite. El índice hipo/hipercolesterolémico y la proporción de ácidos grasos poliinsaturados y saturados presentan valores altos (superiores a 1,0), lo cual indica un buen potencial hipocolesterolémico y valor nutricional del aceite. El contenido de componentes biológicamente activos del aceite de semilla de ortiga muestra que es un producto rico de ácidos grasos esenciales, esteroles y tocoferoles, y por eso se puede utilizar en alimentos, cosméticos y productos farmacéuticos

Carbon monoxide neurotoxicity is triggered by oxidative stress induced by ROS production from three distinct cellular sources

Carbon monoxide (CO) poisoning is one of the leading causes of toxic mortality and morbidity. We have studied the generation of reactive oxygen species in cortical neurons in culture in response to toxic doses of CO exposure. Fluorescence microscopy was used to measure the rate of free radical generation, lipid peroxidation, GSH level and also mitochondrial metabolism. We have found that toxic concentrations of CO released from CORM-401 induced mitochondrial depolarisation and inhibition of NADH dependent respiration to a lesser degree than when compared to ischaemia. Energy collapse was not observed within 40 min of CO exposure. We have found that CO induces the generation of reactive oxygen species resulting in lipid peroxidation and a decrease in GSH via three different mechanisms: from mitochondria during the first minutes of CO exposure, from xanthine oxidase at around 20 min exposure due to energy deprivation, and considerable ROS production from NADPH oxidase in the post CO exposure period (re-oxygenation). Inhibition of these different phases with mitochondrial antioxidants, inhibitors of xanthine oxidase, or NADPH oxidase, protected neurons and astrocytes against CO-induced oxidative stress and cell death. The most profound effect was seen during NADPH oxidase inhibition. Thus, oxidative stress has a remarkably significant role in CO-induced neuronal cell death and preventing its occurrence during reoxygenation is of great importance in the consideration of a positive, neurologically protective therapeutic outcome for CO exposed patients

Determination of the critical values of power density in laser marking of textile materials

Представлено фізичну модель процесу лазерного маркування текстильних матеріалів. Визначено межі застосування лазерного маркування для бавовняних і поліефірних тканин.Представлена физическая модель процесса лазерной маркировки текстильных материалов. Определены границы применимости лазерной маркировки для хлопчатобумажных и полиэфирных тканей.A physical model of the process of laser marking of textile materials is presented. The limits of applicability of laser marking for cotton and polyester fabrics have been defined

Hyperammonemia induces mitochondrial dysfunction and neuronal cell death

BACKGROUND & AIMS: In liver cirrhosis, astrocytic swelling is believed to be the principal mechanism of ammonia neurotoxicity leading to hepatic encephalopathy (HE). The role of neuronal dysfunction in HE is not clear. We aimed to explore the impact of hyperammonemia on mitochondrial function in primary co-cultures of neurons and astrocytes and in acute brain slices of cirrhotic rats using live cell imaging. METHODS: To primary co-cultures of astrocytes and neurons, low concentrations (1 and 5μM) of NH4Cl were applied. In rats with bile-duct ligation (BDL)-induced cirrhosis, a model known to induce hyperammonemia and minimal HE, acute brain slices were studied. One group of BDL rats were treated twice daily with the ammonia scavenger ornithine phenylacetate (OP, 0.3g/kg). Fluorescence measurements of changes in mitochondrial membrane potential (ΔΨm), cytosolic and mitochondrial reactive oxygen species (ROS) production, lipid peroxidation (LP) rates, and cell viability were performed using confocal microscopy. RESULTS: Neuronal cultures treated with NH4Cl exhibited mitochondrial dysfunction, ROS overproduction and reduced cell viability (27.8±2.3% and 41.5±3.7%, respectively) compared to untreated cultures (15.7±1.0%, both p<0.0001). BDL led to increased cerebral LP (p=0.0003) and cytosolic ROS generation (p<0.0001), which was restored by OP (both p<0.0001). Mitochondrial function was severely compromised in BDL resulting in hyperpolarization of ΔΨm with consequent overconsumption of ATP and augmentation of mitochondrial ROS production. Administration of OP restored ΔΨm. In BDL animals, neuronal loss was observed in hippocampal areas, which was partially prevented by OP. CONCLUSIONS: Our results elucidate that low-grade hyperammonemia in cirrhosis can severely impact on brain mitochondrial function. Profound neuronal injury was observed in hyperammonemic conditions, which was partially reversible by OP. This points towards a novel mechanism of HE development. LAY SUMMARY: The impact of hyperammonemia, a common finding in patients with liver cirrhosis, on brain mitochondrial function was investigated in this study. The results show that ammonia in concentrations commonly seen in patients induces severe mitochondrial dysfunction, overproduction of damaging oxygen molecules and profound injury and death of neurons in rat brain cells. These findings point towards a novel mechanism of ammonia-induced brain injury in liver failure and potential novel therapeutic targets

Inorganic polyphosphate regulates AMPA and NMDA receptors and protects against glutamate excitotoxicity via activation of P2Y receptors

Glutamate is one of the most important neurotransmitters in the process of signal transduction in the central nervous system. Excessive amounts of this neurotransmitter lead to glutamate excitotoxicity which is accountable for neuronal death in acute neurological disorders including stroke, trauma, and in neurodegenerative diseases. Inorganic polyphosphate (PolyP) plays multiple roles in the mammalian brain, including function as a calcium-dependent gliotransmitter mediating communication between astrocytes, while its role in the regulation of neuronal activity is unknown. Here we studied the effect of polyP on glutamate-induced calcium signal in primary rat neurons in both physiological and pathological conditions. We found that pre-incubation of primary neurons with polyP reduced glutamate- and AMPA- but not the NMDA-induced calcium signal. However, in rat hippocampal acute slices polyP reduced ion flux through NMDA and AMPA receptors in native neurons. The effect of polyP on glutamate and specifically on the AMPA receptors was dependent on the presence of P2Y1 but not of P2X receptor inhibitors and also could be mimicked by P2Y1 agonist 2MeSADP. Pre-incubation of cortical neurons with polyP significantly reduced the initial calcium peak as well as the number of neurons with delayed calcium deregulation in response to high concentrations of glutamate and resulted in protection of neurons against glutamate-induced cell death. As a result, activation of P2Y1 receptors by polyP reduced calcium signal acting through AMPA receptors, thus protecting neurons against glutamate excitotoxicity by reduction of the calcium overload and restoration of mitochondrial function.Significance StatementOne of the oldest polymers in the evolution of living matter is the inorganic polyphosphate. It is shown to play a role of gliotransmitter in the brain; however, the role of polyphosphate in neuronal signalling is not clear. Here we demonstrate that inorganic polyphosphate is able to reduce calcium signal, induced by physiological or high concentrations of glutamate. The effect of polyphosphate on glutamate-induced calcium signal in neurons is due to the effect of this polymer on the AMPA receptors.The effect of polyP on glutamate- and AMPA-induced calcium signal is dependent on P2Y receptor antagonist. The ability of polyphosphate to restrict glutamate-induced calcium signal lies in the basis of its protection of neurons against glutamate excitotoxicity

Raman study of self-assembled InAs/InP quantum wire stacks with varying spacer thickness

Self-assembled InAs/InP (001) quantum wire stacks have been investigated by means of Raman scattering. The characteristics of the observed vibrational modes show clear evidence of confinement and atomic intermixing between As and P atoms from the wire and the spacer. The change in the intermixing with spacer layer thickness and growth temperature is investigated. Likewise, the effect of annealing on the exchange of As and P atoms is also studied. Resonance effects in confined and interface phonons are discussed for excitation in the vicinity of the InAs E1 critical point. Finally, the energy of the interface modes is related to the structural characteristics of the wires by comparing the experimental data with a lattice dynamic calculation based on the dielectric continuum [email protected] [email protected] [email protected]

Monomeric alpha-synuclein exerts a physiological role in brain ATP synthase

Misfolded α-synuclein is a key factor in the pathogenesis of Parkinson's disease (PD). However, knowledge about a physiological role for the native, unfolded α-synuclein is limited. Using brains of mice lacking α-, β-, and γ-synuclein, we report that extracellular monomeric α-synuclein enters neurons and localizes to mitochondria, interacts with ATP synthase subunit α, and modulates ATP synthase function. Using a combination of biochemical, live-cell imaging and mitochondrial respiration analysis, we found that brain mitochondria of α-, β-, and γ-synuclein knock-out mice are uncoupled, as characterized by increased mitochondrial respiration and reduced mitochondrial membrane potential. Furthermore, synuclein deficiency results in reduced ATP synthase efficiency and lower ATP levels. Exogenous application of low unfolded α-synuclein concentrations is able to increase the ATP synthase activity that rescues the mitochondrial phenotypes observed in synuclein deficiency. Overall, the data suggest that α-synuclein is a previously unrecognized physiological regulator of mitochondrial bioenergetics through its ability to interact with ATP synthase and increase its efficiency. This may be of particular importance in times of stress or PD mutations leading to energy depletion and neuronal cell toxicity

Lipid peroxidation is involved in calcium dependent upregulation of mitochondrial metabolism in skeletal muscle

BACKGROUND: Skeletal muscle cells continuously generate reactive oxygen species (ROS). Excessive ROS can affect lipids resulting in lipid peroxidation (LPO). Here we investigated the effects of myotube intracellular calcium-induced signaling eliciting contractions on the LPO induction and the impact of LPO-product 4-hydroxynonenal (4-HNE) on physiology/pathology of myotubes using C2C12 myoblasts. METHODS: C2C12 myoblasts were differentiated into myotubes, stimulated with caffeine and analyzed for the induction of LPO and formation of 4-HNE protein adducts. Further effects of 4-HNE on mitochondrial bioenergetics, NADH level, mitochondrial density and expression of mitochondrial metabolism genes were determined. RESULTS: Short and long-term caffeine stimulation of myotubes promoted superoxide production, LPO and formation of 4-HNE protein adducts. Furthermore, low 4-HNE concentrations had no effect on myotube viability and cellular redox homeostasis, while concentrations from 10 μM and above reduced myotube viability and significantly disrupted homeostasis. A time and dose-dependent 4-HNE effect on superoxide production and mitochondrial NADH-autofluorescence was observed. Finally, 4-HNE had strong impact on maximal respiration, spare respiratory capacity, ATP production, coupling efficiency of mitochondria and mitochondrial density. CONCLUSION: Data presented in this work make evident for the first time that pathological 4-HNE levels elicit damaging effects on skeletal muscle cells while acute exposure to physiological 4-HNE induces transient adaptation. GENERAL SIGNIFICANCE: This work suggests an important role of 4-HNE on the regulation of myotube's mitochondrial metabolism and cellular energy production. It further signifies the importance of skeletal muscle cells hormesis in response to acute stress in order to maintain essential biological functions

Alpha-Synuclein Oligomers Interact with Metal Ions to Induce Oxidative Stress and Neuronal Death in Parkinson's Disease

Protein aggregation and oxidative stress are both key pathogenic processes in Parkinson's disease, although the mechanism by which misfolded proteins induce oxidative stress and neuronal death remains unknown. In this study, we describe how aggregation of alpha-synuclein (α-S) from its monomeric form to its soluble oligomeric state results in aberrant free radical production and neuronal toxicity

Measuring farmland biodiversity

About one-third of the world’s land surface is used for farming, a fact that bears important implications for biodiversity. In Europe, for instance, an estimated 50 percent of all wild species are reliant on agricultural habitats, while agricultural productivity often depends on the presence or absence of particular species. Despite this close coupling, surprisingly little is known about the status and evolution of farmland biodiversity. A team of European and African researchers, hoping to fill this gap in information, recently invented and piloted a new toolbox called the BioBio indicator set, which measures 23 different instances of biodiversity across a variety of farm types and scales in Europe. Applications were also tested in Tunisia, Ukraine, and Uganda, where they proved a feasible starting point for adaptation to the agricultural context of different countries