X-ray diffraction and Raman study of nanogranular BaTiO3-CoFe2O4thin films deposited by laser ablation on Si/Pt substrates

Nanocomposite thin films composed by (BaTiO3)1-x-(CoFe2O4)x with different cobalt ferrite concentrations (x) have been deposited by pulsed laser ablation on platinum covered Si(001) substrates. The films structure was studied by X-ray diffraction and Raman spectroscopy. It was found that the CoFe2O4 phase unit cell was compressed along the growth direction of the films, and it relaxed with increasing x. The opposite behavior was observed in the BaTiO3 phase where the lattice parameters obtained from the X-ray measurements presented a progressive distortion of its unit cell with increasing x. The presence of the strain in the films induced a blueshift of the Raman peaks of CoFe2O4 that decreased with increasing CoFe2O4 concentration. Cation disorder in the cobalt ferrite was observed for lower x, where the nanograins are more isolated and subjected to more strain, which was progressively decreased for higher CoFe2O4 content in the films.This work has been financially supported by the Portuguese Foundation for Science and Technology (FCT), through the project POCI/CTM/60181/2004 and the Bilateral Research Action nºB48-06 between CRUP (Portugal) and British Council (UK)

Nanogranular BaTiO3–CoFe2O4 thin films deposited by pulsed laser ablation

Detailed structural and magnetic measurements were performed on nanostructured composite thin films of cobalt ferrite (CoFe2O4 - magnetostrictive) dispersed in a barium titanate (BaTiO3 - piezoelectric) matrix, with different CoFe2O4 concentrations (ranging from x=20% to x=70%). The films were deposited by laser ablation on platinum covered Si(100). Their structure was studied by X-ray diffraction and Raman spectroscopy. The magnetic properties were measured with a SQUID magnetometer. The nanocomposite films were polycrystalline and composed by a mixture of tetragonal-BaTiO3 and CoFe2O4 with the cubic spinel structure. The lattice parameter of the CoFe2O4 phase varied from 8.26Å (x=20%) to 8.35Å (x=70%), and, comparing with bulk CoFe2O4, it was under compressive stress that relaxed as its concentration progressively increased. In the tetragonal-BaTiO3 phase, the lattice parameter a was contracted relative to the bulk phase and decreases with x. The lattice parameter c increased from 4.088 Å (x=20%) to 4.376 Å (x=70%), so that the BaTiO3 c axes was increasingly expanded as the quantity of the barium titanate phase was reduced. This behavior was the opposite of that observed in CoFe2O4. The magnetic measurements showed that the coercive fields decreased from 6.6 kOe (x=20%) to 2.3 kOe (x=70%) which was attributed to the progressive relaxation of the stress in the films as well as to the increase of particle agglomeration in bigger polycrystalline clusters with increasing cobalt ferrite concentration. For higher temperatures T=300 K the reduction of magnetocrystalline anisotropy induced a strong reduction of the coercive field.This work has been financially supported by the Portuguese Foundation for Science and Technology (FCT), through the project POCI/CTM/60181/2004

Structural and magnetic properties of nanogranular BaTiO3-CoFe2O4 thin films deposited by laser ablation on Si/Pt substrates

Thin film nanogranular composites of cobalt ferrite (CoFe2O 4) dispersed in a barium titanate (BaTiO3) matrix were deposited by laser ablation with different cobalt ferrite concentrations (x). The films were polycrystalline and composed by a mixture of tetragonal- BáTiO3 and CoFe2O4 with the cubic spinnel structure. A slight (111) barium titanate phase orientation and (311) CoFe2O4 phase orientation was observed. As the concentration of the cobalt ferrite increased, the grain size of the BaTiO 3 phase decreased, from 91nm to 30nm, up to 50% CoFe 2O4 concentration, beyond which the BaTiO3 grain size take values in the range 30-35nm. On the other hand the cobalt ferrite grain size did not show a clear trend with increasing cobalt ferrite concentration, fluctuating in the range 25nm to 30nm. The lattice parameter of the CoFe2O4 phase increased with increasing x. However, it was always smaller than the bulk value indicating that, in the films, the cobalt ferrite was under compressive stress that was progressively relaxed with increasing CoFe2O4 concentration. The magnetic measurements showed a decrease of coercive field with increasing x, which was attributed to the relaxation of the stress in the films and to the increase of particle agglomeration in bigger polycrystalline clusters with increasing cobalt ferrite concentration.This work has been financially supported by the Portuguese Foundation for Science and Technology (FCT), through the project POCI/CTM/60181/2004

Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging

SummaryEver since eukaryotes subsumed the bacterial ancestor of mitochondria, the nuclear and mitochondrial genomes have had to closely coordinate their activities, as each encode different subunits of the oxidative phosphorylation (OXPHOS) system. Mitochondrial dysfunction is a hallmark of aging, but its causes are debated. We show that, during aging, there is a specific loss of mitochondrial, but not nuclear, encoded OXPHOS subunits. We trace the cause to an alternate PGC-1α/β-independent pathway of nuclear-mitochondrial communication that is induced by a decline in nuclear NAD+ and the accumulation of HIF-1α under normoxic conditions, with parallels to Warburg reprogramming. Deleting SIRT1 accelerates this process, whereas raising NAD+ levels in old mice restores mitochondrial function to that of a young mouse in a SIRT1-dependent manner. Thus, a pseudohypoxic state that disrupts PGC-1α/β-independent nuclear-mitochondrial communication contributes to the decline in mitochondrial function with age, a process that is apparently reversible

Blueberry consumption challenges hepatic mitochondrial bioenergetics and elicits transcriptomics reprogramming in healthy wistar rats

An emergent trend of blueberries’ (BB) “prophylactic” consumption, due to their phytochemicals’ richness and well-known health-promoting claims, is widely scaled-up. However, the benefits arising from BB indiscriminate intake remains puzzling based on incongruent preclinical and human data. To provide a more in-depth elucidation and support towards a healthier and safer consumption, we conducted a translation-minded experimental study in healthy Wistar rats that consumed BB in a juice form (25 g/kg body weight (BW)/day; 14 weeks’ protocol). Particular attention was paid to the physiological adaptations succeeding in the gut and liver tissues regarding the acknowledged BB-induced metabolic benefits. Systemically, BB boosted serum antioxidant activity and repressed the circulating levels of 3-hydroxybutyrate (3-HB) ketone bodies and 3-HB/acetoacetate ratio. Moreover, BB elicited increased fecal succinic acid levels without major changes on gut microbiota (GM) composition and gut ultra-structural organization. Remarkably, an accentuated hepatic mitochondrial bioenergetic challenge, ensuing metabolic transcriptomic reprogramming along with a concerted anti-inflammatory pre-conditioning, was clearly detected upon long-term consumption of BB phytochemicals. Altogether, the results disclosed herein portray a quiescent mitochondrial-related metabolomics and hint for a unified adaptive response to this nutritional challenge. The beneficial or noxious consequences arising from this dietary trend should be carefully interpreted and necessarily claims future research.info:eu-repo/semantics/publishedVersio

Altered mitochondrial metabolism in the insulin-resistant heart.

Obesity-induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this case, cardiac dysfunction is characterized by metabolic disturbances such as impaired glucose oxidation and an increased reliance on fatty acid (FA) oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from FA-induced lipotoxicity and uncoupling of oxidative phosphorylation. In this review, we address the metabolic changes in the diabetic heart, focusing on the loss of metabolic flexibility and cardiac mitochondrial function. We consider the alterations observed in mitochondrial substrate utilization, bioenergetics and dynamics, and highlight new areas of research which may improve our understanding of the cause and effect of cardiac mitochondrial dysfunction in diabetes. Finally, we explore how lifestyle (nutrition and exercise) and pharmacological interventions can prevent and treat metabolic and mitochondrial dysfunction in diabetes.COST Action MitoEAGL

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Hyperglycemia decreases mitochondrial function: The regulatory role of mitochondrial biogenesis

Increased generation of reactive oxygen species (ROS) is implicated in "glucose toxicity" in diabetes. However, little is known about the action of glucose on the expression of transcription factors in hepatocytes, especially those involved in mitochondrial DNA (mtDNA) replication and transcription. Since mitochondrial functional capacity is dynamically regulated, we hypothesized that stressful conditions of hyperglycemia induce adaptations in the transcriptional control of cellular energy metabolism, including inhibition of mitochondrial biogenesis and oxidative metabolism. Cell viability, mitochondrial respiration, ROS generation and oxidized proteins were determined in HepG2 cells cultured in the presence of either 5.5 mM (control) or 30 mM glucose (high glucose) for 48 h, 96 h and 7 days. Additionally, mtDNA abundance, plasminogen activator inhibitor-1 (PAI-1), mitochondrial transcription factor A (TFAM) and nuclear respiratory factor-1 (NRF-1) transcripts were evaluated by real time PCR. High glucose induced a progressive increase in ROS generation and accumulation of oxidized proteins, with no changes in cell viability. Increased expression of PAI-1 was observed as early as 96 h of exposure to high glucose. After 7 days in hyperglycemia, HepG2 cells exhibited inhibited uncoupled respiration and decreased MitoTracker Red fluorescence associated with a 25% decrease in mtDNA and 16% decrease in TFAM transcripts. These results indicate that glucose may regulate mtDNA copy number by modulating the transcriptional activity of TFAM in response to hyperglycemia-induced ROS production. The decrease of mtDNA content and inhibition of mitochondrial function may be pathogenic hallmarks in the altered metabolic status associated with diabetes.http://www.sciencedirect.com/science/article/B6WXH-4PC8RDJ-3/1/56d34862ca326b7c56cae828eb44677

Biosensor plates detect mitochondrial physiological regulators and mutations in vivo

http://www.sciencedirect.com/science/article/B6W9V-4TMBPVF-7/2/3e75ce2b20adb3707a2d6c0aef2493a