Top PDF Iron accumulation with age, oxidative stress and functional decline.

Iron accumulation with age, oxidative stress and functional decline.

Iron accumulation with age, oxidative stress and functional decline.

The increases in non-heme iron levels in the young CR animals could have lead to more free radical damage. However, young CR animals i) are better protected against oxidative stress because of increased antioxidant defense systems [49] ii) CR animals may have greater levels of ferritin and frataxin proteins to store and transport iron and iii) non-heme iron may be tighter bound to proteins rendering them less redox active. It is also unknown what % of the non-heme iron is potentially redox active because we could not measure free iron. Redox free iron measurements using the bleomycin/iron-dependent DNA degradation assay in these samples is challenging. This method is used to indirectly quantify the labile iron pool and involves the measurement of bleomycin/ iron-dependent DNA degradation or the direct assay of oxidized 2-deoxyribose in homogenized tissue samples [50]. The bleomycin assay for ‘‘free’’ iron was introduced by Gutteridge et al. in 1981 as a first attempt to detect and measure reactive iron species in biological fluids, and has since allowed the detection of several new clinical states of plasma iron overload. Moreover, the labile iron pool has been quantitated by several other techniques, including the use of DFO-chelatable iron-59 [51] and electron paramagnetic resonance spectroscopy [52]. It is, however, difficult to measure free iron concentration in tissue precisely. For example, the bleomycin molecule is a non-physiological iron chelator (Ka 10 15 ) that forms an iron complex with non-biological redox properties, and this has led some to criticize the data obtained using the assay [53]. Most importantly, disrupting the cells by tissue homogena- tion alters the existing equilibrium between free and bound iron, as well as its oxidation state [47]. Therefore, the bleomycin assay is mostly used in biological fluids such as plasma to indirectly quantify the labile iron pool; in this study, the measurement of non-heme iron concentrations gives a much better overall status of the iron pool.
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HFE gene mutation and oxidative damage biomarkers in patients with  syndromes and its relation to transfusional iron oload : an observational crosssectional study

HFE gene mutation and oxidative damage biomarkers in patients with syndromes and its relation to transfusional iron oload : an observational crosssectional study

Myelodysplastic syndromes (MDS) comprise a heteroge- neous range of haematopoietic diseases characterised by bone marrow failure and a variable propensity to evolve into acute myeloid leukaemia. Most patients have anaemia at some point in the course of the disease and many develop transfusion dependence and consequent iron overload (IOL), considered to be a negative inde- pendent prognostic factor associated with a higher risk of leukaemic transformation and shorter survival. 1 The pathogenesis of MDS is complex and involves the haem- atopoietic stem cells, bone marrow microenvironment and the interaction between them. Recently, attention has been focused on oxidative stress and its negative effect on self-renewal and the number of haematopoietic stem cells. Nuclear and mitochondrial DNA can be dir- ectly damaged by hydroxyl radicals resulting in genomic instability contributing to disease progression. 2 3 Excess of iron due to multiple transfusions is toxic through the production of free radicals derived from activated oxygen species, which eventually form hydroxyl radicals from superoxide or hydrogen peroxide resulting in organ dysfunction. 4 Hereditary haemochromatosis (HH) is an autosomal recessive disorder characterised by the enhanced intestinal absorption of dietary iron associated with the presence of variations in the HFE gene located in the short arm of chromosome 6. 5 The gene variations result in a tyrosine substitution by cysteine residue at position 282 (C282Y allele), exchange of histidine to aspartic acid at amino acid position 63 (H63D allele) and substitution of cysteine for serine at amino acid pos- ition 65 (S65C allele). Patients with HH are most fre- quently either homozygous for C282Y or compound heterozygous for C282Y/H63D. 6 HFE gene variants cor- relate with body iron levels and have shown association with cancer risk including childhood acute lympho- blastic leukaemia (ALL). 7 Increased IOL and iron- mediated oxidative stress may be directly involved in the pathogenesis of MDS. We hypothesise if the presence of HH gene variations in homozygous as well as heterozy- gous forms could contribute to a significantly higher rate of iron accumulation in the context of transfusion dependence. 8 The aim of this study was to evaluate the presence of variations in the HFE gene and the oxida- tive status in patients with MDS with IOL and compare these findings with those of patients without IOL and healthy individuals.
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Rev. Bras. Hematol. Hemoter.  vol.35 número1

Rev. Bras. Hematol. Hemoter. vol.35 número1

The analysis of the biochemical and oxidative stress parameters, as well as IL-10 levels, showed a clear increase of inlammation and tissue injury in the iron overload group. While each class of biomarker is traditionally thought to represent one of these processes, it is important to note that they are not distinct entities and have considerable interaction. Oxidative stress can initiate tissue injury and/or inlammation. Plasma MDA is a marker of tissue injury and oxidative stress. The free iron accumulation, due to transfusions, acts as a catalyst for oxidation with subsequent production of superoxide and hydroxyl radicals. The authors introduced the heme-oxidase-1 (HO-1) as one of the mechanisms induced by the reduction of bioavailability of nitric oxide. Heme-oxygenase is the rate-limiting enzyme in the degradation of heme groups to biliverdin, carbon monoxide (CO) and iron. Bilirubin is created by the activity of biliverdin reductase on biliverdin (5) , however, no signiicant differences in bilirubin
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Two kinds of ferritin protect ixodid ticks from iron overload and consequent oxidative stress.

Two kinds of ferritin protect ixodid ticks from iron overload and consequent oxidative stress.

Ticks are obligate hematophagous parasites that have successfully developed counteractive means against their hosts’ immune and hemostatic mechanisms, but their ability to cope with potentially toxic molecules in the blood remains unclear. Iron is important in various physiological processes but can be toxic to living cells when in excess. We previously reported that the hard tick Haemaphysalis longicornis has an intracellular (HlFER1) and a secretory (HlFER2) ferritin, and both are crucial in successful blood feeding and reproduction. Ferritin gene silencing by RNA interference caused reduced feeding capacity, low body weight and high mortality after blood meal, decreased fecundity and morphological abnormalities in the midgut cells. Similar findings were also previously reported after silencing of ferritin genes in another hard tick, Ixodes ricinus. Here we demonstrated the role of ferritin in protecting the hard ticks from oxidative stress. Evaluation of oxidative stress in Hlfer-silenced ticks was performed after blood feeding or injection of ferric ammonium citrate (FAC) through detection of the lipid peroxidation product, malondialdehyde (MDA) and protein oxidation product, protein carbonyl. FAC injection in Hlfer-silenced ticks resulted in high mortality. Higher levels of MDA and protein carbonyl were detected in Hlfer-silenced ticks compared to Luciferase-injected (control) ticks both after blood feeding and FAC injection. Ferric iron accumulation demonstrated by increased staining on native HlFER was observed from 72 h after iron injection in both the whole tick and the midgut. Furthermore, weak iron staining was observed after Hlfer knockdown. Taken together, these results show that tick ferritins are crucial antioxidant molecules that protect the hard tick from iron- mediated oxidative stress during blood feeding.
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Lycopene and ß-carotene protect in vivo iron-induced oxidative stress damage in rat prostate

Lycopene and ß-carotene protect in vivo iron-induced oxidative stress damage in rat prostate

or ß-carotene for 5 days prior to Fe-NTA treatment showed a reduction of about 70% in 8-oxodGuo levels to almost control levels. Compared with control rats, the prostate of Fe-NTA-treated animals showed a 78% increase in malondialdehyde accumulation. Lycopene or ß- carotene pre-treatment almost completely prevented lipid damage. Epidemiological studies have suggested a lower risk of prostate cancer in men reporting a higher consumption of tomato products. However, before associating this effect with tomato sauce constitu- ents, more information is required. The results described here may contribute to the understanding of the protective effects of carotenoids against iron-induced oxidative stress.
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Age related changes in NAD+ metabolism oxidative stress and Sirt1 activity in wistar rats.

Age related changes in NAD+ metabolism oxidative stress and Sirt1 activity in wistar rats.

Multiple degenerative processes are implicated in natural senescence. As aging is associated with progressive decline in organ function, elucidating the complex pathways controlling the rate of aging is of significant clinical importance [1]. An important mechanism contributing to aging is oxidative stress. The ‘‘free- radical theory of aging’’, initially proposed by Harman (1956) suggests that oxidative damage occurs with advanced aging due to an imbalance between free radical and reactive species (ROS) production, and cellular antioxidant defense mechanisms [2]. Elevated levels of intracellular ROS through hydrogen peroxide treatment, or deficiency of ROS scavenging enzymes such as superoxide dismutase (SOD1) knockdown, has been shown to induce premature senescence and reduce cellular life span [3,4,5]. The mitochondria, represents the main producer of cellular ROS in the human body, and approximately 1–2% of the oxygen molecules consumed during normal respiration are converted into highly reactive superoxide anion, which is rapidly dismutated to H 2 O 2 by the superoxide dismutases [6]. Other pathways and
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Déficits de memória associados ao envelhecimento e ao acúmulo de ferro cerebral : uso de rosuvastatina na estratégia de neuroproteção

Déficits de memória associados ao envelhecimento e ao acúmulo de ferro cerebral : uso de rosuvastatina na estratégia de neuroproteção

one possible mechanism by which rosuvastatin promoted the cog- nitive improvement seen in our study may be associated with its anti-oxidative properties. In previous studies we have demon- strated that neonatal iron treatment is associated with increased oxidative stress in brain regions related to memory formation (de Lima et al., 2005a), and that reduction of oxidative damage to pro- teins in the cortex and hippocampus in aged rats was associated with amelioration of age-induced memory impairment (Pietá Dias et al., 2007). While further studies will be required in order to pre- cise understand the mechanisms by which rosuvastatin amelio- rated iron-induced memory deficits, we do not know why the lowest dose used in the present study was effective and the highest was not. However, a number of studies examining the effects of injections of both memory-enhancing (McGaugh, 1989) and mem- ory-impairing drugs show that many treatments produce an in- verted-U dose–response curve where specific doses are optimal whereas both lower and higher doses are ineffective.
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Increased parameters of oxidative stress and its relation to transfusion iron oload in patients with  syndromes

Increased parameters of oxidative stress and its relation to transfusion iron oload in patients with syndromes

Seventy-six patients were enrolled, 20 (26.3%) with and 56 (73.7%) without IOL. The average age was 66.8 years and 68.6 years, respectively. The cntrol group consisted of 45 healthy volunteers with a mean age of 74.2 years. Demographic and laboratory data and WHO classification are shown in table 1.

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Memory decline in Down syndrome and its relationship to iPF2alpha, a urinary marker of oxidative stress.

Memory decline in Down syndrome and its relationship to iPF2alpha, a urinary marker of oxidative stress.

It has been suggested that oxidative stress is an important consequence of the specific biology of DS, and is likely to play a role in some of the co-morbidities associated with DS, including the tendency to develop AD [4]. Oxidative damage may lead to enhanced amyloid beta peptide (Ab) production [21–24] and in a recent study, Cenini et al. showed that soluble and insoluble Ab and oligomers increase as a function of age in DS frontal cortex, and that Ab40 correlated with protein carbonyls (an oxidative stress marker), which suggests that oxidative damage may contribute to the onset and progression of AD pathogenesis in DS [25]. The exact mechanism is still unknown, but Yang et al. showed that ROS enhanced amyloid toxicity in the neurons of APP/PS1 mice [26], an AD mouse model with excessive amyloid production which is also found in DS, while Di Domenico et al demonstrated that oxidation of proteins is an early event in DS and might contribute to neurodegenerative phenomena [27].
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Are iron oxide nanoparticles safe? Current knowledge and future perspectives

Are iron oxide nanoparticles safe? Current knowledge and future perspectives

eters were observed in Sprague-Dawley rats orally administered, daily over a 13-week period [99]. Ansciaux et al. [107] function- alized several ultrasmall iron oxide particles with peptides that present an affinity for amyloid- ␤ peptide, for being used in early diagnosis of Alzheimer’s disease. The particles coupled to peptide C-IPLPFYN-C demonstrated ability to cross the blood-brain barrier in mice without any facilitating strategy, and accumulated in brain 90 min after their intravenous injection. However, no toxic effects were observed after exposure and none of the derivatives tested was found in any organ one week after administration; elimina- tion half-life was about 3 h. Recently, Yang et al. [108] investigated the size-dependent in vivo kinetics, toxicity and gene expression changes caused by carboxyl-coated ION (magnetite, diameters 10, 20, 30, and 40 nm). They demonstrated that ION accumulated primarily in liver and spleen of Kunming mice on the first day post-intravenous injection, following a size-dependent pattern, with 10 nm nanoparticles showing the highest uptake by liver and 40 nm nanoparticles the highest uptake by spleen. Moreover, 10 nm ION were cleared faster from liver and kidneys, but entered more readily brain and uterus, whereas 40 nm ION accumulated more readily but were easily eliminated in spleen. No apparent signs of acute toxicity were observed, but ION exposure was able to change the expression level of sensitive genes related to oxidative stress, iron transport, metabolic processes, and apoptosis, among others. Likewise, Chamorro et al. [101] reported accumulation of nanopar- ticles in liver, spleen, or duodenum of growing chickens chronically exposed to low doses of ION ( ␥-Fe 2 O 3 ) by oral route; faeces were
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Beneficial effects of a Q-ter based nutritional mixture on functional performance, mitochondrial function, and oxidative stress in rats.

Beneficial effects of a Q-ter based nutritional mixture on functional performance, mitochondrial function, and oxidative stress in rats.

representative measurements in functional aging [69,70]. Our previous studies have shown that aged rats with advanced muscle atrophy exhibited reduced grip strength [55,56]. In the present study, muscle mass and grip strength decreased significantly with age in control groups (Table 3). Eufortyn H supplementation significantly ameliorated the decline in grip strength in 21-month- old rats, however, did not have a significant effect when initiated in 29-month-old rats. This suggests there may be a critical time period during which this nutritional combination is effective and they may no longer be beneficial after a threshold is reached. Another possibility is that the time period of Eufortyn H supplementation (4 weeks while grip strength was measured and total of 6 weeks in this study) and the dosage used were not sufficient to achieve this goal in late middle aged animals.
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Polyhydroxyfullerene binds cadmium ions and alleviates metal-induced oxidative stress in saccharomyces cerevisiae

Polyhydroxyfullerene binds cadmium ions and alleviates metal-induced oxidative stress in saccharomyces cerevisiae

Complementarily to the antioxidant role of PHF, electrochem- ical stripping analyses showed extracellular binding of Cd to PHF in a concentration- and pH-dependent manner that led to a re- duction in the concentration of bioavailable Cd. The binding ef- fects of PHF in the presence of YPD medium suggested that the binding was additive. Cd binding by PHF resulted in up to a 10- fold decrease of free Cd, which translated into a significant pro- tection against Cd toxicity. Also, SEM-EDX analysis showed that Cd ions were surrounded by PHF nanoparticles, supporting the idea that the functionalized surface hydroxyl groups of PHF could trap Cd while still having a facet available for interacting with yeast cells. In addition, the more pronounced decrease in Cd toxicity promoted by PHF at higher pHs was probably due to greater avail- ability of unbound and/or nonaggregated PHF nanoparticles with unmasked hydroxyl groups to interact with Cd ions, as disclosed by the shift toward smaller nanoparticles and lower PdIs at higher pHs (see Table S1 in the supplemental material). These results provided the mechanistic explanation for the alleviating effects of PHF on Cd-induced cytotoxicity. Thus, along with hydroxyl rad- icals or ROS-scavenging properties, PHF directly interacted with Cd, and pH was a key factor for the stability and availability of PHF nanoparticles to the yeast cells. Figure 3 schematically sum- marizes the possible modes of action of Cd and PHF in yeast cells based on our results and data from literature.
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Functional Role of Parkin against Oxidative Stress in Neural Cells

Functional Role of Parkin against Oxidative Stress in Neural Cells

To examine differences in efficiency of neural differentiation, WT and PKO ES cells were differentiated into neurons by the adherent monolayer culture method. Morphological changes were observed during a differentiation period, and immunocy- tochemistry was performed with MAP2, a mature neuron marker. There were no differences in the morphology or differ- entiation of MAP2-positive cells between WT and PKO cells (Fig. 1A). Specifically, the efficiency of neural differentiation into dopaminergic neurons showed no difference between WT and PKO ES cells, as determined by immunocytochemistry with TH, a dopaminergic neuron marker (Fig. 1B). Real-time RT-PCR analysis with dopaminergic neuron markers such as Nurr1, Pitx3, AADC, TH, and D2R also showed no difference
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Arq. Bras. Oftalmol.  vol.80 número4

Arq. Bras. Oftalmol. vol.80 número4

Detailed ophthalmologic examinations were performed, in- cluding visual acuity testing, slit-lamp biomicroscopy, retinoscopy, intrao cular pressure measurement via Goldmann applanation tono- metry, optical coherence tomography, and luorescein angiography. Patients included in the study had either choroidal neovascularisa- tion or disciform scars. Participants with any systemic disease that could afect TDH, such as a chronic inlammatory disease, rheumato- logic disease, diabetes mellitus, hypertension, cardiovascular disease, or malignancy, as well as smokers, alcoholics, patients with a body mass index greater than 30 kg/m 2 , and anyone taking antioxidant
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Seasonal alterations in serum iron levels in elite football players

Seasonal alterations in serum iron levels in elite football players

of preseason values (20.64± 6.58 vs. 16.38±5.51 µmol/l). CONCLUSION A significant decrease in serum iron level among footballers during both half-seasons is most probably due to an increased loss and/or diminished absorption resulting from a high intensity training process. Because the decline in serum iron may be an early sign of iron store depletion and iron de- ficiency anaemia, it is very important to evaluate it regularly, along with other factors of iron metabolism and oxygen trans- port system.

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Vanadium and cadmium in vivo effects in cardiac muscle: metal accumulation and oxidative stress markers

Vanadium and cadmium in vivo effects in cardiac muscle: metal accumulation and oxidative stress markers

Several biological studies have associated metals, such as lead, cadmium, copper, zinc, mercury, arsenate and vanadium, with the ability to produce reactive oxygen species (ROS), resulting in lipid peroxidation and antioxidant enzymes alterations, leading to oxidative stress (Hu, 2000). Vanadium and cadmium are two metals involved in such effects. In the ocean seawater, the concentrations of vanadium and cadmium range from approxi- mately 1 to 3 μg/L and 0.01 to 42 μg/L (Miramand and Fowler, 1998; Hu, 2000). Cadmium are among the most abundant toxic metals in our environment, with no biological function in superior organisms described so far, which is very toxic even at very low concentrations. The adverse effects of this toxic metal have been studied in many animal species – such as fish – in reproductive, respiratory and haematological systems and in specific target organs, such as the liver and kidney (Verbost et al., 1989; Ricard et al., 1998; Sarkar et al., 1998; Vaglio and Landriscina, 1999; Hu, 2000; Soares et al., 2003; Risso-de Faverney et al., 2004). Besides the toxic effects of this metal has yet to be completely understood, it is well known that cadmium-induced oxidative stress leads to lipid peroxidation and changes in antioxidants enzymes activity (Viarengo, 1989; Correia et al., 1998; Kostic et al., 1993; Shukla et al., 2000). Although cadmium has been studied most extensively, toxicity (such as hepatotoxicity) occurs upon exposure to many metals, including vanadium (Dong et al., 1998; Valko et al., 2005). In contrast, vanadium is involved in many physiological systems, although not considered an essential element (Nechay et al., 1986; Harland and Harden-Williams, 1994). Its physiological role is still far from a clear identification. At higher concentrations (N1–10 nM), vanadium becomes toxic to the cells inducing several injury effects at specific target organs, such as liver and kidney, inducing oxidative damage, lipid peroxidation and changes in haematological, reproductive and respiratory systems (Zychlinski et al., 1991; Zaporowska and Wasilewski, 1992; Stohs and Bagchi, 1995; Domingo, 1996; Byczkowski and Kulkarni, 1998). In order to not generalize the toxic effects promoted by metallic elements a comparative approach in toxicological studies is always needed to precisely characterize the exact effects promoted by different metals and therefore to define the appropriated stress markers to each metal in study.
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Distinct Responses of Mycobacterium smegmatis to Exposure to Low and High Levels of Hydrogen Peroxide.

Distinct Responses of Mycobacterium smegmatis to Exposure to Low and High Levels of Hydrogen Peroxide.

using FastPrep Purification kits (MP Bio) according to the manufacturer’s instructions. Con- struction and sequencing of the cDNA libraries of the various mycobacterial strains was per- formed by BGI-Shenzhen (China). Briefly, total RNA from treated mc 2 155 strains was treated using a Ribominus Transcriptome Isolation Kit (Thermo Fisher Scientific) to remove rRNA contaminations. NEXTflex RNA Fragmentation Buffer (Bioo Scientific) was added to separate the mRNA into short fragments. Using these short fragments as templates, random hexamer- primers were used to synthesize the first strand of cDNA. The second strand of cDNA was syn- thesized using buffer, dNTPs, RNase H and DNA polymerase I. The short fragments were puri- fied with a QIAQuick PCR extraction kit (QIAGEN) and resolved with EB buffer for end reparation and addition of poly(A). The short fragments were subsequently connected with sequencing adaptors. For amplification by PCR, we selected suitable fragments as templates, based on results of agarose gel electrophoresis. The library was then sequenced using Illumina HiSeq 2000. Clean reads were mapped to the reference genome and the gene sequences using SOAP2 [22]. The RNA-sequencing dataset obtained has been submitted to ArrayExpress under the accession number E-MTAB-3594.
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Oxidative stress

Oxidative stress

Reaktivnìe kislorodnìe vidì, harakterizuÓçie okislitelÝnìy stress sposobnìe napastÝ vse glavnìe klassì biologi~eskih makromolekul, to estÝ proteinov DNK i RNK molekulov, a osobenno lipidov. Pod vliÔniem svo- bodnìh radikalov prihodit do perokisleniÔ lipidov kleto~nìh membran, oksil- itelÝnìh povrre`deniy DNK i RNK molekul, razvitiÔ geneti~eskih mutaciy, fragmentacii i izmeneniÔ funkcii samìh razli~nìh proteinìh molekul. VsÒ Ìto imeet svoim posledstviem: naru{enie pronicaemosti kleto~nìh membran, ras- stroystv kleto~noy signalizacii i gomeostaza ionov, umenÝ{{eniÔ ili poteri funkciy povre`dënnìh proteinov, i t.p. Potomu svobodnìe radikalì osvobo`da- emìe v te~enie okslitelÝnogo stressa, s~itaÓtsÔ patogennìmi agentami mnogih bolezney i stareniÔ. Kotoriy vid povre`deniÔ slu~itsÔ i kogda, zavisit ot pri- rodì svobodnìh radikalov, mesta deystvovaniÔ i ih isto~nika.
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Iron overload alters glucose homeostasis, causes liver steatosis, and increases serum triacylglycerols in rats

Iron overload alters glucose homeostasis, causes liver steatosis, and increases serum triacylglycerols in rats

energy-transducing capabilities arising from a reduction in the respiratory chain enzyme activities. Such irreversible oxidative anomalies caused a dramatic drop in tissue ATP levels. In addition, Ceccarelli et al [34] observed induction of lipid peroxidation and consequential abnormalities in mitochondria and calcium transport, after feeding rats with a diet supplemented with 2.5% of iron pentacarbonyl for 40 days. The present study revealed that, irrespective of the diet applied, iron treatment did not dramatically stress the antioxidant system, as indicated by the absence of alteration in the levels of free and total SH radicals and total antioxidant status in the serum. In contrast, Lykkesfeldt et al [35] have recently demonstrated an increase in the biochemical markers of oxidative stress and damage in response to increasing concentrations of iron in the liver. In our study, we observed that iron treatment produced an increase in AST activity, which is a marker for mitochon- drial lesions. A reduction in mitochondrial capacity and impaired ATP production would lead to reduced levels of gluconeogenesis, and this could explain the observed reduction in serum glucose and glycated hemoglobin levels. Paraoxonase is a serum enzyme that is closely associated with HDL and prevents and inhibits lipoprotein oxidation, a basic mechanism involved in the initiation and progression of atherosclerosis. Under certain conditions, oxidative stress is associated with the reduction of PON activity [36,37]. In the present study, arylesterase activity toward phenyl acetate was decreased in rats fed a hyperlipidemic diet, which is in agreement with previous reports [37,38]. Moreover, Nguyen and Sok [39] proposed that metal-catalyzed oxidation may be a primary cause for the decrease in HDL-associated PON1 activity observed under oxidative stress. Administration of iron might, therefore, give rise to a reduction in PON activity. This hypothesis is supported by Trudel et al [40] who reported that PON activity was decreased in rat and human liver microsomes in the presence of increased iron concentrations. However, these authors found that the administration of iron did not alter PON activity in rat serum, a result that was confirmed in the present study. It is likely that the iron dextran treatment used in our investiga- tion did not cause the oxidative stress required to bring about an alteration in PON activity. This possibility is supported by the finding that MDA and HAE levels were altered by diet but not by administration of iron dextran.
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Trends and strategies to enhance triacylglycerols and high-value compounds in microalgae

Trends and strategies to enhance triacylglycerols and high-value compounds in microalgae

Microalgae are important sources of triacylglycerols (TAGs) and high-value compounds such as carotenoids and long-chain polyunsaturated fatty acids (LC-PUFAs). TAGs are feedstocks for biofuels or edible oils; carotenoids are used as pigments in the food and feed industries; and LC-PUFAs are beneficial for human health, being also key to the correct development of fish in aquaculture. Current trends in microalgal biotechnology propose the combined production of biofuels with high-value compounds to turn large-scale production of microalgal biomass into an economically feasible venture. As TAGs, carotenoids and LC-PUFAs are lipophilic biomolecules, they not only share biosynthetic precursors and storage sinks, but also their regulation often depends on common environmental stimuli. In general, stressful conditions favor carotenoid and TAGs biosynthesis, whereas the highest accumulation of LC-PUFAs is usually obtained under conditions promoting growth. However, there are known exceptions to these general rules, as a few species are able to accumulate LC-PUFAs under low light, low temperature or long-term stress conditions. Thus, future research on how microalgae sense, transduce and respond to environmental stress will be crucial to understand how the biosynthesis and storage of these lipophilic molecules are regulated. The use of high-throughput methods (e.g. fluorescent activated cell sorting) will provide an excellent opportunity to isolate triple-producers, i.e. microalgae able to accumulate high levels of LC-PUFAs, carotenoids and TAGs simultaneously. Comparative transcriptomics between wild type and triple- producers could then be used to identify key gene products involved in the regulation of these biomolecules even in microalgal species not amenable to reverse genetics. This combined approach could be a major step towards a better understanding of the microalgal metabolism under di fferent stress conditions. Moreover, the generation of triple-producers would be essential to raise the biomass value in a biore finery setting and contribute to meet the world's rising demand for food, feed and energy.
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