Showing papers on "Methylglyoxal published in 2021"

Glutathione Metabolism in Plants under Stress: Beyond Reactive Oxygen Species Detoxification

Abstract: Glutathione is an essential metabolite for plant life best known for its role in the control of reactive oxygen species (ROS). Glutathione is also involved in the detoxification of methylglyoxal (MG) which, much like ROS, is produced at low levels by aerobic metabolism under normal conditions. While several physiological processes depend on ROS and MG, a variety of stresses can dramatically increase their concentration leading to potentially deleterious effects. In this review, we examine the structure and the stress regulation of the pathways involved in glutathione synthesis and degradation. We provide a synthesis of the current knowledge on the glutathione-dependent glyoxalase pathway responsible for MG detoxification. We present recent developments on the organization of the glyoxalase pathway in which alternative splicing generate a number of isoforms targeted to various subcellular compartments. Stress regulation of enzymes involved in MG detoxification occurs at multiple levels. A growing number of studies show that oxidative stress promotes the covalent modification of proteins by glutathione. This post-translational modification is called S-glutathionylation. It affects the function of several target proteins and is relevant to stress adaptation. We address this regulatory function in an analysis of the enzymes and pathways targeted by S-glutathionylation.

Benefits, deleterious effects and mitigation of methylglyoxal in foods: A critical review

Abstract: Background Methylglyoxal, a reactive carbonyl compound widely present in thermally processed foods, is produced from sugar degradation and lipid oxidation. Methylglyoxal can yield various aroma compounds by reacting with amino acids and act as a precursor to generate other toxins, including advanced glycation end products, acrylamide and 4(5)-methylimidazole. Scope and approach: This review highlights the formation and the transformation of methylglyoxal, its benefits and its deleterious effects as well as the interaction with dietary ingredients and scavenging reagents. Moreover, the role of amino acids and phenolic compounds in methylglyoxal mitigation in foods and the possible consequences of the intake of the derived adducts was discussed. Key findings and conclusions: The formation and the transformation of methylglyoxal simultaneously occur during food processing. Amino acids and phenolic compounds can efficiently scavenge methylglyoxal, thereby forming numerous adducts, due to their highly nucleophilic reactivity with methylglyoxal. The absorption, metabolism and toxicology of dietary methylglyoxal–phenolic adducts remain largely unknown and require further investigation before applying polyphenols to control methylglyoxal in foods. The selective addition of amino acids may provide a satisfactory strategy to control methylglyoxal in foods, but their effects on food quality and the toxicity of derived adducts should be deeply investigated.

Vitexin Inhibits Protein Glycation through Structural Protection, Methylglyoxal Trapping, and Alteration of Glycation Site.

Abstract: In this study, the antiglycation potential and mechanisms of vitexin were explored in vitro by multispectroscopy, microscope imaging, high-resolution mass spectrometry, and computational simulations. Vitexin was found to show much stronger antiglycation effects than aminoguanidine. The inhibition against the fluorescent advanced glycation end products was more than 80% at 500 μM vitexin in both bovine serum albumin (BSA)-fructose and BSA-methylglyoxal (MGO) models. Treated with 100 and 200 μM vitexin for 24 h, the contents of MGO were reduced to 4.97 and 0.2%, respectively, and only one vitexin-mono-MGO adduct was formed. LC-Orbitrap-MS/MS analysis showed that vitexin altered the glycated sites and reduced the glycation degree of some sites. The mechanisms of vitexin against protein glycation were mainly through BSA structural protection, MGO trapping, and alteration of glycation sites induced by interaction with BSA. These findings provided valuable information about the functional development of vitexin as a potential antiglycation agent.

Nitrate reductase is required for salicylic acid-induced water stress tolerance of pepper by upraising the AsA-GSH pathway and glyoxalase system.

Abstract: A trial was conducted to evaluate whether nitrate reductase (NR) participates in salicylic acid (SA)-improved water stress (WS) tolerance in pepper (Capsicum annuum L.) plants. Before starting WS treatment, 0.5 mM SA was applied to half of the well-watered (WW) plants as well as to WS-plants as a foliar spray once a day for a week. The soil water holding capacity was maintained at 40 and 80% of the full water storing capacity for WS and and well-watered (WW) plants, respectively. Water stress caused substantial decreases in total plant dry weight, Fv /Fm , chlorophyll a and b, relative water content, leaf water potential (ΨI) by 53, 37, 49, 21, 36 and 33%, respectively relative to control, but significant increases in malondialdehyde (MDA), hydrogen peroxide (H2 O2 ), electrolyte leakage (EL), methylglyoxal (MG), proline, key antioxidant enzymes' activities, NO and NR activity. The SA reduced oxidative stress, but improved antioxidant defence system, ascorbate-glutathione (AsA-GSH) cycle enzymes, glyoxalase system-related enzymes, glyoxalase I (Gly I) and glyoxalase II (Gly II), plant growth, photosynthetic traits, NO, NR and proline. SA-induced WS tolerance was further improved by supplementation of sodium nitroprusside (SNP), a donor of NO. NR inhibitor, sodium tungstate (ST) was applied in conjunction with SA and SA + SNP to the WW and WS-plants to assess whether NR contributes to SA-improved WS tolerance. ST abolished the beneficial effects of SA by reducing NO and NR activity in WS-pepper, but the application of SNP along with SA + ST reversed negative effects of ST, showing that NO and NR are jointly needed for SA-induced WS tolerance of pepper plants.

Protein glycation - biomarkers of metabolic dysfunction and early-stage decline in health in the era of precision medicine.

Abstract: Protein glycation provides a biomarker in widespread clinical use, glycated hemoglobin HbA1c (A1C). It is a biomarker for diagnosis of diabetes and prediabetes and of medium-term glycemic control in patients with established diabetes. A1C is an early-stage glycation adduct of hemoglobin with glucose; a fructosamine derivative. Glucose is an amino group-directed glycating agent, modifying N-terminal and lysine sidechain amino groups. A similar fructosamine derivative of serum albumin, glycated albumin (GA), finds use as a biomarker of glycemic control, particularly where there is interference in use of A1C. Later stage adducts, advanced glycation endproducts (AGEs), are formed by the degradation of fructosamines and by the reaction of reactive dicarbonyl metabolites, such as methylglyoxal. Dicarbonyls are arginine-directed glycating agents forming mainly hydroimidazolone AGEs. Glucosepane and pentosidine, an intense fluorophore, are AGE covalent crosslinks. Cellular proteolysis of glycated proteins forms glycated amino acids, which are released into plasma and excreted in urine. Development of diagnostic algorithms by artificial intelligence machine learning is enhancing the applications of glycation biomarkers. Investigational glycation biomarkers are in development for: (i) healthy aging; (ii) risk prediction of vascular complications of diabetes; (iii) diagnosis of autism; and (iv) diagnosis and classification of early-stage arthritis. Protein glycation biomarkers are influenced by heritability, aging, decline in metabolic, vascular, renal and skeletal health, and other factors. They are applicable to populations of differing ethnicities, bridging the gap between genotype and phenotype. They are thereby likely to find continued and expanding clinical use, including in the current era of developing precision medicine, reporting on multiple pathogenic processes and supporting a precision medicine approach.

Unexpected Oligomerization of Small α-Dicarbonyls for Secondary Organic Aerosol and Brown Carbon Formation.

Abstract: Large amounts of small α-dicarbonyls (glyoxal and methylglyoxal) are produced in the atmosphere from photochemical oxidation of biogenic isoprene and anthropogenic aromatics, but the fundamental mechanisms leading to secondary organic aerosol (SOA) and brown carbon (BrC) formation remain elusive. Methylglyoxal is commonly believed to be less reactive than glyoxal because of unreactive methyl substitution, and available laboratory measurements showed negligible aerosol growth from methylglyoxal. Herein, we present experimental results to demonstrate striking oligomerization of small α-dicarbonyls leading to SOA and BrC formation on sub-micrometer aerosols. Significantly more efficient growth and browning of aerosols occur upon exposure to methylglyoxal than glyoxal under atmospherically relevant concentrations and in the absence/presence of gas-phase ammonia and formaldehyde, and nonvolatile oligomers and light-absorbing nitrogen-heterocycles are identified as the dominant particle-phase products. The distinct aerosol growth and light absorption are attributed to carbenium ion-mediated nucleophilic addition, interfacial electric field-induced attraction, and synergetic oligomerization involving organic/inorganic species, leading to surface- or volume-limited reactions that are dependent on the reactivity and gaseous concentrations. Our findings resolve an outstanding discrepancy concerning the multiphase chemistry of small α-dicarbonyls and unravel a new avenue for SOA and BrC formation from atmospherically abundant, ubiquitous carbonyls and ammonia/ammonium sulfate.

Silicon attenuates the negative effects of chromium stress in tomato plants by modifying antioxidant enzyme activities, ascorbate–glutathione cycle and glyoxalase system

Abstract: Among the heavy metal pollutants, Cr (VI) is very toxic to plants because of its mobile nature. Silicon (Si) is a metalloid and is reported to ease the negative effects of heavy metal stress in plants. Thus, the current study was conducted to examine the influence of chromium (Cr) toxicity and the mitigating role of silicon (Si) in tomato plants. Chromium toxicity induced high accumulation of Cr in roots and shoots, thereby decreasing plant growth and biomass yield. Silicon supplementation enhanced the afore-mentioned parameters except Cr accumulation. Silicon also enhanced the translocation factor, total chlorophyll, Fv/Fm, ΦPSII, Φexc and qp but at the same time it decreased NPQ in Cr-stressed plants. The gaseous exchange and relative water content (LRWC) of leaf were improved by Si, that were initially decreased by Cr noxiousness. Malondialdehyde (MDA), hydrogen peroxide, (H2O2) and electrolyte leakage (EL) increased with Cr toxicity, but were reduced with Si application. Cr toxicity boosts the enzyme concentration, and Si supplementation thereafter increased the activities of the enzymes as well as metabolite cycle (Asc–Glu). Chromium stress increased methylglyoxal (MG) by 116.87%, which was reduced by Si supplementation. Silicon increased GlyI (EC: 4.4.1.5) and GlyII (EC: 3.1.2.6) thereby making the glyoxalase system more active for providing tolerance to tomato plants. In conclusion, Cr toxicity triggers detrimental effect on plant growth and physio-biochemical processes. However, Si supplementation reversed partially the Cr toxicity by modulating the levels of osmoprotectants, antioxidant enzyme activities, Asc–Glu cycle and the glyoxalase system.

Dicarbonyl stress, protein glycation and the unfolded protein response

Abstract: The reactive dicarbonyl metabolite, methylglyoxal (MG), is increased in obesity and diabetes and is implicated in the development of insulin resistance, type 2 diabetes mellitus and vascular complications of diabetes. Dicarbonyl stress is the metabolic state of abnormal high MG concentration. MG is an arginine-directed glycating agent and precursor of the major advanced glycation endproduct, arginine-derived hydroimidazolone MG-H1. MG-H1 is often formed on protein surfaces and an uncharged hydrophobic residue, inducing protein structural distortion and misfolding. Recent studies indicate that dicarbonyl stress in human endothelial cells and fibroblasts in vitro induced a proteomic response consistent with activation of the unfolded protein response (UPR). The response included: increased abundance of heat shock proteins and ubiquitin ligases catalysing the removal of proteins with unshielded surface hydrophobic patches and formation of polyubiquitinated chains to encapsulate misfolded proteins; and increased low grade inflammation. Activation of the UPR is implicated in insulin resistance. An effective strategy to counter increased MG is inducing increased expression of glyoxalase-1 (Glo1). An optimized inducer of Glo1 expression, trans-resveratrol and hesperetin combination, normalized increased MG concentration, corrected insulin resistance and decreased low grade inflammation in overweight and obese subjects. We propose that dicarbonyl stress, through increased formation of MG-glycated proteins, may be an important physiological stimulus of the UPR and Glo1 inducers may provide a route to effective suppression and therapy. With further investigation and validation, this may provide key new insight into physiological activators of the UPR and association with dicarbonyl stress.

Methylglyoxal-Dependent Glycative Stress Is Prevented by the Natural Antioxidant Oleuropein in Human Dental Pulp Stem Cells through Nrf2/Glo1 Pathway.

Abstract: Methylglyoxal (MG) is a potent precursor of glycative stress (abnormal accumulation of advanced glycation end products, AGEs), a relevant condition underpinning the etiology of several diseases, including those of the oral cave. At present, synthetic agents able to trap MG are known; however, they have never been approved for clinical use because of their severe side effects. Hence, the search of bioactive natural scavengers remains a sector of strong research interest. Here, we investigated whether and how oleuropein (OP), the major bioactive component of olive leaf, was able to prevent MG-dependent glycative stress in human dental pulp stem cells (DPSCs). The cells were exposed to OP at 50 µM for 24 h prior to the administration of MG at 300 µM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2. Our results suggest that OP holds great promise for the development of preventive strategies for MG-derived AGEs-associated oral diseases and open new paths in research concerning additional studies on the protective potential of this secoiridoid.

Supplemental Selenium and Boron Mitigate Salt-Induced Oxidative Damages in Glycine max L.

Abstract: The present investigation was executed with an aim to evaluate the role of exogenous selenium (Se) and boron (B) in mitigating different levels of salt stress by enhancing the reactive oxygen species (ROS) scavenging, antioxidant defense and glyoxalase systems in soybean. Plants were treated with 0, 150, 300 and 450 mM NaCl at 20 days after sowing (DAS). Foliar application of Se (50 µM Na2SeO4) and B (1 mM H3BO3) was accomplished individually and in combined (Se+B) at three-day intervals, at 16, 20, 24 and 28 DAS under non-saline and saline conditions. Salt stress adversely affected the growth parameters. In salt-treated plants, proline content and oxidative stress indicators such as malondialdehyde (MDA) content and hydrogen peroxide (H2O2) content were increased with the increment of salt concentration but the relative water content decreased. Due to salt stress catalase (CAT), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), glyoxalase I (Gly I) and glyoxalase II (Gly II) activity decreased. However, the activity of ascorbate peroxidase (APX), glutathione reductase (GR), glutathione peroxidase (GPX), glutathione S-transferase (GST) and peroxidase (POD) increased under salt stress. On the contrary, supplementation of Se, B and Se+B enhanced the activities of APX, MDHAR, DHAR, GR, CAT, GPX, GST, POD, Gly I and Gly II which consequently diminished the H2O2 content and MDA content under salt stress, and also improved the growth parameters. The results reflected that exogenous Se, B and Se+B enhanced the enzymatic activity of the antioxidant defense system as well as the glyoxalase systems under different levels of salt stress, ultimately alleviated the salt-induced oxidative stress, among them Se+B was more effective than a single treatment.

Naringenin, a dietary flavanone, enhances insulin-like growth factor 1 receptor-mediated antioxidant defense and attenuates methylglyoxal-induced neurite damage and apoptotic death.

Abstract: Objectives: Recent studies revealed the neuroprotective effects of naringenin (NGEN), a common dietary bioflavonoid contained in citrus fruits. However, there are limited data on its protection aga...

Menadione sodium bisulfite alleviated chromium effects on wheat by regulating oxidative defense, chromium speciation, and ion homeostasis

Abstract: Menadione sodium bisulfite (MSB) is a crucial growth regulator mediating plant defense response. MSB-mediated regulation of defense mechanisms in wheat under chromium (Cr) toxicity has not been reported in the literature. Therefore, the present study was undertaken to appraise the efficacy of exogenous MSB on circumventing Cr phytotoxic effects on wheat. We also compared the effects of water-soluble MSB with that of water-insoluble menadiol diacetate (MD). The levels used in the present investigation for MSB and MD were 100 and 200 mg L-1. Wheat plants grown in soil contaminated with 25 mg kg-1 Cr in the form of K2Cr2O7 showed a notable reduction in growth, chlorophyll molecules, relative water contents, grain yield, total soluble sugars, phenolics, flavonoids, ascorbic acid, activities of antioxidant enzymes (SOD, POD, CAT), and uptake of essential nutrients (K, P, and Ca). Cr toxicity caused a noticeable accretion in total free amino acids, proline, malondialdehyde, H2O2, O2•-, relative membrane permeability, methylglyoxal contents, activities of enzymes (lipoxygenase, glutathione-S-transferase, and ascorbate peroxidase), nitric oxide and H2S contents, glutathione and oxidized glutathione contents, total Cr contents, and Cr6+ and Cr3+ accumulation. MSB application significantly reduced lipid peroxidation, ROS overproduction, methylglyoxal levels, total Cr contents, and maintained higher Cr3+:Cr6+ ratio in aerial parts. Besides, Cr-mediated inhibition in essential nutrient uptake was significantly circumvented by exogenous MSB. Consequently, MSB enhanced wheat growth by lessening oxidative damage, total Cr contents in aerial parts, and strengthening antioxidant enzyme activities. MD was not effective in mediating defense responses in wheat under Cr toxicity.

Classically activated mouse macrophages produce methylglyoxal that induces a TLR4- and RAGE-independent proinflammatory response.

Abstract: The highly reactive compound methylglyoxal (MG) can cause direct damage to cells and tissues by reacting with cellular macromolecules. MG has been identified as a biomarker associated with increased sepsis-induced mortality. Patients undergoing septic shock have significantly elevated circulating MG levels compared to postoperative patients and healthy controls. Furthermore, MG has been implicated in the development of type II diabetes mellitus and Alzheimer's disease. Because MG is generated during glycolysis, we hypothesized that MG may be produced by classically activated (M1) macrophages, possibly contributing to the inflammatory response. LPS and IFN-γ-treated macrophages acquired an M1 phenotype (as evidenced by M1 markers and enhanced glycolysis) and formed MG adducts, MG-H1, MG-H2, and MG-H3, which were detected using antibodies specific for MG-modified proteins (methylglyoxal 5-hydro-5-methylimidazolones). MG adducts were also increased in the lungs of LPS-treated mice. Macrophages treated with LPS and IFN-γ also exhibited decreased expression of glyoxalase 1 (Glo1), an enzyme that metabolizes MG. Concentrations of exogenous, purified MG > 0.5 mM were toxic to macrophages; however, a nontoxic dose of 0.3 mM induced TNF-α and IL-1β, albeit to a lesser extent than LPS stimulation. Despite prior evidence that MG adducts may signal through "receptor for advanced glycation endproducts" (RAGE), MG-mediated cell death and cytokine induction by exogenous MG was RAGE-independent in primary macrophages. Finally, RAGE-deficient mice did not exhibit a significant survival advantage following lethal LPS injection. Overall, our evidence suggests that MG may be produced by M1 macrophages during sepsis, following IFN-γ-dependent down-regulation of Glo1, contributing to over-exuberant inflammation.

The metabolite methylglyoxal-mediated gene expression is associated with histone methylglyoxalation.

Abstract: Methylglyoxal (MG) is a byproduct of glycolysis that functions in diverse mammalian developmental processes and diseases and in plant responses to various stresses, including salt stress. However, it is unknown whether MG-regulated gene expression is associated with an epigenetic modification. Here we report that MG methylglyoxalates H3 including H3K4 and increases chromatin accessibility, consistent with the result that H3 methylglyoxalation positively correlates with gene expression. Salt stress also increases H3 methylglyoxalation at salt stress responsive genes correlated to their higher expression. Following exposure to salt stress, salt stress responsive genes were expressed at higher levels in the Arabidopsis glyI2 mutant than in wild-type plants, but at lower levels in 35S::GLYI2 35S::GLYII4 plants, consistent with the higher and lower MG accumulation and H3 methylglyoxalation of target genes in glyI2 and 35S::GLYI2 35S::GLYII4, respectively. Further, ABI3 and MYC2, regulators of salt stress responsive genes, affect the distribution of H3 methylglyoxalation at salt stress responsive genes. Thus, MG functions as a histone-modifying group associated with gene expression that links glucose metabolism and epigenetic regulation.

Methyl jasmonate ameliorates lead toxicity in Oryza sativa by modulating chlorophyll metabolism, antioxidative capacity and metal translocation.

Abstract: Lead (Pb) not only negatively alters plant growth and yield but may also have potentially toxic risks to human health. Nevertheless, the interaction between rice (Oryza sativa L.) plants and the molecular cell dynamics induced by lead-methyl jasmonate (MJ) remains unknown. Here, plants were hydroponically exposed to Pb (150 and 300 µM) alone or in combination with 0.5 and 1 µM MJ. The application of MJ modulated the expression of the HMAs, PCS1, PCS2 and ABCC1 genes, thereby immobilizing the Pb in the roots and lessening its translocation to the aerial parts of the rice plant. The supplementation of MJ improved the growth and yield of Pb-stressed rice by adjusting the proline and chlorophyll metabolism, increasing the phytochelatins (PCs) accumulation and diminishing the accumulation of Pb in the shoots. the application of MJ alleviated the oxidative stress of rice plants exposed to Pb toxicity by enhancing the activity of antioxidant enzymes and enzymes of the glyoxalase system (glyoxalase I and II) and decreasing the endogenous levels of malondialdehyde (MDA), hydrogen peroxide (H2O2) and methylglyoxal (MG). Therefore, the results of the present study could provide a molecular insight and cellular interplay scheme for the development of a promising strategy in Pb-contaminated areas to produce healthy food.

Non-enzymatic glycation of protein induces cancer cell proliferation and its inhibition by quercetin: Spectroscopic, cytotoxicity and molecular docking studies.

Abstract: Methylglyoxal (MG) is a potent glycating agent which reacts with proteins to form advanced glycation end products (AGEs). These chemically stable AGEs crosslink with proteins and could lead to amyl...

Methylglyoxal-Mediated Dopamine Depletion, Working Memory Deficit, and Depression-Like Behavior Are Prevented by a Dopamine/Noradrenaline Reuptake Inhibitor

Abstract: Methylglyoxal (MGO) is an endogenous toxin, mainly produced as a by-product of glycolysis that has been associated to aging, Alzheimer’s disease, and inflammation. Cell culture studies reported that MGO could impair the glyoxalase, thioredoxin, and glutathione systems. Thus, we investigated the effect of in vivo MGO administration on these systems, but no major changes were observed in the glyoxalase, thioredoxin, and glutathione systems, as evaluated in the prefrontal cortex and the hippocampus of mice. A previous study from our group indicated that MGO administration produced learning/memory deficits and depression-like behavior. Confirming these findings, the tail suspension test indicated that MGO treatment for 7 days leads to depression-like behavior in three different mice strains. MGO treatment for 12 days induced working memory impairment, as evaluated in the Y maze spontaneous alternation test, which was paralleled by low dopamine and serotonin levels in the cerebral cortex. Increased DARPP32 Thr75/Thr34 phosphorylation ratio was observed, suggesting a suppression of phosphatase 1 inhibition, which may be involved in behavioral responses to MGO. Co-treatment with a dopamine/noradrenaline reuptake inhibitor (bupropion, 10 mg/kg, p.o.) reversed the depression-like behavior and working memory impairment and restored the serotonin and dopamine levels in the cerebral cortex. Overall, the cerebral cortex monoaminergic system appears to be a preferential target of MGO toxicity, a new potential therapeutic target that remains to be addressed.

High-Resolution Mass Spectrometry Analysis of Melanoidins and Their Precursors Formed in a Model Study of the Maillard Reaction of Methylglyoxal with l-Alanine or l-Lysine.

Abstract: Despite more than 100 years of research, formation of food melanoidins from carbohydrates and amino acids in the course of the Maillard reaction is still not fully understood. Experiments with relevant precursors are commonly used to limit the pathways of the complex reaction and to elucidate the formation mechanisms of the colored end-products. Here as a simple model, methylglyoxal was incubated with l-alanine or l-lysine in aqueous solutions at 100 °C and pH 5. The reaction mixtures were analyzed for color formation, molecular weight distribution, and conversion of methylglyoxal. High-resolution mass spectrometry was used to characterize the variety of products formed. With the help of Kendrick and van Krevelen analyses, the complex data sets were investigated for common substructures and reaction patterns. This study revealed that methylglyoxal forms oligomers via aldol reaction under involvement of its prevalent reaction products such as formaldehyde, acetaldehyde, acetol, and aminoacetone with amino acids.

Coumarin improves tomato plant tolerance to salinity by enhancing antioxidant defence, glyoxalase system and ion homeostasis.

Abstract: Salinity is a severe threat to crop growth, development and even to world food sustainability. Plant possess natural antioxidant defense tactics to mitigate salinity-induced oxidative stress. Phenolic compounds are non-enzymatic antioxidants with specific roles in protecting plant cells against stress-mediated reactive oxygen species (ROS) generation. Coumarin (COU) is one of these compounds, however, to date, little is known about antioxidative roles of exogenous COU in enhancing plant tolerance mechanisms under salt stress. The involvement of COU in increasing tomato salt tolerance was examined in the present study using COU as a pre-treatment at 20 or 30 µM for 2 days against salt stress (100 or 160 NaCl; 5 days). The COU-mediated stimulation of plant antioxidant defence and glyoxalase systems to suppress salt-induced ROS and methylglyoxal (MG) toxicity, respectively, were the main hypotheses examined in the present study. Addition of COU suppressed salt-induced excess accumulation of ROS and MG, and significantly reduced membrane damage, lipid peroxidation and Na+ toxicity. These results demonstrate COU-improved plant growth, biomass content, photosynthetic pigment content, water retention and mineral homeostasis upon imposition of salinity. Finally, this present study suggests that COU has potential roles as a phytoprotectant in stimulating plant antioxidative mechanisms and improving glyoxalase enzyme activity under salinity stress.

An Unrecognized Hazard in E-Cigarette Vapor: Preliminary Quantification of Methylglyoxal Formation from Propylene Glycol in E-Cigarettes.

Abstract: Up to 95% of the liquid volume in an e-cigarette consists of propylene glycol. Previous research has shown that propylene glycol can generate diacetyl and formaldehyde when heated. New research shows that propylene glycol can also generate methylglyoxal, an alpha di-carbonyl compound recently shown to cause epithelial necrosis at even lower concentrations than diacetyl, the flavoring chemical associated with bronchiolitis obliterans ("Popcorn Lung"). We analyzed chemical emissions from 13 JUUL pod flavors. Diacetyl and methylglyoxal was detected in 100% of samples with median concentration (range) of 20 µg/m3 (less than limit of quantification: 54 µg/m3) and 4219 µg/m3 (677-15,342 µg/m3), respectively. We also detected acetaldehyde (median concentration: 341 µg/m3) and propionaldehyde (median concentration: 87 µg/m3) in all samples. The recent evidence that methylglyoxal is more cytotoxic to airway epithelial cells than diacetyl makes this an urgent public health concern. Current smokers considering e-cigarettes as a smoking cessation tool, and never users, who may be under the impression that e-cigarettes are harmless, need information on emissions and potential risks to make informed decisions.