Oxidative Energy Metabolism Research Articles

Duchenne muscular dystrophy is associated with the inhibition of calcium uniport in mitochondria and an increased sensitivity of the organelles to the calcium-induced permeability transition

Duchenne muscular dystrophy (DMD) is characterized by a pronounced and progressive degradation of the structure of skeletal muscles, which decreases their strength and lowers endurance of the organism. At muscular dystrophy, mitochondria are known to undergo significant functional changes, which is manifested in a decreased efficiency of oxidative phosphorylation and impaired energy metabolism of the cell. It is believed that the DMD-induced functional changes of mitochondria are mainly associated with the dysregulation of Ca2+ homeostasis. This work examines the kinetic parameters of Ca2+ transport and the opening of the Ca2+-dependent MPT pore in the skeletal-muscle mitochondria of the dystrophin-deficient C57BL/10ScSn-mdx mice. As compared to the organelles of wild-type animals, skeletal-muscle mitochondria of mdx mice have been found to be much less efficient in respect to Ca2+ uniport, with the kinetics of Na+-dependent Ca2+ efflux not changing. The data obtained indicate that the decreased rate of Ca2+ uniport in the mitochondria of mdx mice may be associated with the increased level of the dominant negative subunit of Ca2+ uniporter (MCUb). The experiments have also shown that in mdx mice, skeletal-muscle mitochondria have low resistance to the induction of MPT, which may be related to a significantly increased expression of adenylate translocator (ANT2), a possible structural element of the MPT pore. The paper discusses how changes in the expression of calcium uniporter and putative components of the MPT pore caused by the development of DMD can affect Ca2+ homeostasis of skeletal-muscle mitochondria.

Dynamic Alterations of Brain Injury, Functional Recovery, and Metabolites Profile after Cerebral Ischemia/Reperfusion in Rats Contributes to Potential Biomarkers.

Cerebral ischemia-reperfusion (I/R) is characterized by initial transient cerebral ischemia followed by reperfusion. Various pathophysiological processes are involved in brain injury and functional recovery during cerebral I/R. There are few studies on dynamic metabolic process after cerebral I/R. The present study was to observe dynamic alteration of brain injury, functional recovery, and metabolites after cerebral I/R in rats and discover potential metabolic markers. The cerebral I/R model was established by middle cerebral artery occlusion (MCAO) for 90min, following reperfusion in rats. The results of cerebral infarction area, cerebral edema, and behavior test showed that there were dynamic changes in brain injury and functional recovery at different periods after cerebral I/R. Further analysis showed that the brain injury was severe on the first day of cerebral I/R, and there was a significant functional recovery from the 7th day of cerebral I/R, followed by an aggravation trend of brain injury from the days 7 to 28. Furthermore, Matrix-assisted laser desorption ionization mass spectrometry imaging analysis showed that the expression of ATP, glucose, and citric acid on 7th day was the highest during cerebral I/R, which indicated that energy metabolism and oxidative phosphorylation played important roles during cerebral I/R. In addition, the untargeted metabolomic results showed that the level of isocitric acid, the ratio of oxyglutaric acid/glutamic acid, and the level of pyruvic acid associated with the TCA cycle were also the highest on the 7th day during cerebral I/R, which indicated that the transient spontaneous recovery of ischemic brain on the 7th day after ischemia-reperfusion might be related to oxidative phosphorylation and energy metabolism in the brain in this period. In conclusion, the results suggest that some small molecule metabolites participate in the brain injury and functional recovery during cerebral I/R, which is of great significance to the development of therapeutic drugs and diagnostic markers.

Stress responses linked to antimicrobial resistance in Acinetobacter species

Since the last 20years, bacteria of the genus Acinetobacter have been the leading cause of hospital-acquired infections. In addition to the ability of Acinetobacter species to acquire rapid antibiotic resistance, limited knowledge on the mechanisms of multidrug resistance to antibiotics limits the treatment options for such infections. Here, we present a review of cellular processes, including oxidative stress defense, energy metabolism, ppGpp signaling, toxin-antitoxin system, and quorum sensing network in Acinetobacter species and their roles in antimicrobial resistance. Although inhibition of stress responses is an attractive approach to the development of effective antimicrobial therapeutic agents, it is crucial to understand the mechanisms that cause antibiotic resistance in Acinetobacter species, as they are not as well studied as those in other pathogenic bacteria. RelA/SpoT has been shown to be involved in ppGpp synthesis in all 50 genomes of 35 Acinetobacter species. However, toxin-antitoxin (TA) systems are present in less than 30% of the 50 genomes (28/30% of SplT/A; 14/14% of HigB/A; 4/6% of HicA/B), except the RelE/B system (30/78%). These data suggested that ppGpp signaling is conserved in Acinetobacter species, but TA systems are not. This review describes our current knowledge on stress responses with respect to antibiotic resistance or tolerance in pathogenic and non-pathogenic Acinetobacter species.

Proteomic analysis and antibacterial resistance mechanisms of Salmonella Enteritidis submitted to the inhibitory effect of Origanum vulgare essential oil, thymol and carvacrol

Biological properties of natural products are an important research target and essential oils (EO) from aromatic plants with antimicrobial properties are well documented. However, their uses are limited, and the mechanisms underlying their antibacterial activity are still not well known. Therefore, our objective was to evaluate the antibacterial activities of Origanum vulgare EO, thymol and carvacrol against Salmonella Enteritidis ATCC 13076 strain, particularly regarding the bacterial proteic profile, enzymatic activities and DNA synthesis. Bacterial expressed proteins were evaluated using an untreated assay control and treatments with sublethal concentrations of oregano EO, carvacrol and thymol. The same protein extracts were also assayed for oxidative stress and energy metabolism enzyme activities, as well as effect on DNA synthesis. Protein expression outcomes revealed by 2D-SDS-PAGE, from antimicrobial actions, showed a stress response with differential expressions of chaperones and cellular protein synthesis mediated by the bacterial signaling system. In addition, Salmonella used a similar mechanism in defense against oxidative stress, for its survival. Thus, the antibacterial inhibitory activity of EO was preferentially associated with the presence of thymol and there was interference in protein regulation as well as DNA synthesis affected by these compounds. SignificanceAntimicrobial activity of essential oils (EO) is already known. In this way, the understanding of how this activity occurs is a fundamental part to provide the practical and rational use of these substances. In the current scenario, where the emergence of resistant bacteria or even multiresistant bacteria against conventional antimicrobials, the search for alternatives becomes essential, since the discovery of new inhibitory substances does not occur at the same speed. The anti-Salmonella action allied to the knowledge about the biological processes affected by O. vulgare EO contribute to these bioactive compounds being effectively used as agents in the safety and shelf life of food in a future product, packaging or process where the antibacterial activity is safe and best used.

Energy Metabolism Impairment in Migraine.

Migraine is a common disabling neurological disorder which is characterised by a recurring headache associated with a variety of sensory and autonomic symptoms. The pathophysiology of migraine remains not entirely understood, although many mechanisms involving the central and peripheral nervous system are now becoming clear. In particular, it is widely accepted that migraine is associated with energy metabolic impairment of the brain. The purpose of this review is to present an updated overview of the energy metabolism involvement in the migraine pathophysiology. Several biochemical, morphological and magnetic resonance spectroscopy studies have confirmed the presence of energy production deficiency together with an increment of energy consumption in migraine patients. An increment of energy demand over a certain threshold creates metabolic and biochemical preconditions for the onset of the migraine attack. The defect of oxidative energy metabolism in migraine is generalized. It remains to be determined if the mitochondrial deficit in migraine is primary or secondary. Riboflavin and Co-Enzyme Q10, both physiologically implicated in mitochondrial respiratory chain functioning, are effective in migraine prophylaxis, supporting the hypothesis that improving brain energy metabolism may reduce the susceptibility to migraine.

Omega-3 polyunsaturated fatty acids have beneficial effects on visceral fat in diet-induced obesity model.

This study evaluated the effects of omega-3 polyunsaturated fatty acids (PUFAs) on oxidative stress and energy metabolism parameters in the visceral fat of a high-fat-diet induced obesity model. Energy intake, body mass, and visceral fat mass were also evaluated. Male Swiss mice received either a control diet (control group) or a high-fat diet (obese group) for 6 weeks. After this period, the groups were divided into control + saline, control + omega-3, obese + saline, and obese + omega-3, and to these groups 400 mg·(kg body mass)-1·day-1 of fish oil (or saline) was administered orally, for 4 weeks. Energy intake and body mass were monitored throughout the experiment. In the 10th week, the animals were euthanized and the visceral fat (mesenteric) was removed. Treatment with omega-3 PUFAs did not affect energy intake or body mass, but it did reduced visceral fat mass. In visceral fat, omega-3 PUFAs reduced oxidative damage and alleviated changes to the antioxidant defense system and the Krebs cycle. The mitochondrial respiratory chain was neither altered by obesity nor by omega-3 PUFAs. In conclusion, omega-3 PUFAs have beneficial effects on the visceral fat of obese mice because they mitigate changes caused by the consumption of a high-fat diet.

Proteome-based identification of chicken egg yolk proteins associated with antioxidant activity on the Qinghai-Tibetan Plateau

In this study, a proteome analysis of Tibetan chicken egg yolk as well as the comparison to that of lowland chicken were performed by label-free quantitative proteomics. A total of 135 proteins were identified and abundances of 19 of these proteins were significantly different between these two groups. These differential proteins were mainly associated with oxidative stress, defense, energy metabolism and tissue development through bioinformatics analysis. To further verify the species-specific diversity of the antioxidant capacity, the antioxidative activities of egg yolk proteins were further invested in vitro and in Caco-2 cells. It was observed that both Tibetan and lowland chicken egg yolk proteins showed antioxidant activities, but the former exerted a much stronger effect. PIT54 and glutathione peroxidase 3 were considered to be antioxidant-related candidate proteins. These results provide substantial evidence for the molecular mechanisms of enhancing physical activity levels of egg yolk proteins, especially with regard to the cross-species protective mechanisms against oxidative stress.

Age-associated changes in human CD4+ T cells point to mitochondrial dysfunction consequent to impaired autophagy.

To gain understanding on the mechanisms that drive immunosenescence in humans, we examined CD4+ T cells obtained from younger (20-39 years-old) and older (70+ years-old) healthy participants of the Baltimore Longitudinal Study on Aging (BLSA). We found that mitochondrial proteins involved in the electron transport chain were overrepresented in cells from older participants, with prevalent dysregulation of oxidative phosphorylation and energy metabolism molecular pathways. Surprisingly, gene transcripts coding for mitochondrial proteins pertaining to oxidative phosphorylation and electron transport chain pathways were underrepresented in older individuals. Paralleling the observed decrease in gene expression, mitochondrial respiration was impaired in CD4+ T cells from older subjects. Though mitochondrial number in both naïve and memory cells visualized with electron microcopy was similar in older versus younger participants, there were a significantly higher number of autophagosomes, many of them containing undegraded mitochondria, in older individuals. The presence of mitochondria inside the accumulated autophagic compartments in CD4+ T cells from older individuals was confirmed by immunofluorescence. These findings suggest that older age is associated with persistence of dysfunctional mitochondria in CD4+ T lymphocytes caused by defective mitochondrial turnover by autophagy, which may trigger chronic inflammation and contribute to the impairment of immune defense in older persons.

Skeletal muscle proteome of piglets is affected in a muscle-dependent manner by a limiting total sulfur amino acid supply.

A total sulfur amino acid (TSAA) deficient diet can affect the amino acid composition of skeletal muscles. However, it is unknown how the different muscle proteins are affected by the TSAA deficiency. The proteomic profiles of the fast-twitch glycolytic longissimus (LM) and the slow-twitch oxidative rhomboideus (RM) muscles were compared in 42-day-old piglets fed either a 28% deficient (TSAA-) or a sufficient (TSAA+) diet in TSAA for 10 days. Differentially regulated proteins were identified and submitted to Gene Ontology Pathways Analysis to identify biological processes affected by TSAA deficiency. A total of 36 proteins in LM and 24 proteins in RM differed in abundance between the two dietary treatments. In both muscles, an increased oxidative energy metabolism was observed in TSAA- piglets. However, a greater mitochondrial oxidation of pyruvate generated from glycolysis was observed in LM of TSAA- piglets, whereas fatty acid β-oxidation and glycogen sparing were favored in RM. This suggests a muscle-specific reorientation of energy metabolism in response to a TSAA- deficiency. In both muscles, the protein abundance and enzyme activity of superoxide dismutase were increased in TSAA- piglets. Other enzymes involved in antioxidant defense, heat shock proteins coping with cellular stress, and annexins involved in the regulation of apoptosis were generally found to be more expressed in the LM of TSAA- piglets, with no or minor changes in RM. Skeletal muscle proteome in young growing piglets was modulated in a muscle-dependent manner by a deficient TSAA supply, with accentuated changes in fast-twitch glycolytic muscle.

The effect of Mycoplasma gallisepticum infection on energy metabolism in chicken lungs: Through oxidative stress and inflammation

Mycoplasma gallisepticum (Mg) causes chronic respiratory disease (CRD) in chickens. However, the effect of Mg infection on energy metabolism in chicken lungs is still unknown. The present study was aimed to investigate the effect of Mg infection on energy metabolism in chicken lungs. Four-weeks-old white leghorn chickens were randomly divided into control group (L1) and Mg infection group (L2). Histopathology, transmission electron microscopy, qRT-PCR and Western blot were used to determine the hallmarks of ultrastructural analysis, inflammation and energy metabolism. Results revealed that Mg infection induced oxidative stress in the chicken lungs and serum cytokine activities were enhanced at the three time points. Chickens infected with Mg revealed abnormal morphology and cellular damage including increased inflammatory cells infiltrate, cellular debris and exudate, mitochondrial and DNA damage in the lungs. The mRNA and protein expression level of inflammation-related genes were significantly increased in L2 group, showing that Mg induced inflammation in chicken lungs. In addition, ATPase activities were reduced in L2 group compared to L1 group. Meanwhile, the expression of energy metabolism related genes were decreased at both mRNA and protein level at all assessed time points, which showed that Mg infection weakened energy metabolism in chicken lungs. In summary, the data suggested that Mg infection induced oxidative stress, inflammation and energy metabolism dysfunction in the chicken lungs, exploring new therapeutic targets and providing a reference for comparative veterinary medicine.

Dietary EPA Increases Rat Mortality in Diabetes Mellitus, A Phenomenon Which Is Compensated by Green Tea Extract.

Diabetes is characterized by a high mortality rate which is often associated with heart failure. Green tea and eicosapentaenoic acid (EPA) are known to lessen some of the harmful impacts of diabetes and to exert cardio-protection. The aim of the study was to determine the effects of EPA, green tea extract (GTE), and a combination of both on the cardiac consequences of diabetes mellitus, induced in Wistar rats by injection of a low dose of streptozotocin (33 mg/kg) combined with a high fat diet. Cardiac mechanical function, coronary reactivity, and parameters of oxidative stress, inflammation, and energy metabolism were evaluated. In the context of diabetes, GTE alone limited several diabetes-related symptoms such as inflammation. It also slightly improved coronary reactivity and considerably enhanced lipid metabolism. EPA alone caused the rapid death of the animals, but this effect was negated by the addition of GTE in the diet. EPA and GTE combined enhanced coronary reactivity considerably more than GTE alone. In a context of significant oxidative stress such as during diabetes mellitus, EPA enrichment constitutes a risk factor for animal survival. It is essential to associate it with the antioxidants contained in GTE in order to decrease mortality rate and preserve cardiac function.

Alpha-calcitonin gene-related peptide prevents pressure-overload induced heart failure: role of apoptosis and oxidative stress.

Alpha‐calcitonin gene‐related peptide (α‐CGRP) is a 37‐amino acid neuropeptide that plays an important protective role in modulating cardiovascular diseases. Deletion of the α‐CGRP gene increases the vulnerability of the heart to pressure‐induced heart failure and the administration of a modified α‐CGRP agonist decreases this vulnerability. Systemic administration of α‐CGRP decreases blood pressure in normotensive and hypertensive animals and humans. Here we examined the protective effect of long‐term administration of native α‐CGRP against pressure‐overload heart failure and the likely mechanism(s) of its action. Transverse aortic constriction (TAC) was performed to induce pressure‐overload heart failure in mice. We found that TAC significantly decreased left ventricular (LV) fractional shortening, ejection fraction, and α‐CGRP content, and increased hypertrophy, dilation, and fibrosis compared to sham mice. Administration of α‐CGRP‐filled mini‐osmotic pumps (4 mg/kg bwt/day) in TAC mice preserved cardiac function and LV α‐CGRP levels, and reduced LV hypertrophy, dilation, and fibrosis to levels comparable to sham mice. Additionally, TAC pressure‐overload significantly increased LV apoptosis and oxidative stress compared to the sham mice but these increases were prevented by α‐CGRP administration. α‐CGRP administration in TAC animals decreased LV AMPK phosphorylation levels and the expression of sirt1, both of which are regulatory markers of oxidative stress and energy metabolism. These results demonstrate that native α‐CGRP is protective against pressure‐overload induced heart failure. The mechanism of this cardio‐protection is likely through the prevention of apoptosis and oxidative stress, possibly mediated by sirt1 and AMPK. Thus, α‐CGRP is a potential therapeutic agent in preventing the progression to heart failure, and the cardio‐protective action of α‐CGRP is likely the result of a direct cellular effect; however, a partial vasodilatory blood pressure‐dependent mechanism of α‐CGRP cannot be excluded.

Mitoferrin-1 is required for brain energy metabolism and hippocampus-dependent memory

Disturbed iron (Fe) ion homeostasis and mitochondrial dysfunction have been implicated in neurodegeneration. Both processes are related, because central Fe ion consuming biogenetic pathways take place in mitochondria and affect their oxidative energy metabolism. Iron is imported into mitochondria by the two homologous Fe ion importers mitoferrin-1 and mitoferrin-2. To elucidate more specifically the role of mitochondrial Fe ions for brain energy metabolism and for proper neuronal function, we generated mice with a neuron-specific knockout of mitoferrin-1 (Slc25a37−/− or mfrn-1−/−) and compared them with corresponding control littermates (mfrn-1flox/flox). Mice lacking neuronal mfrn-1 exhibited no obvious anatomical or behavioral abnormalities as neonates, young or adult animals. However, they exhibited a moderate decrease in brain mitochondrial O2-consumption with complex-I substrates of the electron transport chain (p < 0.05), indicating a moderate suppression of electron transport. While these mice did not exhibit altered basal fear levels, inquisitiveness or motor skills in specific neurobiological test batteries, they clearly exhibited decreased spatial learning skills and missing establishment of stable spatial memory in Morris water maze, as compared to floxed controls (p < 0.05). We thus conclude that mitochondrial Fe ion supply is an important player in neuronal energy metabolism and proper brain function and that the carrier mitoferrin-1 cannot be completely replaced by mitoferrin-2 or other as yet unknown Fe ion carriers.

Gene expression signatures of site-specificity in cancer metastases.

We have previously shown that metastases are generally characterized by a core program of gene expression that induces the oxidative energy metabolism, activates vascularization/tissue remodeling, silences extracellular matrix interactions, and alters ion homeostasis. This core program distinguishes metastases from their originating primary tumors as well as from their target host tissues. We hypothesized that organ preference is reflected in additional, site-selective components within the metastatic gene expression programs. Expanding our prior analysis of 653 human gene expression profiles plus data from a murine model, we find that the release from the primary tumor is associated with a suppression of functions that are important for the identity of the organ of origin, such as a down-regulation of steroid hormone responsiveness in the disseminated foci derived from prostate cancer. Metastases adjust to their target microenvironment by up-regulating-even overexpressing-genes and genetic programs that are characteristic of that organ. Finally, alterations in RNA and protein processing as well as immune deviation are common. In the clinic, metastases are mostly treated with the chemotherapy protocols devised for their primary tumors. Adjustments that account for the gene expression differences between primary and metastatic cancers have the potential to improve the currently dismal success rates.

Waterborne zinc induced lobe-dependent effect on oxidative stress and energy metabolism in hepatopancreas of Larimichthys crocea

The study aimed to compare differences in oxidative stress and energy metabolism between the left and right lobe of hepatopancreas in large yellow croaker Larimichthys crocea exposed to 0 (control), 20, and 100 μM Zn for 96 h. Tipical biomarkers were examined including the proportion of white hepatopancreas, lipid content, malondialdehyde (MDA) level, glutathione (GSH) content, activity levels of enzymes (Cu/Zn-superoxide dismutase, Cu/Zn-SOD; catalase, CAT; glutathione peroxidase, GPx; glutathione reductase, GR; mitochondrial ATP synthase, F-ATPase; malate dehydrogenase, MDH; succinate dehydrogenase, SDH; hepatic lipase, HTGL; lipoprotein lipase, LPL), mRNA levels of genes encoding these enzymes (sod1, cat, gpx1a, gr, atp5b, mdh, sdh, htgl, and lpl), and gene expression of signaling molecules the NF-E2-related nuclear factor 2 (nrf2) and Kelch-like ECH-associated protein 1 (keap1). A whitish color in the left lobe of hepatopancreas was observed in the control and Zn-exposed fish. Contrarily, the right lobe of hepatopancreas tended towards red with increasing Zn levels. The phenomenon was further confirmed by that lipid content was reduced in the right lobe and was not significantly affected in the left lobe by Zn. The right lobe showed higher energy consumption than the left lobe as reflected by the up-regulation of activity levels of HTGL, LPL, F-ATPase, MDH, and SDH. Lipid peroxidation declined by 20 μM Zn and was unchanged by 100 μM Zn in both lobes, which could be explained by increased activity levels of Cu/Zn-SOD and GPx. However, the magnitude of increase in Cu/Zn-SOD activity was greater in the right lobe than that in the left one. The difference in enzyme activity between two lobes may be involved in changes in mRNA levels of sod1, gr, atp5b, sdh, htgl, lpl, and nrf2, which was further confirmed by positive relationships between enzyme activity and gene expression. Our data also showed positive correlations between nrf2 expression and mRNA levels of its target genes, suggesting that Nrf2 was required for the protracted induction of these genes. Our results demonstrated the potential molecular mechanism of Zn-induced differences between lobes of hepatopancreas, suggesting that the sampling part of hepatopancreas should be considered with caution when assessing metal contamination.

Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen.

Hydrogen sulfide (H2S) is one of the main pollutants in the atmosphere, which is a serious threat to human health. The decomposition of sulfur-containing organics in chicken houses could produce a large amount of H2S, thereby damaging poultry health. In this study, one-day-old broilers were selected and exposed to 4 or 20 ppm of H2S gas (0-3 weeks: 4 ± 0.5 ppm, 4-6 weeks: 20 ± 0.5 ppm). The spleen samples were collected immediately after the chickens were euthanized at 2, 4, and 6 weeks. The histopathological and ultrastructural observations showed obvious necrosis characteristics of H2S-exposed spleens. H2S exposure suppressed GSH, CAT, T-AOC, and SOD activities; increased NO, H2O2, and MDA content and iNOS activity; and induced oxidative stress. ATPase activities and the expressions of energy metabolism-related genes were significantly decreased. Also, the expressions of related necroptosis (RIPK1, RIPK3, MLKL, TAK1, TAB2, and TAB3) were significantly increased, and the MAPK pathway was activated. Besides, H2S exposure activated the NF-κB classical pathway and induced TNF-α and IL-1β release. Taken together, we conclude that H2S exposure induces oxidative stress and energy metabolism dysfunction; evokes necroptosis; activates the MAPK pathway, eventually triggering the NF-κB pathway; and promotes inflammatory response in chicken spleens.

Physiology and proteomics of two maize genotypes with different drought resistance

The aim of this study was to investigate the physiological basis and molecular mechanism of genotypic variation in drought response of maize seedlings. Comparative physiological and proteomic analyses were conducted in the leaves of drought-tolerant Liyu 35 (LY) and drought-sensitive Denghai 605 (DH) maize genotype seedlings. Drought induced a significant decrease of relative water content and osmotic potential of leaves, length and volume of roots, and total dry weight, but significantly increased malondialdehyde in DH seedlings. However, root dry weight , proline content and antioxidant enzyme activities increased more in LY than in DH. Forty-two spots in LY and 17 spots in DH that showed significant abundance variations were identified by matrix-assisted laser desorption/ionization time-of-flight/time-of-flight mass spectrometry. These drought-responsive proteins were mainly involved in biological processes of photosynthesis, defense and oxidative stress, carbohydrate and energy metabolism, protein synthesis and processing, and cell wall biogenesis and degradation. Among them, proteins involved in defense and oxidative stress, and protein synthesis and processing were largely enriched in the LY genotype, which may contribute to a natural variation of drought resistance between LY and DH genotypes. The altered protein abundance and corresponding physiological-biochemical response shed some light on molecular mechanisms related to drought tolerance in drought-tolerant maize and provide key candidate proteins for genetic improvement of maize.

Effects of triclosan on early development of Solea senegalensis: from biochemical to individual level

Harmful effects of triclosan (TCS) have been reported on several organisms; however, effects on early life stages of marine vertebrates are limited. Therefore, the objective of this work was to assess the effects of TCS during early development of the flatfish Solea senegalensis after initial characterization of cholinesterases (ChEs) and determination of selected biochemical markers baseline levels.Characterization of ChEs and determination of biochemical markers baseline levels of cholinergic activity, energy metabolism and oxidative stress were analysed in sole at 3 days after hatching (dah) and at the onset and end of metamorphosis. To assess TCS effects, fish were exposed during 96h to 30-500 μg L−1 TCS until 3 dah. Fish at 13 dah were exposed during 48h to 200-1,500 μg L−1 TCS and maintained until complete metamorphosis. Effects on survival, malformations, length, metamorphosis progression and biochemical markers were evaluated.The main ChE active form present in sole early life stages is acetylcholinesterase and baseline levels of oxidative stress and energy metabolism biomarkers changed according to fish developmental stage. Triclosan induced malformations (EC50 = 180 μg L−1 at 3 dah), decreased growth (95 μg L−1 at 3 dah; 548 μg L−1 at 24 dah) and affected metamorphosis progression (391 μg L−1 at 17 dah). Impairment of antioxidant system was observed, with TCS affecting catalase at the end of metamorphosis test, however, no oxidative damage on lipids was detected. Glutathione S-transferase was the most sensitive endpoint during early larval test (LOEC = 30 μg L−1).Exposure to TCS affected S. senegalensis at individual and sub-individual levels, both at early larval stage and during the critical period of metamorphosis.

Photobiomodulation rescues cognitive flexibility in early stressed subjects

Neglectful parenting is one of the most prevalent forms of child mistreatment. This early life stress leads to long-term alterations in all the psychological domains, as well as brain alterations. Animal models have been developed to emulate and further study this early life stress, and one of most widely used models is maternal separation. In both human and animal models, cognitive flexibility has been found to be altered. In this study, we performed maternal separation (10 days, 4 h per day) in rats, and in adulthood, we tested their spatial navigation and cognitive flexibility. In addition, we delivered photobiomodulation treatment (Low-level light therapy: 1064 nm, 30 mW, 60 cycles) on the rats’ brains, and we tested energy oxidative metabolism using cytochrome c oxidase histochemistry. Early life stress delivered in the form of maternal separation on the first 10 postnatal days leads to cognitive flexibility impairment and a general increase in energy metabolism in adulthood. Low-level light therapy seems to be useful for treating these unwanted outcomes, because it rescued cognitive flexibility and returned the oxidative energy metabolism to balanced scores, without harming controls’ brains or behavior. Photobiomodulation is a promising tool in the treatment of chronic stress-related consequences because it rescued cognitive flexibility.

Proteomic profiles during adventitious rooting of Eucalyptus species relevant to the cellulose industry

Adventitious rooting (AR) is an obligatory step for vegetative propagation of commercial woody species. Paper industries have interest in Eucalyptus globulus Labill and its hybrids due to low lignin and lipid contents, which facilitate cellulose extraction. However, this species and some of its hybrids are recalcitrant to rooting, often requiring exogenous auxin supply. Here we performed a comparative analysis of proteome changes during AR of E. globulus and the easy-to-root species Eucalyptus grandis W. Hill and the effects of exogenous auxin in different phases of the process (induction and formation), using a label-free quantification method. We identified 398 differentially abundant proteins, which were predicted to be involved in different biological pathways, mainly oxidative stress, energy metabolism and photosynthesis. Notable differences between species included proteins involved in oxidative stress, carbon and secondary metabolism. Exogenous auxin appeared to affect the availability of carbon sources and other phytohormones, besides cell cycle and microtubule—related proteins. Important players were also identified in each phase of AR. This is the first in depth analysis of protein changes during AR in Eucalyptus. The findings can be used in future studies to evaluate rooting competence in different genotypes and provide leads for AR improvement.