Non-enzymatic Mechanisms Research Articles

OXIDATIVE STRESS AND THE STATE OF ANTIOXIDANT DEFENCES IN HEMORRHAGIC FEVER WITH RENAL SYNDROME

Abstract: Hemorrhagic fever with renal syndrome (HFRS) is zoonotic viral disease with domination of the destabilization of cell membranes in the pathogenesis. An increase in lipid peroxidation is important in membrane damage. Circulating lipid peroxidation products affect the cell membranes of the vascular endothelium, early damage to which by the HFRS virus inevitably leads to vascular dysfunction with marked disturbance of microcirculation processes and development of organ and tissue hypoxia. The manifestation of the damaging effects of peroxide compounds is prevented by a complex system that diminishes the formation of peroxides and provides its breaking. The antioxidant system includes both enzymatic and non-enzymatic mechanisms to protect cells and subcellular structures. Therefore, at the same time study of the mechanism of the development of primary (initial) links of lipid peroxidation and dynamics of antioxidant system work in HFRS allows using more effective therapy of this severe viral infection, aimed at reducing lipid peroxidation processes and improving the quality of antioxidant system work. The aim of this study is to investigate the rate of primary lipid peroxidation processes in HFRS using the example of changes in the concentration of primary lipid peroxidation products: diene conjugates and diene ketones, and the functioning of the body's antioxidant system using the example of superoxide dismutase as the first line of defence. For a more complete evaluation of the primary lipid peroxidation processes the KDC coefficient, the ratio of diene conjugate concentrations to diene ketones, was introduced. This coefficient shows how the rate of the initial lipid peroxidation processes changes, namely the change in the concentration of diene conjugates and its further transformation to diene ketones. From the change in this coefficient, we could consider the course of the disease. When the KDC coefficient decreased, there was an increase in superoxide dismutase activity, which was accompanied by a reduction in clinical manifestations and improvement in the well-being of the patients. In the case of an increase in the KDC ratio, the activity of superoxide dismutase increases slightly, indicating an increase in the rate of the initial lipid peroxidation processes and further cell membrane damage. It seems to be associated with more severe complications that occur in the presence of some associated diseases.

Biostimulant Capacity of an Enzymatic Extract From Rice Bran Against Ozone-Induced Damage in Capsicum annum.

Ozone is a destructive pollutant, damaging crops, and decreasing crop yield. Therefore, there is great interest in finding strategies to alleviate ozone-induced crop losses. In plants, ozone enters leaves through the stomata and is immediately degraded into reactive oxygen species (ROS), producing ROS stress in plants. ROS stress can be controlled by ROS-scavenging systems that include enzymatic or non-enzymatic mechanisms. Our research group has developed a product from rice bran, a by-product of rice milling which has bioactive molecules that act as an antioxidant compound. This product is a water-soluble rice bran enzymatic extract (RBEE) which preserves all the properties and improves the solubility of proteins and the antioxidant components of rice bran. In previous works, the beneficial properties of RBEE have been demonstrated in animals. However, to date, RBEE has not been used as a protective agent against oxidative damage in agricultural fields. The main goal of this study was to investigate the ability of RBEE to be used as a biostimulant by preventing oxidative damage in plants, after ozone exposure. To perform this investigation, pepper plants (Capsicum annuum) exposed to ozone were treated with RBEE. RBEE protected the ozone-induced damage, as revealed by net photosynthetic rate and the content of photosynthetic pigments. RBEE also decreased the induction of antioxidant enzyme activities in leaves (catalase, superoxide dismutase, and ascorbate peroxidase) due to ozone exposure. ROS generation is a common consequence of diverse cellular traumas that also activate the mitogen-activated protein kinase (MAPK) cascade. Thus, it is known that the ozone damages are triggered by the MAPK cascade. To examine the involvement of the MAPK cascade in the ozone damage CaMPK6-1, CaMPK6-2, and CaMKK5 genes were analyzed by qRT-PCR. The results showed the involvement of the MAPK pathway in both, not only in ozone damage but especially in its protection by RBEE. Taken together, these results support that RBEE protects plants against ozone exposure and its use as a new biostimulant could be proposed.

Genotype-dependent and temperature-induced modulation of secondary metabolites, antioxidative defense and gene expression profile in Solanum viarum Dunal

The medicinal plant, Solanum viarum Dunal includes a number of compounds with important pharmacological effects. The effect of temperature (heat and cold) stress on growth, secondary metabolite levels and defense mechanism in two genotypes (prickled and prickleless) of S. viarum was evaluated. The two thermal regimes (4 °C for cold and 35 °C for heat stress) were found to be the most optimum for the accumulation of metabolites (steroidal alkaloids and glycoalkaloids, phenolic acids as well as flavonoids). Prickleless genotype showed 4.08 and 1.51 fold higher total alkaloids/glycoalkaloid content at 35 °C and 4 °C temperatures respectively, in comparison with prickled plants. Prickleless plants also registered 2.03 and 2.28 higher fresh and dry biomass accumulation respectively, under cold stress over the control plants. The accretion of phenolic and flavonoid compounds under heat and cold stress is mainly contributed by gallic and ferulic acid in both the genotypes. The quantitative real-time PCR expression analysis showed the abundance of gene transcript involve in the biosynthesis of alkaloids/glycoalkaloid and phenolics/flavonoids that corroborates with the accumulation of their respective metabolites in prickleless plants under temperature stress. Results revealed that the prickleless plants inhibiting the reactive oxygen species (ROS) mediated oxidative damage by activating the enzymatic (superoxide dismutase, peroxidase, catalase and ascorbate peroxidase) and non-enzymatic (alkaloids, phenols, flavonoids, carotenoids and proline) antioxidants mechanism that confirms its efficiency to tolerate thermal stress under both the thermal regimes. The overall result showed that the prickleless genotype served as a better accumulator of biomass, secondary metabolites with an improved antioxidative mechanism in comparison to prickled genotype. Our findings suggest that thermal stress responses differ significantly between genotypes, emphasizing the necessity of maintaining genotypic diversity in adaptive evolution as in the context of global warming and climate change. The present study also opens the possibility of exploiting improved prickleless genotype of S. viarum as a potential system that can be cultivated under different temperature stress conditions to attain the phytopharmaceutical benefits.

Manganese-Oxidizing Antarctic Bacteria (Mn-Oxb) Release Reactive Oxygen Species (ROS) as Secondary Mn(II) Oxidation Mechanisms to Avoid Toxicity.

Simple SummaryManganese (Mn)-oxidizing bacteria (MnOxb) are an essential group of microorganisms that oxidize soluble Mn(II) to form precipitate Mn(III) minerals, playing a crucial role in soil formation. The Fildes Peninsula is one of the fastest-warming areas globally and, therefore, the maritime Antarctic soils from this pivotal location allow for the examination of the effect of temperature on bacterial communities. The temperature causes an increase in the microbial respiratory rate, producing reactive oxygen species (ROS), which are harmful to bacteria. We evaluate an evasive secondary non-enzymatic mechanism for ROS production under increasing temperature in MnOxb isolated from Antarctic soils. Bacteria produce ROS capable of oxidizing Mn(II) as temperature increases, contributing to the enzymatic pathway protecting microbial cells from Mn(II) toxicity. In addition, we determine that certain strains, such as Arthobacter oxydans, can use these ROS as mechanisms to protect themselves from Mn toxicity at high concentrations. In conclusion, we describe a secondary mechanism of Mn(II) oxidation in bacterial strains of Antarctic soils.Manganese (Mn) oxidation is performed through oxidative Mn-oxidizing bacteria (MnOxb) as the main bio-weathering mechanism for Mn(III/IV) deposits during soil formation. However, with an increase in temperature, the respiration rate also increases, producing Reactive Oxygen Species (ROS) as by-products, which are harmful to microbial cells. We hypothesize that bacterial ROS oxidize Mn(II) to Mn(III/IV) as a secondary non-enzymatic temperature-dependent mechanism for cell protection. Fourteen MnOxb were isolated from Antarctic soils under the global warming effect, and peroxidase (PO) activity, ROS, and Mn(III/IV) production were evaluated for 120 h of incubation at 4 °C, 15 °C, and 30 °C. ROS contributions to Mn oxidation were evaluated in Arthrobacter oxydans under antioxidant (Trolox) and ROS-stimulated (menadione) conditions. The Mn(III/IV) concentration increased with temperature and positively correlated with ROS production. ROS scavenging with Trolox depleted the Mn oxidation, and ROS-stimulant increased the Mn precipitation in A. oxydans. Increasing the Mn(II) concentration caused a reduction in the membrane potential and bacterial viability, which resulted in Mn precipitation on the bacteria surface. In conclusion, bacterial ROS production serves as a complementary non-enzymatic temperature-dependent mechanism for Mn(II) oxidation as a response in warming environments.

Cardiac Oxidative Stress and the Therapeutic Approaches to the Intake of Antioxidant Supplements and Physical Activity.

Reactive oxygen species (ROS) are strongly reactive chemical entities that include oxygen regulated by enzymatic and non-enzymatic antioxidant defense mechanisms. ROS contribute significantly to cell homeostasis in the heart by regulating cell proliferation, differentiation, and excitation-contraction coupling. When ROS generation surpasses the ability of the antioxidant defense mechanisms to buffer them, oxidative stress develops, resulting in cellular and molecular disorders and eventually in heart failure. Oxidative stress is a critical factor in developing hypoxia- and ischemia-reperfusion-related cardiovascular disorders. This article aimed to discuss the role of oxidative stress in the pathophysiology of cardiac diseases such as hypertension and endothelial dysfunction. This review focuses on the various clinical events and oxidative stress associated with cardiovascular pathophysiology, highlighting the benefits of new experimental treatments such as creatine supplementation, omega-3 fatty acids, microRNAs, and antioxidant supplements in addition to physical exercise

Silicon Improves the Redox Homeostasis to Alleviate Glyphosate Toxicity in Tomato Plants-Are Nanomaterials Relevant?

Given the widespread use of glyphosate (GLY), this agrochemical is becoming a source of contamination in agricultural soils, affecting non-target plants. Therefore, sustainable strategies to increase crop tolerance to GLY are needed. From this perspective and recalling silicon (Si)’s role in alleviating different abiotic stresses, the main goal of this study was to assess if the foliar application of Si, either as bulk or nano forms, is capable of enhancing Solanum lycopersicum L. tolerance to GLY (10 mg kg−1). After 28 day(s), GLY-treated plants exhibited growth-related disorders in both shoots and roots, accompanied by an overproduction of superoxide anion (O2•−) and malondialdehyde (MDA) in shoots. Although plants solely exposed to GLY have activated non-enzymatic antioxidant mechanisms (proline, ascorbate and glutathione), a generalized inhibition of the antioxidant enzymes was found, suggesting the occurrence of great redox disturbances. In response to Si or nano-SiO2 co-application, most of GLY phytotoxic effects on growth were prevented, accompanied with a better ROS removal, especially by an upregulation of the main antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX). Overall, results pointed towards the potential of both sources of Si to reduce GLY-induced oxidative stress, without major differences between their efficacy.

How Do Shipworms Eat Wood? Screening Shipworm Gill Symbiont Genomes for Lignin-Modifying Enzymes.

Shipworms are ecologically and economically important mollusks that feed on woody plant material (lignocellulosic biomass) in marine environments. Digestion occurs in a specialized cecum, reported to be virtually sterile and lacking resident gut microbiota. Wood-degrading CAZymes are produced both endogenously and by gill endosymbiotic bacteria, with extracellular enzymes from the latter being transported to the gut. Previous research has predominantly focused on how these animals process the cellulose component of woody plant material, neglecting the breakdown of lignin – a tough, aromatic polymer which blocks access to the holocellulose components of wood. Enzymatic or non-enzymatic modification and depolymerization of lignin has been shown to be required in other wood-degrading biological systems as a precursor to cellulose deconstruction. We investigated the genomes of five shipworm gill bacterial symbionts obtained from the Joint Genome Institute Integrated Microbial Genomes and Microbiomes Expert Review for the production of lignin-modifying enzymes, or ligninases. The genomes were searched for putative ligninases using the Joint Genome Institute’s Function Profile tool and blastp analyses. The resulting proteins were then modeled using SWISS-MODEL. Although each bacterial genome possessed at least four predicted ligninases, the percent identities and protein models were of low quality and were unreliable. Prior research demonstrates limited endogenous ability of shipworms to modify lignin at the chemical/molecular level. Similarly, our results reveal that shipworm bacterial gill-symbiont enzymes are unlikely to play a role in lignin modification during lignocellulose digestion in the shipworm gut. This suggests that our understanding of how these keystone organisms digest and process lignocellulose is incomplete, and further research into non-enzymatic and/or other unknown mechanisms for lignin modification is required.

New insights into the mechanisms of age-related protein-protein crosslinking in the human lens

Although protein crosslinking is often linked with aging as well as some age-related diseases, very few molecular details are available on the nature of the amino acids involved, or mechanisms that are responsible for crosslinking. Recent research has shown that several amino acids are able to generate reactive intermediates that ultimately lead to covalent crosslinking through multiple non-enzymatic mechanisms. This information has been derived from proteomic investigations on aged human lenses and the mechanisms of crosslinking, in each case, have been elucidated using model peptides. Residues involved in spontaneous protein-protein crosslinking include aspartic acid, asparagine, cysteine, lysine, phosphoserine, phosphothreonine, glutamic acid and glutamine. It has become clear, therefore, that several amino acids can act as potential sites for crosslinking in the long-lived proteins that are present in aged individuals. Moreover, the lens has been an invaluable model tissue and source of crosslinked proteins from which to determine crosslinking mechanisms that may lead to crosslinking in other human tissues.

Analysis of antioxidant response in pomelo fruitlets subjected to external injury stress: Significance of naringin biosynthesis

We simulated 2 types of external injuries in fruitlets—throwing and cutting with knife, and evaluated the degree of putrefaction. The external injury-induced toxicity was determined by observing changes in the spatial structure of the cells. Next, we determined the contents of lignin and total flavonoids, and the expression of phenylpropanoid pathway-related genes encoding enzymes that alleviate peroxidation toxicity. By measuring the content of naringin, we uncovered a non-enzymatic antioxidant mechanism that eliminates excessive reactive oxygen species (ROS) in fruitlets. We also determined that external injury triggers an increased activity of antioxidant enzymes. Overall, in fruitlets, external injuries activate naringin biosynthesis in response to stress.

Apoptotic DNase network: Mutual induction and cooperation among apoptotic endonucleases.

DNA fragmentation produced by apoptotic DNases (endonucleases) leads to irreversible cell death. Although apoptotic DNases are simultaneously induced following toxic/oxidative cell injury and/or failed DNA repair, the study of DNases in apoptosis has generally been reductionist in approach, focusing on individual DNases rather than their possible cooperativity. Coordinated induction of DNases would require a mechanism of communication; however, mutual DNase induction or activation of DNases by enzymatic or non‐enzymatic mechanisms is not currently recognized. The evidence presented in this review suggests apoptotic DNases operate in a network in which members induce each other through the DNA breaks they produce. With DNA breaks being a common communicator among DNases, it would be logical to propose that DNA breaks from other sources such as oxidative DNA damage or actions of DNA repair endonucleases and DNA topoisomerases may also serve as triggers for a cooperative DNase feedback loop leading to elevated DNA fragmentation and subsequent cell death. Therefore, mutual induction of apoptotic DNases has serious implications for studies focused on activation or inhibition of specific DNases as a strategy for therapeutic intervention aimed at modulation of cell death.

Toxic effect of antidepressants on male reproductive system cells: evaluation of possible fertility reduction mechanism.

Depression is acknowledged as a major public health problem. Pharmacological treatment may cause adverse drug reactions and sexual side effects. At the same time, the knowledge of the molecular mechanisms associated with antidepressant-mediated toxicity to reproductive cells is fragmentary. The aim of this study was the multilevel evaluation of the potential toxicity of several antidepressants or antipsychotic drugs (amitriptyline, 10 μM; escitalopram, 30 μM; fluoxetine, 5 μM; imipramine, 20 μM; mirtazapine, 150 μM; olanzapine, 40 μM; reboxetine, 30 μM; venlafaxine, 250 μM) on the cells of the spermatogenesis pathway. Effects of various drugs were monitored by several methods including mitochondrial activity MTT test, fluorescent staining, real-time PCR, morphology analysis, immunofluorescence, and Western blots. Obtained results suggest the concentration- and the time-dependent cytotoxic effect. The molecular mechanism of cytotoxic effect is mediated by disturbances in the redox balance (increased production of reactive oxygen species and reactive nitrogen species), failure of enzymatic and non-enzymatic cell protection mechanisms (glutathione system, nuclear factor-κB and fibroblast growth factor 2-mediated pathways), and impairment of mitochondrial functions. In addition, we provide for the first time, to our knowledge, evidence that antidepressant treatment may contribute to spindle apparatus assembly defects and organelle distribution during cell division in vitro (alterations in the levels of small C terminal domain phosphatase-1 and -3, NuMa, and calnexin protein levels). This study sheds new light on the pathomechanisms of antidepressants action and their associated toxicity towards the reproductive system, emerging issues linked with animal or human reproductive health, and treatment of mood disorders.

The crucial role of non-enzymatic NO-production in plants. An EPR study

Polyamines and polyamides have a fundamental role in the biology of plants, and the presence of NO seems compulsory to account for their actions. In general, the NO production has claimed to occur through an enzymatic process, but not involving polyamines and polyamides. Nevertheless, a non-enzymatic mechanism, such as an electron transfer process among polyamines or polyamides and an acid nitrite solution, could account for rapid production of NO, even in anoxic conditions. EPR experiments, carried out with these substrates, proved the formation of NO. This evidence supports a non-enzymatic mechanism as an alternative source of NO, even in plants. So, since the NO production seems directly dependent on polyamines or polyamides presence, and these responsible for many activities in plants, it comes plausibly to consider crucial the involvement of NO in their actions. Furthermore, as for mammals, these results would confirm that, even in plants, NO production can occur through both enzymatic and non-enzymatic mechanisms.

What the Wild Things Do: Mechanisms of Plant Host Manipulation by Bacterial Type III-Secreted Effector Proteins.

Phytopathogenic bacteria possess an arsenal of effector proteins that enable them to subvert host recognition and manipulate the host to promote pathogen fitness. The type III secretion system (T3SS) delivers type III-secreted effector proteins (T3SEs) from bacterial pathogens such as Pseudomonas syringae, Ralstonia solanacearum, and various Xanthomonas species. These T3SEs interact with and modify a range of intracellular host targets to alter their activity and thereby attenuate host immune signaling. Pathogens have evolved T3SEs with diverse biochemical activities, which can be difficult to predict in the absence of structural data. Interestingly, several T3SEs are activated following injection into the host cell. Here, we review T3SEs with documented enzymatic activities, as well as T3SEs that facilitate virulence-promoting processes either indirectly or through non-enzymatic mechanisms. We discuss the mechanisms by which T3SEs are activated in the cell, as well as how T3SEs modify host targets to promote virulence or trigger immunity. These mechanisms may suggest common enzymatic activities and convergent targets that could be manipulated to protect crop plants from infection.

A distinct non-enzymatic role for Indoleamine-2,3-dioxygenase (IDO)2 vs. IDO1 in autoimmune arthritis

Abstract IDO1 and IDO2 are closely related immune modulating enzymes encoded by linked genes. Whereas IDO1 is best known for its immunoregulatory role in tumor immune evasion, IDO2 acts as a proinflammatory effector of B cell-mediated autoimmunity. Given their opposing roles in inflammatory responses, interpretation of results obtained using IDO1 or IDO2 single knockout (ko) mice have been complicated by the expression of the other enzyme. Using single and double knockout (dko) mice and the KRN arthritis model, we distinguished differential roles for IDO1 and IDO2 in autoreactive B vs. T cell responses driving arthritis. Both autoreactive T and B cell responses and severity of arthritis were decreased in IDO2, but not IDO1, ko mice. Despite a similar attenuation of disease, only autoreactive B cell responses were reduced in dko mice, demonstrating that IDO2 directly mediates autoreactive B cell responses, while autoreactive T cell responses are indirectly affected by IDO1. Like IDO1, IDO2 was originally identified as a tryptophan catabolizing enzyme. However, we recently showed that the enzymatic activity of IDO2 is not required to drive arthritis. To define the non-enzymatic mechanism mediating IDO2 function, we identified IDO2-interacting proteins using a yeast two-hybrid screen. Specific interaction between IDO2, but not IDO1, and several candidate proteins was confirmed using overexpressing cell lines and co-IP/Western. Using site-directed mutagenesis and an in vitro IDO2-expression model, we identified potential regions outside of the catalytic site on IDO2 that mediate these interactions, providing the first evidence for the non-enzymatic mechanism by which IDO2 mediates proinflammatory B cell responses.

Multi-omics analysis provides insights into lignocellulosic biomass degradation by Laetiporus sulphureus ATCC 52600

BackgroundWood-decay basidiomycetes are effective for the degradation of highly lignified and recalcitrant plant substrates. The degradation of lignocellulosic materials by brown-rot strains is carried out by carbohydrate-active enzymes and non-enzymatic Fenton mechanism. Differences in the lignocellulose catabolism among closely related brown rots are not completely understood. Here, a multi-omics approach provided a global understanding of the strategies employed by L. sulphureus ATCC 52600 for lignocellulose degradation.ResultsThe genome of Laetiporus sulphureus ATCC 52600 was sequenced and phylogenomic analysis supported monophyletic clades for the Order Polyporales and classification of this species within the family Laetiporaceae. Additionally, the plasticity of its metabolism was revealed in growth analysis on mono- and disaccharides, and polysaccharides such as cellulose, hemicelluloses, and polygalacturonic acid. The response of this fungus to the presence of lignocellulosic substrates was analyzed by transcriptomics and proteomics and evidenced the occurrence of an integrated oxidative–hydrolytic metabolism. The transcriptomic profile in response to a short cultivation period on sugarcane bagasse revealed 125 upregulated transcripts, which included CAZymes (redox enzymes and hemicellulases) as well as non-CAZy redox enzymes and genes related to the synthesis of low-molecular-weight compounds. The exoproteome produced in response to extended cultivation time on Avicel, and steam-exploded sugarcane bagasse, sugarcane straw, and Eucalyptus revealed 112 proteins. Contrasting with the mainly oxidative profile observed in the transcriptome, the secretomes showed a diverse hydrolytic repertoire including constitutive cellulases and hemicellulases, in addition to 19 upregulated CAZymes. The secretome induced for 7 days on sugarcane bagasse, representative of the late response, was applied in the saccharification of hydrothermally pretreated grass (sugarcane straw) and softwood (pine) by supplementing a commercial cocktail.ConclusionThis study shows the singularity of L. sulphureus ATCC 52600 compared to other Polyporales brown rots, regarding the presence of cellobiohydrolase and peroxidase class II. The multi-omics analysis reinforces the oxidative–hydrolytic metabolism involved in lignocellulose deconstruction, providing insights into the overall mechanisms as well as specific proteins of each step.

Sirtuin 2 Regulates Protein LactoylLys Modifications.

Post-translational modifications (PTMs) play roles in both physiological and pathophysiological processes through the regulation of enzyme structure and function. We recently identified a novel PTM, lactoylLys, derived through a nonenzymatic mechanism from the glycolytic by-product, lactoylglutathione. Under physiologic scenarios, glyoxalase 2 prevents the accumulation of lactoylglutathione and thus lactoylLys modifications. What dictates the site-specificity and abundance of lactoylLys PTMs, however, remains unknown. Here, we report sirtuin 2 as a lactoylLys eraser. Using chemical biology and CRISPR-Cas9, we show that SIRT2 controls the abundance of this PTM both globally and on chromatin. These results address a major gap in our understanding of how nonenzymatic PTMs are regulated and controlled.

High-Intensity Interval Training Remodels the Proteome and Acetylome of Human Skeletal Muscle

Exercise is an effective strategy in the prevention and treatment of metabolic diseases. Alterations in the skeletal muscle proteome, including post-translational modifications, regulate its metabolic adaptations to exercise. Here, we examined the effect of high-intensity interval training (HIIT) on the proteome and acetylome of human skeletal muscle, revealing the response of 3168 proteins and 1263 lysine acetyl-sites on 464 acetylated proteins. We identified global protein adaptations to exercise training involved in metabolism, excitation-contraction coupling, and myofibrillar calcium sensitivity. Furthermore, HIIT increased the acetylation of mitochondrial proteins, particularly those of complex V, likely via non-enzymatic mechanisms. We also highlight the regulation of exercise-responsive histone acetyl-sites. These data demonstrate the plasticity of the skeletal muscle proteome and acetylome, providing insight into the regulation of contractile, metabolic and transcriptional processes within skeletal muscle. Herein, we provide a substantial hypothesis-generating resource to stimulate further mechanistic research investigating how exercise improves metabolic health.

Lipid Metabolism and Ferroptosis

Simple SummaryFerroptosis is a type of cell death, which is morphologically and mechanistically distinct from other type of cell death pathways such as apoptosis and necroptosis. Lipid peroxidation is a hallmark of ferroptosis and directly destroys cellular membranes, thereby causing ferroptosis. Since lipid peroxidation, which induces ferroptosis, occurs in polyunsaturated fatty acid on specific phospholipids, various lipid metabolic pathways are involved in lipid peroxidation and ferroptosis. Besides, various metabolic and signaling pathways directly and indirectly regulate lipid peroxidation and ferroptosis. Since ferroptosis is associated with a variety of human diseases such as cancer, myocardial infarction, atherosclerosis, kidney diseases, liver diseases, and neuronal diseases, a better understanding of the regulatory mechanisms of ferroptosis can provide insights and treatment strategies for related diseases.Ferroptosis is a type of iron-dependent regulated necrosis induced by lipid peroxidation that occurs in cellular membranes. Among the various lipids, polyunsaturated fatty acids (PUFAs) associated with several phospholipids, such as phosphatidylethanolamine (PE) and phosphatidylcholine (PC), are responsible for ferroptosis-inducing lipid peroxidation. Since the de novo synthesis of PUFAs is strongly restricted in mammals, cells take up essential fatty acids from the blood and lymph to produce a variety of PUFAs via PUFA biosynthesis pathways. Free PUFAs can be incorporated into the cellular membrane by several enzymes, such as ACLS4 and LPCAT3, and undergo lipid peroxidation through enzymatic and non-enzymatic mechanisms. These pathways are tightly regulated by various metabolic and signaling pathways. In this review, we summarize our current knowledge of how various lipid metabolic pathways are associated with lipid peroxidation and ferroptosis. Our review will provide insight into treatment strategies for ferroptosis-related diseases.

Nanoparticles as elicitors and harvesters of economically important secondary metabolites in higher plants: A review.

Nanoparticles possess some unique properties which improve their biochemical reactivity. Plants, due to their stationary nature, are constantly exposed to nanoparticles present in the environment, which act as abiotic stress agents at sub‐toxic concentrations and phytotoxic agents at higher concentrations. In general, nanoparticles exert their toxicological effect by the generation of reactive oxygen species to which plants respond by activating both enzymatic and non‐enzymatic anti‐oxidant defence mechanisms. One important manifestation of the defence response is the increased or de novo biosynthesis of secondary metabolites, many of which have commercial application. The present review extensively summarizes current knowledge about the application of different metallic, non‐metallic and carbon‐based nanoparticles as elicitors of economically important secondary metabolites in different plants, both in vivo and in vitro. Elicitation of secondary metabolites with nanoparticles in plant cultures, including hairy root cultures, is discussed. Another emergent technology is the ligand‐harvesting of secondary metabolites using surface‐functionalized nanoparticles, which is also mentioned. A brief explanation of the mechanism of action of nanoparticles on plant secondary metabolism is included. Optimum conditions and parameters to be evaluated and standardized for the successful commercial exploitation of this technology are also mentioned.

Physiological responses and phytoremediation capability of Avicennia marina to oil contamination

The impact of oil pollution on coastal vulnerable ecosystems has been a major concern especially, in the Persian Gulf area. The current study was carried out to assess to what extent Avicennia marina can tolerate oil contamination and degrade crude oil polycyclic aromatic hydrocarbons (PAHs) from rhizosphere soil. Seeds of A. marina were grown in control and crude oil-contaminated (2.5, 5.0, 7.5, and 10% w/w) soil under ambient greenhouse conditions. Four-month-old plants were collected, measured for their biometry, and assayed for physiological characteristics in relation to degradation of PAHs. A. marina exposed to petroleum responded by allocating proportionally more biomass to root than shoot, activating enzymatic and non-enzymatic antioxidative mechanisms and removing of PAHs, particularly in lower concentrations of crude oil in the soil. The content of total PAHs in A. marina rhizosphere soil, grown on 2.5, 5.0, 7.5 and 10% oil-treated soils were, respectively, 37 ± 0.4, 21.84 ± 0.27, 12.78 ± 0.11 and 14.74 ± 0.03% lower than non-rhizosphere soil. Comparison of PAHs content of rhizospheric and non-rhizospheric soil also indicated that the highest rate of PAH removal was for acenaphthene (74.63 ± 0.78) in control, fluoranthene (71.18 ± 0.56) in 2.5%, and anthracene (69.45 ± 6.33, 55.66 ± 4.38 and 35.97 ± 0.22) in 5.0, 7.5 and 10% oil-contaminated soil and acenaphthene (74.63 ± 0.78) in control. Activities of peroxidase, ascorbate peroxidase, and polyphenol oxidase were more prominent in the roots of plants exposed to increasing concentrations of oil in soil than control plants. Conversely, the activity of superoxide dismutase decreased. These findings render A. marina as a phytoremediation candidate for small scale oil spills and residual oil pollution in coastal marine environments.