Iron oxidation on the surface of adventitious roots and its relation to aerenchyma formation in rice genotypes

Establishment of the water layer in an irrigated rice crop leads to consumption of free oxygen in the soil which enters in a chemical reduction process mediated by anaerobic microorganisms, changing the crop environment. To maintain optimal growth in an environment without O2, rice plants develop pore spaces (aerenchyma) that allow O2 transport from air to the roots. Carrying capacity is determined by the rice genome and it may vary among cultivars. Plants that have higher capacity for formation of aerenchyma should theoretically carry more O2 to the roots. However, part of the O2 that reaches the roots is lost due to permeability of the roots and the O2 gradient created between the soil and roots. The O2 that is lost to the outside medium can react with chemically reduced elements present in the soil; one of them is iron, which reacts with oxygen and forms an iron plaque on the outer root surface. Therefore, evaluation of the iron plaque and of the formation of pore spaces on the root can serve as a parameter to differentiate rice cultivars in regard to the volume of O2 transported via aerenchyma. An experiment was thus carried out in a greenhouse with the aim of comparing aerenchyma and iron plaque formation in 13 rice cultivars grown in flooded soils to their formation under growing conditions similar to a normal field, without free oxygen. The results indicated significant differences in the volume of pore spaces in the roots among cultivars and along the root segment in each cultivar, indicating that under flooded conditions the genetic potential of the plant is crucial in induction of cell death and formation of aerenchyma in response to lack of O2. In addition, the amount of Fe accumulated on the root surface was different among genotypes and along the roots. Thus, we concluded that the rice genotypes exhibit different responses for aerenchyma formation, oxygen release by the roots and iron plaque formation, and that there is a direct relationship between porosity and the amount of iron oxidized on the root surface.

Roles of multiple acyl-CoA oxidases in the routing of carbon flow towards β-oxidation and polyhydroxyalkanoate biosynthesis in Yarrowia lipolytica.

The oleaginous yeast Yarrowia lipolytica possesses six acyl-CoA oxidase (Aox) isoenzymes encoded by genes POX1-POX6. The respective roles of these multiple Aox isoenzymes were studied in recombinant Y. lipolytica strains that express heterologous polyhydroxyalkanoate (PHA) synthase (phaC) of Pseudomonas aeruginosa in varying POX genetic backgrounds, thus allowing assessment of the impact of specific Aox enzymes on the routing of carbon flow to β-oxidation or to PHA biosynthesis. Analysis of PHA production yields during growth on fatty acids with different chain lengths has revealed that the POX genotype significantly affects the PHA levels, but not the monomer composition of PHA. Aox3p function was found to be responsible for 90% and 75% of the total PHA produced from either C9:0 or C13:0 fatty acid, respectively, whereas Aox5p encodes the main Aox involved in the biosynthesis of 70% of PHA from C9:0 fatty acid. Other Aoxs, such as Aox1p, Aox2p, Aox4p and Aox6p, were not found to play a significant role in PHA biosynthesis, independent of the chain length of the fatty acid used. Finally, three known models of β-oxidation are discussed and it is shown that a 'leaky-hose pipe model' of the cycle can be applied to Y. lipolytica.

Characterization of nano-oxide layers fabricated by ion beam oxidation

In this paper, a remote O2 ion source is used for the formation of nano-oxide layers. The oxidation efficiency was measured in CoFe-oxide films, and a decrease of the oxide layer with the pan angle and the oxidation pressure is observed. For the same oxidation pressure, the oxidation efficiency depends on the O2 content in the Ar-O2 plasma. These results were applied in optimizing the fabrication of Al2O3 barrier for tunnel junctions. This method was also used to fabricate junctions with Fe-oxide layers inserted at the Al2O3-CoFe interface. TEM and magnetization data indicate that after anneal at 385°C, a homogeneous ferromagnetic Fe-oxide layer (Fe3O4?) is formed.

Inhibition of Na(+)-K(+)-ATPase by digoxin and its relation with energy expenditure and nutrient oxidation rate.

This study investigates the effects of digoxin, an inhibitor of the Na+ pump (Na(+)-K(+)-ATPase), on resting metabolic rate (RMR), respiratory quotient (RQ), and nutrient oxidation rate. Twelve healthy male subjects followed a double-blind protocol design and received either 1 mg/day digoxin or a placebo 2 days before indirect calorimetry measurements. Digoxin induced a 0.22 +/- 0.07 kJ/min or 3.8 +/- 1.5% (mean +/- SE, P = 0.01) decrease in RMR and a 0.40 +/- 0.13 kJ/min (P = 0.01) decrease in fat oxidation rate, whereas carbohydrate and protein oxidation rates did not change significantly. A dose-response relationship between serum digoxin and RQ was observed. These results suggest that digoxin reduces not only RMR but also fat oxidation rate by mechanisms that remain to be elucidated. Because a linkage and an association between genes coding the Na(+)-K(+)-ATPase and the RQ have been previously observed, the present demonstration of an effect of Na(+)-K(+)-ATPase inhibition on fat oxidation rate strengthens the concept that the activity of this enzyme may play a role in body weight regulation.

Adverse effects of high dose carnitine supplementation of total parenteral nutrition on protein and fat oxidation in the critically ill.

The aim of the present study was to investigate the effects of continuous and acute L-carnitine supplementation of total parenteral nutrition (TPN) on protein and fat oxidation in severe catabolism. A critically ill and severely malnourished male patient received TPN (non protein energy = 41 kcal/kg/day, provided equally as fat and glucose) over 38 days, without L-carnitine for 23 days and with carnitine supplements (15 mg/kg/day) for the following 15 days. Subsequently, he was given carnitine-free enteral nutrition for 60 more days. A four-hour infusion of 100 mg L-carnitine was given on day 11 of each TPN period. Indirect calorimetry was carried out after 11 days of either carnitine-free or supplemented TPN and at the initiation of enteral nutrition. Additional measurements were performed 4 hours and 24 hours after the acute infusions of carnitine. The rate of protein oxidation and the respiratory quotient were found to be higher, and the rate of fat oxidation to be lower, with carnitine-supplemented TPN, than with either carnitine-free TPN or enteral nutrition. Acute infusion of carnitine resulted in an increased rate of protein oxidation and a reduced rate of fat oxidation on both TPN-regimens. These unfavourable effects on protein metabolism may be due to an impairment of fat oxidation by excess amounts of carnitine.

Use of recovered frying oils in chicken and rabbit feeds: effect on the fatty acid and tocol composition and on the oxidation levels of meat, liver and plasma

The addition of some fat co- and by-products to feeds is usual nowadays; however, the regulations of their use are not always clear and vary between countries. For instance, the use of recycled cooking oils is not allowed in the European Union, but they are used in other countries. However, oils recovered from industrial frying processes could show satisfactory quality for this purpose. Here we studied the effects of including oils recovered from the frying industry in rabbit and chicken feeds (at 30 and 60 g/kg, respectively) on the fatty acid (FA) and tocol (tocopherol + tocotrienol) compositon of meat, liver and plasma, and on their oxidative stability. Three dietary treatments (replicated eight times) were compared: fresh non-used oil (LOX); oil discarded from the frying industry, having a high content of secondary oxidation compounds (HOX); and an intermediate level (MOX) obtained by mixing 50 : 50 of LOX and HOX. The FA composition of oil diets and tissues was assessed by GC, their tocol content by HPLC, the thiobarbituric acid value was used to assess tissue oxidation status, and the ferrous oxidation-xylenol orange method was used to assess the susceptibility of tissues to oxidation. Our results indicate that FA composition of rabbit and chicken meat, liver and plasma was scarcely altered by the addition of recovered frying oils to feed. Differences were encountered in the FA composition between species, which might be attributed mainly to differences in the FA digestion, absorption and metabolism between species, and to some physiological dietary factors (i.e. coprophagy in rabbits that involves fermentation with FA structure modification). The α-tocopherol (αT) content of tissues was reduced in response to the lower αT content in the recovered frying oil. Differences in the content of other tocols were encountered between chickens and rabbits, which might be attributable to the different tocol composition of their feeds, as well as to species differences in the digestion and metabolism of tocols. Tissue oxidation and susceptibility to oxidation were in general low and were not greatly affected by the degree of oxidation of the oil added to the feeds. The relative content of polyunsaturated fatty acids/αT in these types of samples would explain the differences observed between species in the susceptibility of each tissue to oxidation. According to our results, oils recovered from the frying industry could be useful for feed uses.

Nanometer-scale oxidation of Si(100) surfaces by tapping mode atomic force microscopy

The nanometer¿scale oxidation of Si(100) surfaces in air is performed with an atomic force microscope working in tapping mode. Applying a positive voltage to the sample with respect to the tip, two kinds of modifications are induced on the sample: grown silicon oxide mounds less than 5 nm high and mounds higher than 10 nm (which are assumed to be gold depositions). The threshold voltage necessary to produce the modification is studied as a function of the average tip¿to¿sample distance.

Mineralization of the recalcitrant oxalic and oxamic acids by electrochemical advanced oxidation processes using a boron-doped diamond anode

Oxalic and oxamic acids are the ultimate and more persistent by-products of the degradation of N-aromatics by electrochemical advanced oxidation processes (EAOPs). In this paper, the kinetics and oxidative paths of these acids have been studied for several EAOPs using a boron-doped diamond (BDD) anode and a stainless steel or an air-diffusion cathode. Anodic oxidation (AO-BDD) in the presence of Fe2+ (AO-BDD-Fe2+) and under UVA irradiation (AO-BDD-Fe2+-UVA), along with electro-Fenton (EF-BDD), was tested. The oxidation of both acids and their iron complexes on BDD was clarified by cyclic voltammetry. AO-BDD allowed the overall mineralization of oxalic acid, but oxamic acid was removed much more slowly. Each acid underwent a similar decay in AO-BDD-Fe2+ and EFBDD, as expected if its iron complexes were not attacked by hydroxyl radicals in the bulk. The faster and total mineralization of both acids was achieved in AO-BDD-Fe2+-UVA due to the high photoactivity of their Fe(III) complexes that were continuously regenerated by oxidation of their Fe(II) complexes. Oxamic acid always released a larger proportion of NH4 + than NO3- ion, as well as volatile NOx species. Both acids were independently oxidized at the anode in AO-BDD, but in AO-BDD-Fe2+-UVA oxamic acid was more slowlydegraded as its content decreased, without significant effect on oxalic acid decay. The increase in current density enhanced the oxidation power of the latter method, with loss of efficiency. High Fe2+ contents inhibited the oxidation of Fe(II) complexes by the competitive oxidation of Fe2+ to Fe3+. Low current densities and Fe2+ contents are preferable to remove more efficiently these acids by the most potent AO-BDD-Fe2+-UVA method.

Analysis of the alternative pathways for the beta-oxidation of unsaturated fatty acids using transgenic plants synthesizing polyhydroxyalkanoates in peroxisomes.

Degradation of fatty acids having cis-double bonds on even-numbered carbons requires the presence of auxiliary enzymes in addition to the enzymes of the core beta-oxidation cycle. Two alternative pathways have been described to degrade these fatty acids. One pathway involves the participation of the enzymes 2, 4-dienoyl-coenzyme A (CoA) reductase and Delta(3)-Delta(2)-enoyl-CoA isomerase, whereas the second involves the epimerization of R-3-hydroxyacyl-CoA via a 3-hydroxyacyl-CoA epimerase or the action of two stereo-specific enoyl-CoA hydratases. Although degradation of these fatty acids in bacteria and mammalian peroxisomes was shown to involve mainly the reductase-isomerase pathway, previous analysis of the relative activity of the enoyl-CoA hydratase II (also called R-3-hydroxyacyl-CoA hydro-lyase) and 2,4-dienoyl-CoA reductase in plants indicated that degradation occurred mainly through the epimerase pathway. We have examined the implication of both pathways in transgenic Arabidopsis expressing the polyhydroxyalkanoate synthase from Pseudomonas aeruginosa in peroxisomes and producing polyhydroxyalkanoate from the 3-hydroxyacyl-CoA intermediates of the beta-oxidation cycle. Analysis of the polyhydroxyalkanoate synthesized in plants grown in media containing cis-10-heptadecenoic or cis-10-pentadecenoic acids revealed a significant contribution of both the reductase-isomerase and epimerase pathways to the degradation of these fatty acids.

Oxidation and ubiquitination in neurodegeneration.

It is widely accepted that protein oxidation is involved in a variety of diseases, including neurodegenerative diseases. Especially during aging, a reduction in anti-oxidant defence mechanisms leads to an increased formation of free radical oxygen species and consequently results in a damage of proteins, including mitochondrial and synaptic ones. Even those proteins involved in repair and protein clearance via the ubiquitin proteasome and lysosomal system are subject to damage and show a reduced function. Here, we will discuss a variety of mechanisms and provide examples where cognition is affected and where repair mechanisms are no longer sufficient to compensate for a dysfunction of damaged proteins or even may become toxic. Next to physiological deficits, an accumulation of deficient proteins in aggresomes may occur and result in a formation of pathological hallmark structures typical for aging and disease. A major challenge is how to prevent aberrant oxidation, given that oxidation plays an essential role in aging and neurodegenerative diseases. Particularly interesting are the possibilities to reduce the formation of radical oxygen species leading to a dysfunction of protein repair and protein clearance, or to a formation of toxic byproducts accelerating neurodegeneration.

Changes in sleeping and basal energy expenditure and substrate oxidation induced by short term thyroxin administration in man.

The present study was designed to explore the thermogenic effect of thyroid hormone administration and the resulting changes in nitrogen homeostasis. Normal male volunteers (n = 7) received thyroxin during 6 weeks. The first 3-week period served to suppress endogenous thyroid secretion (180 micrograms T4/day). This dose was doubled for the next 3 weeks. Sleeping energy expenditure (respiratory chamber) and BMR (hood) were measured by indirect calorimetry, under standardized conditions. Sleeping heart rate was continuously recorded and urine was collected during this 12-hour period to assess nitrogen excretion. The changes in energy expenditure, heart rate and nitrogen balance were then related to the excess thyroxin administered. After 3 weeks of treatment, serum TSH level fell to 0.15 mU/L, indicating an almost complete inhibition of the pituitary-thyroid axis. During this phase of treatment there was an increase in sleeping EE and sleeping heart rate, which increased further by doubling the T4 dose (delta EE: +8.5 +/- 2.3%, delta heart rate +16.1 +/- 2.2%). The T4 dose, which is currently used as a substitutive dose, lead to a borderline hyperthyroid state, with an increase in EE and heart rate. Exogenous T4 administration provoked a significant increase in urinary nitrogen excretion averaging 40%. It is concluded that T4 provokes an important stimulation of EE, which is mostly mediated by an excess protein oxidation.

Effect of a 1-hour single bout of moderate-intensity exercise on fat oxidation kinetics.

The present study aimed to examine the effects of a prior 1-hour continuous exercise bout (CONT) at an intensity (Fat(max)) that elicits the maximal fat oxidation (MFO) on the fat oxidation kinetics during a subsequent submaximal incremental test (IncrC). Twenty moderately trained subjects (9 men and 11 women) performed a graded test on a treadmill (Incr), with 3-minute stages and 1-km.h(-1) increments. Fat oxidation was measured using indirect calorimetry and plotted as a function of exercise intensity. A mathematical model (SIN) including 3 independent variables (dilatation, symmetry, and translation) was used to characterize the shape of fat oxidation kinetics and to determine Fat(max) and MFO. On a second visit, the subjects performed CONT at Fat(max) followed by IncrC. After CONT performed at 57% +/- 3% (means +/- SE) maximal oxygen uptake (Vo(2max)), the respiratory exchange ratio during IncrC was lower at every stage compared with Incr (P < .05). Fat(max) (56.4% +/- 2.3% vs 51.5% +/- 2.4% Vo(2max), P = .013), MFO (0.50 +/- 0.03 vs 0.40 +/- 0.03 g.min(-1), P < .001), and fat oxidation rates from 35% to 70% Vo(2max) (P < .05) were significantly greater during IncrC compared with Incr. However, dilatation and translation were not significantly different (P > .05), whereas symmetry tended to be greater in IncrC (P = .096). This study showed that the prior 1-hour continuous moderate-intensity exercise bout increased Fat(max), MFO, and fat oxidation rates over a wide range of intensities during the postexercise incremental test. Moreover, the shape of the postexercise fat oxidation kinetics tended to have a rightward asymmetry.

Ion-beam induced oxidation of GaAs and AlGaAs

The oxidation of GaAs and AlxGa1−xAs targets by oxygen irradiation has been studied in detail. It was found that the oxidation process is characterized by the strong preferential oxidation of Al as compared to Ga, and of Ga as compared to As. This experimental observation, which has been accurately quantified by using x‐ray photoelectron spectroscopy, is connected to the different heats of formation of the corresponding oxides. The oxide grown by ion beam oxidation shows a strong depletion in As and relatively low oxidation of As as well. The depletion can be associated with the preferential sputtering of the As oxide in respect to other compounds whereas the low oxidation is due to the low heat of formation. In contrast Al is rapidly and fully oxidized, turning the outermost layer of the altered layer to a single Al2O3 overlayer, as observed by transmission electron microscopy. The radiation enhanced diffusion of oxygen and aluminum in the altered layer explains the large thickness of these altered layers and the formation of Al oxides on top of the layers. For the case of ion‐beam oxidation of GaAs a simulation program has been developed which describes adequately the various growth mechanisms experimentally observed

Effects of weight loss and exercise on insulin resistance, and intramyocellular triacylglycerol, diacylglycerol and ceramide.

AIMS/HYPOTHESIS: Intramyocellular lipids, including diacylglycerol (DAG) and ceramides, have been linked to insulin resistance. This randomised repeated-measures study examined the effects of diet-induced weight loss (DIWL) and aerobic exercise (EX) on insulin sensitivity and intramyocellular triacylglycerol (IMTG), DAG and ceramide. METHODS: Sixteen overweight to obese adults (BMI 30.6 ± 0.8; 67.2 ± 4.0 years of age) with either impaired fasting glucose, or impaired glucose tolerance completed one of two lifestyle interventions: DIWL (n = 8) or EX (n = 8). Insulin sensitivity was determined using hyperinsulinaemic-euglycaemic clamps. Intramyocellular lipids were measured in muscle biopsies using histochemistry and tandem mass spectrometry. RESULTS: Insulin sensitivity was improved with DIWL (20.6 ± 4.7%) and EX (19.2 ± 12.9%). Body weight and body fat were decreased by both interventions, with greater decreases in DIWL compared with EX. Muscle glycogen, IMTG content and oxidative capacity were all significantly (p < 0.05) decreased with DIWL and increased with EX. There were decreases in DAG with DIWL (-12.4 ± 14.6%) and EX (-40.9 ± 12.0%). Ceramide decreased with EX (-33.7 ± 11.2%), but not with DIWL. Dihydroceramide was decreased with both interventions. Sphingosine was decreased only with EX. Changes in total DAG, total ceramides and other sphingolipids did not correlate with changes in glucose disposal. Stearoyl-coenzyme A desaturase 1 (SCD1) content was decreased with DIWL (-19.5 ± 8.5%, p < 0.05), but increased with EX (19.6 ± 7.4%, p < 0.05). Diacylglycerol acyltransferase 1 (DGAT1) was unchanged with the interventions. CONCLUSIONS/INTERPRETATION: Diet-induced weight loss and exercise training both improved insulin resistance and decreased DAG, while only exercise decreased ceramides, despite the interventions having different effects on IMTG. These alterations may be mediated through differential changes in skeletal muscle capacity for oxidation and triacylglycerol synthesis. TRIAL REGISTRATION: ClinicalTrials.gov NCT00766298.

Pancreatic islet adaptation to fasting is dependent on peroxisome proliferator-activated receptor alpha transcriptional up-regulation of fatty acid oxidation.

The cellular response to fasting and starvation in tissues such as heart, skeletal muscle, and liver requires peroxisome proliferator-activated receptor-alpha (PPARalpha)-dependent up-regulation of energy metabolism toward fatty acid oxidation (FAO). PPARalpha null (PPARalphaKO) mice develop hyperinsulinemic hypoglycemia in the fasting state, and we previously showed that PPARalpha expression is increased in islets at low glucose. On this basis, we hypothesized that enhanced PPARalpha expression and FAO, via depletion of lipid-signaling molecule(s) for insulin exocytosis, are also involved in the normal adaptive response of the islet to fasting. Fasted PPARalphaKO mice compared with wild-type mice had supranormal ip glucose tolerance due to increased plasma insulin levels. Isolated islets from the PPARalpha null mice had a 44% reduction in FAO, normal glucose use and oxidation, and enhanced glucose-induced insulin secretion. In normal rats, fasting for 24 h increased islet PPARalpha, carnitine palmitoyltransferase 1, and uncoupling protein-2 mRNA expression by 60%, 62%, and 82%, respectively. The data are consistent with the view that PPARalpha, via transcriptionally up-regulating islet FAO, can reduce insulin secretion, and that this mechanism is involved in the normal physiological response of the pancreatic islet to fasting such that hypoglycemia is avoided.