Severe Oxidative Stress Research Articles

Kynurenine Pathway of Tryptophan Metabolism Is Associated with Hospital Mortality in Patients with Acute Respiratory Distress Syndrome: A Prospective Cohort Study.

Acute respiratory distress syndrome (ARDS) involves dysregulated immune-inflammatory responses, characterized by severe oxidative stress and high mortality. Metabolites modulating the inflammatory and immune responses may play a central role in the pathogenesis of ARDS. Most biogenic amines may induce the production of reactive oxygen species, oxidative stress, mitochondrial dysfunction, and programmed cell death. We conducted a prospective study on metabolic profiling specific to the amino acids and biogenic amines of 69 patients with ARDS. Overall, hospital mortality was 52.2%. Between day 1 and day 7 after ARDS onset, plasma kynurenine levels and the kynurenine/tryptophan ratio were significantly higher among non-survivors than in survivors (all p < 0.05). Urine metabolic profiling revealed a significantly higher prevalence of tryptophan degradation and higher concentrations of metabolites downstream of the kynurenine pathway among non-survivors than among survivors upon ARDS onset. Cox regression models revealed that plasma kynurenine levels and the plasma kynurenine/tryptophan ratio on day 1 were independently associated with hospital mortality. The activation of the kynurenine pathway was associated with mortality in patients with ARDS. Metabolic phenotypes and modulating metabolic perturbations of the kynurenine pathway could perhaps serve as prognostic markers or as a target for therapeutic interventions aimed at reducing oxidative stress and mortality in ARDS.

Toxic and bioaccumulative effects of zinc nanoparticle exposure to goldfish, Carassius auratus (Linnaeus, 1758)

The widespread use of produced metal oxide nanoparticles (NPs) has increased major concerns about their impact on human as well as aquatic animal health. The present study shows that exposure to different concentrations of zinc oxide (ZnO) NPs led to high accumulations of Zn ions in the metabolic organs of fish (liver and gills), resulting in severe oxidative stress in Carassius auratus. The goldfish (C. auratus) was chosen as an aquatic species for the evaluation of the potential toxicity of aqueous ZnO-NPs (Treatments of hemoglobin and neutrophils (0, 0.5, 1, and 1.5 mg L− 1) following 14 days of exposure. A range of histological and hematological factors were examined. Exposure to the NPs produced significant reduction of red blood cell and white blood cell counts, hematocrit) were found to produce no significant differences in lymphocyte, monocyte, and eosinophil counts; as well as the mean corpuscular hemoglobin concentrations index (P > 0.05). Moreover, the results revealed significant alterations in serum biochemical parameters, hepatic enzyme levels, and immune and antioxidant responses; except for total protein and superoxide dismutase (SOD) of C. auratus exposed to ZnO-NPs, particularly at the 1 and 1.5 mg L− 1 concentrations. Fish exposed to 1 and 1.5 mg L−1 ZnO-NPs displayed a significant reduction in alternative complement pathway activity, lysozyme, and total protein contents of mucus compared to those in the control group. The results showed that hepatic SOD and catalase, and gill catalase activity were significantly decreased, and their malondialdehyde levels increased at 1 and 1.5 mg L−1 ZnO-NPs compared to the control group (P < 0.05). Significant accumulations of ZnO-NPs were observed in the liver, kidney, and gill tissues of fish leading to severe histopathological alterations in these organs. These results suggest that water-borne ZnO-NPs can easily accumulate in metabolic organs and lead to oxidative stress and destructive effects on the physiological features of C. auratus.

Taurine mitigates the development of pulmonary inflammation, oxidative stress, and histopathological alterations in a rat model of bile duct ligation.

Lung injury is a significant complication associated with cholestasis/cirrhosis. This problem significantly increases the risk of cirrhosis-related morbidity and mortality. Hence, finding effective therapeutic options in this field has significant clinical value. Severe inflammation and oxidative stress are involved in the mechanism of cirrhosis-induced lung injury. Taurine (TAU) is an abundant amino acid with substantial anti-inflammatory and antioxidative properties. The current study was designed to evaluate the role of TAU in cholestasis-related lung injury. For this purpose, bile duct ligated (BDL) rats were treated with TAU (0.5 and 1% w: v in drinking water). Significant increases in the broncho-alveolar lavage fluid (BALF) level of inflammatory cells (lymphocytes, neutrophils, basophils, monocytes, and eosinophils), increased IgG, and TNF-α were detected in the BDL animals (14 and 28days after the BDL surgery). Alveolar congestion, hemorrhage, and fibrosis were the dominant pulmonary histopathological changes in the BDL group. Significant increases in the pulmonary tissue biomarkers of oxidative stress, including reactive oxygen species formation, lipid peroxidation, increased oxidized glutathione levels, and decreased reduced glutathione, were also detected in the BDL rats. Moreover, significant myeloperoxidase activity and nitric oxide levels were seen in the lung of BDL rats. It was found that TAU significantly blunted inflammation, alleviated oxidative stress, and mitigated lung histopathological changes in BDL animals. These data suggest TAU as a potential protective agent against cholestasis/cirrhosis-related lung injury.

CREBH alleviates mitochondrial oxidative stress through SIRT3 mediating deacetylation of MnSOD and suppression of Nlrp3 inflammasome in NASH.

Lipotoxicity and unresolved oxidative stress are key drivers of metabolic inflammation in nonalcoholic steatohepatitis (NASH). cAMP-response element binding protein H(CREBH) is a liver-specific transcription factor and regulates the glucose and lipid metabolism of NASH. However, its role in mitochondrial oxidative stress and its association with sirtuin 3 (SIRT3), a master regulator of deacetylation for mitochondrial proteins, remains elusive. In this study, AML-12cells were treated with palmitic acid to imitate the pathological changes of NASH in vitro and 8-week-old male C57BL/6J mice were fed with a high-fat (HF) diet or a methionine-choline-deficient (MCD) diet to build the widely accepted in vivo model of NASH. We found that lipid overload induced mitochondrial oxidative stress and stimulated the expression of CREBH and SIRT3. CREBH overexpression alleviated the mitochondrial oxidative stress. Moreover, CREBH promoted SIRT3 expression, which regulated the deacetylation of manganese superoxide dismutase (MnSOD) and inhibited NOD-Like Receptor Pyrin Domain Containing 3 (Nlrp3) inflammasome activation whereas suppression of SIRT3 damaged the protecting ability of CREBH in mitochondrial oxidative stress. CREBH knockout mice were highly susceptible to HF and MCD diet-induced NASH with more severe oxidative stress. Collectively, our results firstly provided the support that CREBH could serve as a protective factor in the progression of NASH by regulating the acetylation of MnSOD and the activation of Nlrp3 inflammasome through SIRT3. These results suggest that CREBH might be a valuable therapeutic candidate for NASH.

Combined effects of abamectin and temperature on the physiology and behavior of male lizards (Eremias argus): Clarifying adaptation and maladaptation.

Chemical pollution and global warming are two major threats to organisms, which can interact to affect the normal activities of living beings. In this study, to explore the effects of abamectin and high temperature on adaptability of lizard, male adult Eremias argus (a native Chinese lizard) were exposed to environmentally relevant concentrations of abamectin (0.02 mg·L-1 and 2 mg·L-1) and different temperature (26 °C and 32 °C) for 30 days. The fitness-related behaviors (locomotion, predation, and thermoregulation) of lizards were evaluated. Physiological effects were addressed using biochemical biomarkers related to oxidative stress, detoxification, and neurotransmitter content. The results showed that abamectin could affect the neurotransmitter systems, cause oxidative stress, and alters lizard locomotion and predation-related behaviors of lizards, but lizards up-regulating detoxification metabolic enzymes, exhibiting higher body temperature preference to alleviate the toxicity of abamectin, and compensate the increased energy demand for detoxification and repair damage by increasing food intake. After exposure to high temperature, lizards showed adaptation to high temperature (higher body temperature preference), the thermal compensation mechanisms may involve elevated Hsp70 levels and increased food intake. At the combined effects of abamectin and high temperature, more obvious behavioral disorders and more severe oxidative stress were observed, although lizards avoided the negative effects of overheating and pollutants by seeking thermal shelter and reducing energy expenditure, this may subsequently reduce foraging opportunities and the ability to obtain energy needed for vital physiological functions (i.e., growth, maintenance, and reproduction). From a long-term perspective, these short-term adaptive strategies will be detrimental to individual long-term survival and population sustainability, and may transformed into maladaptation.

How do viruses use oxidative stress?

Oxygen is a vital element for all living beings to continue their life activities and is the main component of oxidant–antioxidant metabolism, which should be in balance. The free radicals formed as a result of this metabolic process in the organism constitute a source of oxidants; external factors (radiation, exposure to sunlight, environmental pollution, cigarettes, etc.), inflammation and microbial agents also cause the formation of oxidants. Oxidative stress occurs when the balance between free radicals and antioxidants (which have an eliminating effect against them) shifts in favour of free radicals. Many studies have reported that oxidative stress may affect the virulence of pathogens during infection. Viruses use a pathological pathway that causes the production of reactive oxygen species (ROS) and the consumption of antioxidants. Thus, after viral infections, higher levels of ROS are often formed. Not only DNA-containing but also RNA-containing viruses were found to be associated with severe oxidative stress supporting DNA damage, high mutagenicity, initiation and/or progression of neoplasia. This review focuses on the relationship between oxidative stress and viruses.

Corynoline ameliorates dextran sulfate sodium-induced colitis in mice by modulating Nrf2/NF-κB pathway

Objective Corynoline is an active substance extracted from Corydalis bungeana Turcz and exerts a therapeutic effect in multiple diseases by alleviating inflammatory response. The present study sought to elucidate the role of corynoline in ulcerative colitis (UC). Methods The experimental colitis models were induced in BALB/c mice via receiving a drinking water supplemented with 3.5% (I) dextran sulfate sodium (DSS) ad libitum for 7 days. Results Corynoline administration inhibited body weight loss, colon shortening, disease activity index and colonic pathomorphological changes in DSS-treated mice. Besides, corynoline down-regulated the levels of pro-inflammatory interleukin (IL)-1β, IL-6 and tumor necrosis factor Alpha (TNF-α), as well as decreased myeloperoxidase (MPO) activity in the colon of DSS-treated mice. In addition, severe oxidative stress in the colonic tissues of DSS-treated was mitigated by corynoline treatment. However, these beneficial effects were reversed by a specific nuclear factor E2-related factor 2 (Nrf2) inhibitor ML385 intervention. Further evidence confirmed that corynoline promoted Nrf2 nuclear migration and heme oxygenase-1 gene expression in the colonic tissues of UC mice. Besides, corynoline treatment restrained colonic nuclear factor-kappa B (NF-κB) activation as proved by the decrease in phosphorylation and nuclear translocation of NF-κB. Conclusions Corynoline ameliorates DSS-induced mouse colitis, which may provide a promising therapeutic strategy for UC treatment.

Luteolin-7-O-Glucuronide Improves Depression-like and Stress Coping Behaviors in Sleep Deprivation Stress Model by Activation of the BDNF Signaling.

Stress exposure is a major risk factor for mental disorders such as depression. Because of the limitations of classical antidepressants such as side effects, low efficacy, and difficulty in long-term use, new natural medicines and bioactive molecules from plants with greater safety and efficacy have recently attracted attention. Luteolin-7-O-glucuronide (L7Gn), a bioactive molecule present in Perilla frutescens, is known to alleviate severe inflammatory responses and oxidative stress in macrophages. However, its antistress and antidepressant effects have not been elucidated. The present study aims to explore the antidepressant the effect of L7Gn on stress-induced behaviors and the underlying mechanism in a mouse sleep deprivation (SD) model. L7Gn treatment improved depression-like and stress coping behaviors induced by SD stress, as confirmed by the tail suspension test and forced swimming test. Furthermore, L7Gn treatment reduced the blood corticosterone and hippocampal proinflammatory cytokine levels which were increased by SD stress, and L7Gn also increased the mRNA and protein levels of hippocampal brain-derived neurotrophic factor (BDNF) which were reduced by SD stress. Additionally, treatment with L7Gn resulted in increases in the phosphorylation of tropomyosin-related kinase B (TrkB), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB), which are downstream molecules of BDNF signaling. These findings suggest that L7Gn have therapeutic potential for SD-induced stress, via activating the BDNF signaling.

Combined ingestion of polystyrene microplastics and epoxiconazole increases health risk to mice: Based on their synergistic bioaccumulation in vivo.

Microplastic and pesticide are two common environmental pollutants whose adverse effects have been widely reported, but it is unclear whether they cause combined toxicity in mammals. In this study, polystyrene microplastics (5µm, 0.012 or 0.120mg/kg) or/and epoxiconazole (0.080mg/kg) were administered orally to mice for 6weeks, their toxicity to liver and kidney was assessed from changes in histopathology, tissue function, oxidative defense system and metabolic profile. In addition, mechanism of combined toxicity was explored in terms of bioaccumulation levels, intestinal barrier, gut microbiota. Results showed that combined ingestion of polystyrene (0.120mg/kg) and epoxiconazole caused more severe tissue damage, dysfunction, oxidative stress, and metabolic disorders compared to single exposure sources. Interestingly, occurrence of combined toxicity was associated with their increased accumulation in tissues. In-depth exploration found that epoxiconazole caused intestinal barrier damage by targeting the gut microbiota, leading to massive invasion and accumulation of polystyrene, which in turn interfered with the metabolic clearance of epoxiconazole in liver. In all, findings highlighted that polystyrene and epoxiconazole could cause combined toxicity in mice through the synergistic effect of their bioaccumulation in vivo, which provided new reference for understanding the health risks of microplastics and pesticides and sheds light on the potential risk to humans of their combined ingestion.

Toxic Effect of Combined Exposure of Microplastics and Copper on Goldfish (Carassius auratus): Insight fromOxidative Stress, Inflammation, Apoptosis and Autophagy in Hepatopancreas and Intestine.

The enhancement of the toxic effect of microplastics (MPs) on heavy metals and its mechanism needs more in-depth and systematic research. In this study, the copper (Cu) accumulation, histological injury, and expression of genes involved in oxidative stress, inflammation, apoptosis, and autophagy of goldfish after single or combined exposure of MPs (1mg/L) and Cu2+ (0.1mg/L) for 7days were determined. The results demonstrated that MPs enhanced the Cu accumulation in hepatopancreas and intestine of goldfishand induced more severe oxidative stress in the hepatopancreas and intestine of goldfish. Additionally, combined exposure of MPs and Cu induced inflammation, excessive apoptosis and insufficient autophagyin the hepatopancreas. Contrary, the inflammation and apoptosis were depressed in the intestine after combined exposure of MPs and Cu, which still requires further exploration.Hence, these findings provide further evidence for the threat of MPs and its adsorbed heavy metals.

The Loss-Function of the Male Sterile Gene ZmMs33/ZmGPAT6 Results in Severely Oxidative Stress and Metabolic Disorder in Maize Anthers

In plants, oxidative stress and metabolic reprogramming frequently induce male sterility, however our knowledge of the underlying molecular mechanism is far from complete. Here, a maize genic male-sterility (GMS) mutant (ms33-6038) with a loss-of-function of the ZmMs33 gene encoding glycerol-3-phosphate acyltransferase 6 (GPAT6) displayed severe deficiencies in the development of a four-layer anther wall and microspores and excessive reactive oxygen species (ROS) content in anthers. In ms33-6038 anthers, transcriptome analysis identified thousands of differentially expressed genes that were functionally enriched in stress response and primary metabolism pathways. Further investigation revealed that 64 genes involved in ROS production, scavenging, and signaling were specifically changed in expression levels in ms33-6038 anthers compared to the other five investigated GMS lines. The severe oxidative stress triggered premature tapetal autophagy and metabolic reprogramming mediated mainly by the activated SnRK1-bZIP pathway, as well as the TOR and PP2AC pathways, proven by transcriptome analysis. Furthermore, 20 reported maize GMS genes were altered in expression levels in ms33-6038 anthers. The excessive oxidative stress and the metabolic reprogramming resulted in severe phenotypic deficiencies in ms33-6038 anthers. These findings enrich our understanding of the molecular mechanisms by which ROS and metabolic homeostasis impair anther and pollen development in plants.

Deciphering the therapeutic mechanism of topical WS2 nanosheets for the effective therapy of burn injuries

Deep burn injuries are complicated traumas accompanying severe oxidative stress and impairment of inherent cellular defense mechanisms against external bacteria. Accordingly, it is required to suppress oxidative stress and support the recovery of intrinsic defense systems in burn wound lesions, but limited topical treatments are clinically available. Herein, antioxidative and anti-inflammatory 2H-WS2 nanosheets are developed as a biocompatible, topical antipyrotic for the treatment of deep burn wounds. The 2H-WS2 nanosheets functionalized with a block copolymer can effectively suppress extrinsic apoptosis, lipid peroxidation, and inflammation in human keratinocytes by scavenging intracellular reactive oxygen species (ROS) and reactive nitrogen species (RNS). Moreover, the 2H-WS2 nanosheets markedly stimulate the up-regulation of innate antioxidant enzymes and antimicrobial peptides in the skin cells, enhancing their intrinsic cellular defense systems. The combined effects of this 2H-WS2 antipyrotic enables a higher efficacy in the deep burn wounds of mice, accelerating re-epithelialization and satisfactory wound healing as compared with commercial silver sulfadiazine (SSD). The therapeutic mechanism of the 2H-WS2 nanosheets for deep burn wounds is proposed herein and found to be distinctly different from that of SSD. The nanotherapeutics of multifunctional 2H-WS2 nanosheets show potential for use in the treatment of other oxidative stress-induced and inflammatory diseases.

Ranolazine Counteracts Strength Impairment and Oxidative Stress in Aged Sarcopenic Mice.

Sarcopenia is defined as the loss of muscle mass associated with reduced strength leading to poor quality of life in elderly people. The decline of skeletal muscle performance is characterized by bioenergetic impairment and severe oxidative stress, and does not always strictly correlate with muscle mass loss. We chose to investigate the ability of the metabolic modulator Ranolazine to counteract skeletal muscle dysfunctions that occur with aging. For this purpose, we treated aged C57BL/6 mice with Ranolazine/vehicle for 14 days and collected the tibialis anterior and gastrocnemius muscles for histological and gene expression analyses, respectively. We found that Ranolazine treatment significantly increased the muscle strength of aged mice. At the histological level, we found an increase in centrally nucleated fibers associated with an up-regulation of genes encoding MyoD, Periostin and Osteopontin, thus suggesting a remodeling of the muscle even in the absence of physical exercise. Notably, these beneficial effects of Ranolazine were also accompanied by an up-regulation of antioxidant and mitochondrial genes as well as of NADH-dehydrogenase activity, together with a more efficient protection from oxidative damage in the skeletal muscle. These data indicate that the protection of muscle from oxidative stress by Ranolazine might represent a valuable approach to increase skeletal muscle strength in elderly populations.

Self-Assembled Maslinic Acid Attenuates Doxorobucin Induced Cytotoxicity via Nrf2 Signaling Pathway: An In Vitro and In Silico Study in Human Healthy Cells.

The clinical applications of some well-known chemotherapeutic drugs for cancer treatment have been restricted nowadays owing to their adverse effects on many physiological systems. In this experimental study, maslinic acid (MA) isolated from Olea europaea (Olive) fruit extract was used to mitigate the cytotoxicity induced by Doxorubicin (DOX) in human healthy peripheral blood mononuclear cells (hPBMCs). Self-assembled maslinic acid (SA-MA) was obtained in ethanol-water mixture (35.5 mM: 4:1 v/v). The morphology of SA-MA was analyzed by various physicochemical characterization techniques, which revealed its micro-metric vesicular architecture as well as nano-vesicular appearances. In this study, treatment of hPBMCs with DOX has been found to generate severe intracellular oxidative stress, which was significantly mitigated after pre-treatment with SA-MA. Alteration of hPBMC morphologies after DOX treatment was also restored notably by pre-treatment with SA-MA. Furthermore, pentoxifylline (TNF-α inhibitor) and indomethacin (COX-2 inhibitor) were used to investigate the responsible pathway by which SA-MA protected hPBMCs from DOX-induced cellular stress. Restoration of hPBMC viability above 92% in both cases confirmed that SA-MA protected the cells by inhibiting inflammatory pathways generated by DOX treatment. Subsequently, in molecular docking study, it was also evaluated that MA could successfully bind with the pocket region of Keap1, while Nrf2 was capable of upregulating cytoprotecting genes.

A Mixture of Multi-Strain Probiotics (Lactobacillus Rhamnosus, Lactobacillus Helveticus, and Lactobacillus Casei)had Anti-Inflammatory, Anti-Apoptotic, and Anti-Oxidative Effects in Oxidative Injuries Induced By Cadmium in Small Intestine and Lung.

Cadmium (Cd) produces severe oxidative stress, which can result in serious clinical consequences and tissue injury. The aim of the present survey was to investigate the protective effects of native Iranian probiotics (Lactobacillus rhamnosus, L. helveticus, and L. casei) against cadmium (Cd)-induced toxicity against the small intestine and lung at histopathological and biochemical levels. Twenty-one adult male Wistar rats were randomized into three groups of seven rats (control, Cd-treated (3mg/kg), and concomitant Cd and mix probiotic treatment for 30days). Histological alterations were appraised via hematoxylin & eosin, Trichrome Masson, and PAS staining. The qRT-PCR technique was applied to assess the expression of pro-apoptotic, anti-apoptotic, and pro-inflammatory genes. Antioxidant enzymes activity was measured via ZellBio kits. Probiotic-treated rats displayed low production of lipid peroxides, reduced malondialdehyde (MDA) level, and elevated contents of superoxide dismutase (SOD) and catalase (CAT) enzymes compared with Cd-treated rats. The results of qRT-PCR demonstrated the up-regulation of Bax, p53, and caspase 3 and down-regulation of Bcl2, TNF-α, and IL-6 genes in both the intestine and lungs of mix probiotic-treated rats compared with Cd-treated animals. Histopathological findings revealed that the probiotic formulation improved Cd-triggered tissue damage in the intestine and lungs. The strong cytoprotective benefits of Iranian probiotics against Cd-induced tissue injury observed in this study may be due to their anti-inflammatory and antioxidant properties. Therefore, additional clinical and experimental research is required to explain the precise mechanisms of probiotics' beneficial impacts and underline their potential therapeutic use.

Efficacy of Prednisolone/Zn Metal Complex and Artemisinin Either Alone or in Combination on Lung Functions after Excessive Exposure to Electronic Cigarettes Aerosol with Assessment of Antibacterial Activity

The use of transition metal complexes as therapeutic compounds has become more and more pronounced. These complexes offer a great diversity of uses in their medicinal applications. Electronic cigarettes (ECs) are an electronic nicotine delivery system that contain aerosol (ECR). The ligation behavior of prednisolone, which is a synthetic steroid that is used to treat allergic diseases and asthma arthritis, and its Zn (II) metal complex were studied and characterized based on elemental analysis, molar conductance, Fourier-transform infrared (FT-IR) spectra, electronic spectra, XRD, scanning electron microscopy (SEM), energy dispersive x-ray (EDX), and transmission electron microscopy (TEM). The FT-IR spectral data revealed that PRD acts as a mono-dentate ligand via oxygen atoms of the carbonyl group. Electronic and FT-IR data revealed that the PRD/Zn (II) metal complexes have square planner geometry. Artemisinin (ART) is the active main constituent of Artemisia annua extract, and it has been demonstrated to exert an excellent antimalarial effect. The experiment was performed on 40 male mice that were divided into the following 7 groups: Control, EC group, PRD/Zn, ART, EC plus PRD/Zn, EC plus ART, and PRD plus combination of PRD/Zn and ART. Serum CRP, IL-6, and antioxidants biomarkers were determined. Pulmonary tissue histology was evaluated. When in combination with Zn administration, PRD showed potent protective effects against pulmonary biochemical alterations induced by ECR and suppressed severe oxidative stress and pulmonary structure alterations. Additionally, PRD/Zn combined with ART prevented any stress on the pulmonary tissues via antioxidant regulation, reducing inflammatory markers CRP and Il-6 and improving antioxidant enzymatic levels more than either PRD or ART alone. Therefore, PRD/Zn combined with ART produced a synergistic effect against any sort of oxidative stress and also improved the histological structure of the lung tissues. These findings are of great importance for saving pulmonary function, especially during pandemic diseases, such as during the COVID-19 pandemic.

Hordeum vulgare L. microgreen mitigates reproductive dysfunction and oxidative stress in streptozotocin-induced diabetes and aflatoxicosis in male rats.

Diabetes mellitus type 2 (DM) is a common chronic disease worldwide, which may be due to increased environmental pollution. Aflatoxin B1 is a likely inevitable contaminant in food and dairy products. Both DM and aflatoxicosis exert a deleterious effect on reproduction urging the exploration of various functional food for protection. This study investigated the effect of barley microgreen (BM) on reproductive disorders caused by DM with or without aflatoxicosis in male rats. Rats were divided into eight groups; G1 control, G2 barley, G3 aflatoxin, G4 aflatoxin‐barley, G5 streptozotocin (STZ), G6 STZ‐barley, G7 STZ‐aflatoxin, and G8 STZ‐aflatoxin‐barley. BM chemical composition revealed elevated calcium, iron, phosphorus, and vitamin A compared with barely seeds. Complete blood picture, lipid profile, serum oxidative stress parameters, relative testicular weight, sperm analysis, chromosomal aberration, and testis histopathology were performed. The lipid profile was altered significantly in G7. Oxidative stress was increased in G3, G5, and G7, whereas it was decreased in BM‐treated groups. Sperm counts were reduced significantly in aflatoxin and/or STZ groups but increased significantly in BM‐treated groups. Sperm morphological abnormalities and chromosomal aberrations were decreased significantly in BM‐treated groups compared with untreated groups. Testicular histopathology revealed moderate diffuse degeneration of seminiferous tubules in aflatoxin and/or STZ groups, which were alleviated in BM‐treated groups. In conclusion, aflatoxin and STZ together caused severe reproductive disorder and oxidative stress more than aflatoxin or STZ alone. BM diet reduced significantly oxidative stress and reproductive disorder associated with DM and aflatoxicosis in rats.

Sustained zeaxanthin-dependent thermal dissipation is induced by desiccation and low temperatures in the fern Polypodium virginianum.

Desiccation and low temperatures inhibit photosynthetic carbon reduction and, in combination with light, result in severe oxidative stress, thus, tolerant organisms must utilize enhanced photoprotective mechanisms to prevent damaging reactions from occurring. We sought to characterize the desiccation tolerance of the fern Polypodium virginianum and to assess the role of the xanthophyll cycle and sustained forms of thermal dissipation in its response to desiccation, as well as to low temperatures during winter. Our results demonstrate that P. virginianum is desiccation-tolerant and that it increases its utilization of sustained forms of zexanthin (Z)-dependent thermal dissipation in response to desiccation and low temperatures during winter. Experiments with detached fronds were conducted in dark and natural light conditions and demonstrated that some dark-formation of Z occurs in this species. In addition, desiccation in the light resulted in more pronounced declines in maximal photochemical efficiency (Fv /Fm ) and higher Z levels than desiccation in the dark, indicating a substantial fraction of the sustained reduction in Fv /Fm is due to Z-dependent sustained dissipation. Recovery from desiccation and from low temperatures exhibited biphasic kinetics with a more rapid phase (1-4 h), which was accompanied by an increase in minimal fluorescence yield (Fo ) but no change in Z, and a slower phase (up to 24 h) correlating with reconversion of Z to violaxanthin. These data suggest that two mechanisms of sustained thermal dissipation occur in response to desiccation and low temperatures, possibly corresponding to sustained forms of the energy-dependent and zeaxanthin-dependent mechanisms of dynamic thermal dissipation.

Curcumin improves D-galactose and normal-aging associated memory impairment in mice: In vivo and in silico-based studies.

Aging-induced memory impairment is closely associated with oxidative stress. D-Galactose (D-gal) evokes severe oxidative stress and mimics normal aging in animals. Curcumin, a natural flavonoid, has potent antioxidant and anti-aging properties. There are several proteins like glutathione S-transferase A1 (GSTA1), glutathione S-transferase omega-1 (GSTO1), kelch-like ECH-associated protein 1 (KEAP1), beta-secretase 1 (BACE1), and amine oxidase [flavin-containing] A (MAOA) are commonly involved in oxidative stress and aging. This study aimed to investigate the interaction of curcumin to these proteins and their subsequent effect on aging-associated memory impairment in two robust animal models: D-Gal and normal aged (NA) mice. The aging mice model was developed by administering D-gal intraperitoneally (i.p). Mice (n = 64) were divided into the eight groups (8 mice in each group): Vehicle, Curcumin-Control, D-gal (100mg/kg; i.p), Curcumin + D-gal, Astaxanthin (Ast) + D-gal, Normal Aged (NA), Curcumin (30mg/kg Orally) + NA, Ast (20mg/kg Orally) + NA. Retention and freezing memories were assessed by passive avoidance (PA) and contextual fear conditioning (CFC). Molecular docking was performed to predict curcumin binding with potential molecular targets. Curcumin significantly increased retention time (p < 0.05) and freezing response (p < 0.05) in PA and CFC, respectively. Curcumin profoundly ameliorated the levels of glutathione, superoxide dismutase, catalase, advanced oxidation protein products, nitric oxide, and lipid peroxidation in mice hippocampi. In silico studies revealed favorable binding energies of curcumin with GSTA1, GSTO1, KEAP1, BACE1, and MAOA. Curcumin improves retention and freezing memory in D-gal and nature-induced aging mice. Curcumin ameliorates the levels of oxidative stress biomarkers in mice. Anti-aging effects of curcumin could be attributed to, at least partially, the upregulation of antioxidant enzymes through binding with GSTA1, GSTO1, KEAP1, and inhibition of oxidative damage through binding with BACE1 and MAOA.

Acetylcholinesterase and butyrylcholinesterase inhibitory activities of antioxidant peptides obtained from enzymatic pea protein hydrolysates and their ultrafiltration peptide fractions.

This study optimized the enzymatic hydrolysis of yellow field pea proteins using alcalase (ACH), chymotrypsin (CHH), flavourzyme (FZH), pancreatin (PCH), pepsin (PEH), and trypsin (TPH) to obtain hydrolysates and ultrafiltered fractions (<1, 1-3, 3-5 and 5-10kDa) that possess antioxidant plus acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) inhibitory activities. The hydrolysates exhibited varying degrees of radical scavenging and inhibition of linoleic acid peroxidation, as well as cholinesterase inhibition activities but the potency generally improved by >10% after UF separation into peptide fractions. ACH, FZH, and PEH exhibited significantly (p< .05) higher (20%-30% increases) radical scavenging activities than the other hydrolysates. The 1 and 3kDa UF fractions of ACH, FZH, and PEH inhibited ~20%-30% AChE activity, while ACH, PCH, TPH, and PEH inhibited ~20%-40% BuChE activity. We conclude that the pea protein hydrolysates and their peptide fractions possess multifunctional properties with potential use against neurodegenerative disorders. PRACTICAL APPLICATIONS: Alzheimer's disease (AD) has multiple pathological pathways in addition to the loss of acetylcholine (ACh) catalyzed by acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). The presence of severe oxidative stress triggered by lipid peroxidation and formation of free radicals is a common trait in AD patients. The concept of AChE and BuChE inhibition as an approach toward AD amelioration involves the use of compounds with a similar structure to ACh, the natural substrate. Peptides derived from food proteins consist of ester bonds with structural similarity to ACh and theoretically possess the ability to interact with AChE and BuChE. Results from the present study imply that pea protein-derived peptides are potential candidates for use as inhibitors of AChE and BuChE activities, with application in the prevention and management of AD.