Impaired Antioxidant Capacity Research Articles

Stable Nitroxide as Diagnostic Tools for Monitoring of Oxidative Stress and Hypoalbuminemia in the Context of COVID-19.

Oxidative stress is a major source of ROS-mediated damage to macromolecules, tissues, and the whole body. It is an important marker in the severe picture of pathological conditions. The discovery of free radicals in biological systems gives a "start" to studying various pathological processes related to the development and progression of many diseases. From this moment on, the enrichment of knowledge about the participation of free radicals and free-radical processes in the pathogenesis of cardiovascular, neurodegenerative, and endocrine diseases, inflammatory conditions, and infections, including COVID-19, is increasing exponentially. Excessive inflammatory responses and abnormal reactive oxygen species (ROS) levels may disrupt mitochondrial dynamics, increasing the risk of cell damage. In addition, low serum albumin levels and changes in the normal physiological balance between reduced and oxidized albumin can be a serious prerequisite for impaired antioxidant capacity of the body, worsening the condition in patients. This review presents the interrelationship between oxidative stress, inflammation, and low albumin levels, which are hallmarks of COVID-19.

Multi-omics analysis reveals a crosstalk between ferroptosis and peroxisomes on steatotic graft failure after liver transplantation.

To identify the mechanism underlying macrosteatosis (MaS)-related graft failure (GF) in liver transplantation (LT) by multi-omics network analysis. The transcriptome and metabolome were assayed in graft and recipient plasma in discovery (n=68) and validation (n=89) cohorts. Differentially expressed molecules were identified by MaS and GF status. Transcriptional regulatory networks were generated to explore the mechanism for MaS-related inferior post-transplant prognosis. The differentially expressed molecules associated with MaS and GF were enriched in ferroptosis and peroxisome-related pathways. Core features of MaS-related GF were presented on decreased transferrin and impaired anti-oxidative capacity dependent upon dysregulation of transcription factors hepatocytenuclear factor 4A (HNF4A) and hypoxia-inducible factor 1A (HIF1A). Furthermore, miR-362-3p and miR-299-5p inhibited transferrin and HIF1A expression, respectively. Lower M2 macrophages but higher memory CD4 T cells were observed in MaS-related GF cases. These results were validated in clinical specimens and cellular models. Systemic analysis of multi-omics data depicted a panorama of biological pathways deregulated in MaS-related GF. Transcriptional regulatory networks centered on transferrin and anti-oxidant responses were associated with poor MaS graft quality, qualifying as potential targets to improve prognosis of patients after LT.

In Silico Evaluation of the Interaction of Marine-derived Bioactive Compounds against Heme-oxygenase 1 – a Putative Ferroptosis Target

Ferroptosis is a novel iron-dependent form of regulated necrotic cell death characterized by extensive lipid peroxidation arising from an impaired antioxidant capacity of the cell. It has been implicated in various pathophysiological conditions such as cancer and neurodegenerative diseases. Heme-oxygenase 1 (HO-1) contributes to ferroptosis through its breakdown of heme, releasing Fe2+, which could challenge the body’s ferritin systems during periods of heightened cellular stress, making HO-1 a promising target to exploit the therapeutic potential of ferroptosis. This study investigated a library of 136 marine-derived bioactive compounds for their interaction with HO-1 using in silico approaches. Based on a co-crystal structure, the compounds were docked on the target protein to assess binding free energies (BFE) and conformations. Clustering analysis yielded BFEs that ranged from 15.9 kcal/mol to –11.8 kcal/mol. Interaction analysis of the top 10 compounds with the most negative BFEs showed comparable interactions with the previously co-crystallized HO-1 inhibitor. Furthermore, the top compounds were subjected to ADMET analysis, and – although all exhibited drug-likeness – Lipinski violations,and toxicity risks were nonetheless predicted. The docking results of the top compound, paraminabeolide F (1), were then validated using molecular dynamics (MD) simulations over 100 ns through RMSD, RMSF, radius of gyration, and molecular mechanics Poisson-Boltzmann surface area (MMPBSA) analyses, which confirmed the favorable interactions with HO-1.

Research progress of ferroptosis and inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a non-specific chronic inflammatory disorder of the gastrointestinal tract, imposing significant burdens on both society and individuals. As a new type of regulated cell death (RCD), ferroptosis is different from classic RCDs such as apoptosis and necrosis in cell morphology, biochemistry and genetics. The main molecular mechanisms of ferroptosis include dysregulation of iron metabolism, impaired antioxidant capacity, mitochondrial dysfunction, accumulation of lipid-associated super-oxides, and membrane disruption. In recent years, increasing evidence has shown that ferroptosis is involved in the pathophysiology of inflammatory bowel disease. However, the exact roles and underlying molecular mechanisms have not been fully elucidated. This article reviews the mechanism of ferroptosis in the occurrence and development of inflammatory bowel disease, in order to provide new ideas for the pathophysiological research of inflammatory bowel disease. Additionally, we discuss potential strategies for the prevention and treatment of inflammatory bowel disease by targeting ferroptosis.

Dietary Lycium barbarum Polysaccharide Modulates Growth Performance, Antioxidant Capacity, and Lipid Metabolism in Common Carp (Cyprinus carpio) Fed with High-Fat Diet.

To investigate the ameliorative effects and mechanism of Lycium barbarum polysaccharide (LBP) on growth performance, oxidative stress, and lipid deposition in common carp (Cyprinus carpio) fed with high-fat diets, fish with an initial weight of 5.29 ± 0.12 g were divided into five experimental groups-including normal-fat diets, high-fat diets, and high-fat diets-supplemented with LBP (0.5, 1.0, and 2.0 g/kg) for 8 weeks. The results showed that high-fat diets resulted in significant decreases in final body weight, weight gain rate, and specific growth rate of fish, as well as causing a significant decrease in hepatic total antioxidant capacity, catalase, and glutathione peroxidase activities. These changes were accompanied by a significant decrease in lipase activity and ATP level and a significant increase in malondialdehyde content. The expression levels of lipid metabolism-related genes (acetyl coenzyme A carboxylase 1, stearoyl coenzyme A desaturase 1, fat synthase, peroxisome proliferator-activated receptor-γ, fructofuranose bisphosphatase, and glucose-6-phosphatase) were also markedly elevated by high-fat diets. Supplementation with 0.5-2.0 g/kg LBP in high-fat diets improved the reduced growth performance, increased hepatic total antioxidant enzymes, catalase, and glutathione peroxidase activities, and lowered malondialdehyde level in fish fed with high-fat diets. Additionally, dietary supplementation with LBP significantly downregulated hepatic gene expression levels of acetyl coenzyme A carboxylase 1, stearoyl coenzyme A desaturase 1, fat synthase, sterol regulatory element-binding protein 1, peroxisome proliferator-activated receptor-γ, fructofuranose bisphosphatase, and glucose-6-phosphatase. In conclusion, fish fed with high-fat diets demonstrated impaired growth performance, antioxidant capacity, and lipid metabolism, and dietary supplementation with 0.5-2.0 g/kg LBP ameliorated the impairments induced by high-fat diets.

Protective effect of Broussonetia papyrifera leaf polysaccharides on intestinal integrity in a rat model of diet-induced oxidative stress

This study aimed to investigate the effect of Broussonetia papyrifera polysaccharides (BPP) on the jejunal intestinal integrity of rats ingesting oxidized fish oil (OFO) induced oxidative stress. Polysaccharides (Mw 16,956 Da) containing carboxyl groups were extracted from Broussonetia papyrifera leaves. In vitro antioxidant assays showed that this polysaccharide possessed antioxidant capabilities. Thirty-two male weaned rats were allocated into two groups orally infused BPP solution and PBS for 26 days, respectively. From day 9 to day 26, half of the rats in each group were fed food containing OFO, where the lipid peroxidation can induce intestinal oxidative stress. OFO administration resulted in diarrhea, decreased growth performance (p < 0.01), impaired jejunal morphology (p < 0.05) and antioxidant capacity (p < 0.01), increased the levels of ROS and its related products, IL-1β and IL-17 (p < 0.01) of jejunum, as well as down-regulated Bcl-2/Bax (p < 0.01) and Nrf2 signaling (p < 0.01) of jejunum in rats. BPP gavage effectively alleviated the negative effects of OFO on growth performance, morphology, enterocyte apoptosis, antioxidant capacity and inflammation of jejunum (p < 0.05) in rats. In the oxidative stress model cell assay, the use of receptor inhibitors inhibited the enhancement of antioxidant capacity by BPP. These results suggested that BPP protected intestinal morphology, thus improving growth performance and reducing diarrhea in rats ingesting OFO. This protective effect may be attributed to scavenging free radicals and activating the Nrf2 pathway, which enhances antioxidant capacity, consequently reducing inflammation and mitigating intestinal cell death.

Chemotherapy impairs ovarian function through excessive ROS-induced ferroptosis

Chemotherapy was conventionally applied to kill cancer cells, but regrettably, they also induce damage to normal cells with high-proliferative capacity resulting in cardiotoxicity, nephrotoxicity, peripheral nerve toxicity, and ovarian toxicity. Of these, chemotherapy-induced ovarian damages mainly include but are not limited to decreased ovarian reserve, infertility, and ovarian atrophy. Therefore, exploring the underlying mechanism of chemotherapeutic drug-induced ovarian damage will pave the way to develop fertility-protective adjuvants for female patients during conventional cancer treatment. Herein, we firstly confirmed the abnormal gonadal hormone levels in patients who received chemotherapy and further found that conventional chemotherapeutic drugs (cyclophosphamide, CTX; paclitaxel, Tax; doxorubicin, Dox and cisplatin, Cis) treatment significantly decreased both the ovarian volume of mice and the number of primordial and antral follicles and accompanied with the ovarian fibrosis and reduced ovarian reserve in animal models. Subsequently, Tax, Dox, and Cis treatment can induce the apoptosis of ovarian granulosa cells (GCs), likely resulting from excessive reactive oxygen species (ROS) production-induced oxidative damage and impaired cellular anti-oxidative capacity. Thirdly, the following experiments demonstrated that Cis treatment could induce mitochondrial dysfunction through overproducing superoxide in GCs and trigger lipid peroxidation leading to ferroptosis, first reported in chemotherapy-induced ovarian damage. In addition, N-acetylcysteine (NAC) treatment could alleviate the Cis-induced toxicity in GCs by downregulating cellular ROS levels and enhancing the anti-oxidative capacity (promoting the expression of glutathione peroxidase, GPX4; nuclear factor erythroid 2-related factor 2, Nrf2 and heme oxygenase-1, HO-1). Our study confirmed the chemotherapy-induced chaotic hormonal state and ovarian damage in preclinical and clinical examination and indicated that chemotherapeutic drugs initiated ferroptosis in ovarian cells through excessive ROS-induced lipid peroxidation and mitochondrial dysfunction, leading to ovarian cell death. Consequently, developing fertility protectants from the chemotherapy-induced oxidative stress and ferroptosis perspective will ameliorate ovarian damage and further improve the life quality of cancer patients.

Integrative transcriptomic and metabolomic analysis reveals alterations in energy metabolism and mitochondrial functionality in broiler chickens with wooden breast

This integrative study of transcriptomics and metabolomics aimed to improve our understanding of Wooden Breast myopathy (WB). Breast muscle samples from 8 WB affected and 8 unaffected male broiler chickens of 47 days of age were harvested for metabolite profiling. Among these 16 samples, 5 affected and 6 unaffected also underwent gene expression profiling. The Joint Pathway Analysis was applied on 119 metabolites and 3444 genes exhibiting differential abundance or expression between WB affected and unaffected chickens. Mitochondrial dysfunctions in WB was suggested by higher levels of monoacylglycerols and down-regulated genes involved in lipid production, fatty acid beta oxidation, and oxidative phosphorylation. Lower levels of carnosine and anserine, along with down-regulated carnosine synthase 1 suggested decreased carnosine synthesis and hence impaired antioxidant capacity in WB. Additionally, Weighted Gene Co-expression Network Analysis results indicated that abundance of inosine monophosphate, significantly lower in WB muscle, was correlated with mRNA expression levels of numerous genes related to focal adhesion, extracellular matrix and intercellular signaling, implying its function in connecting and possibly regulating multiple key biological pathways. Overall, this study showed not only the consistency between transcript and metabolite profiles, but also the potential in gaining further insights from analyzing multi-omics data.

Selenium, Stroke, and Infection: A Threefold Relationship; Where Do We Stand and Where Do We Go?

Stroke is currently the second most common cause of death worldwide and a major cause of serious long-term morbidity. Selenium is a trace element with pleotropic effects on human health. Selenium deficiency has been associated with a prothrombotic state and poor immune response, particularly during infection. Our aim was to synthesize current evidence on the tripartite interrelationship between selenium levels, stroke, and infection. Although evidence is contradictory, most studies support the association between lower serum selenium levels and stroke risk and outcomes. Conversely, limited evidence on the role of selenium supplementation in stroke indicates a potentially beneficial effect of selenium. Notably, the relationship between stroke risk and selenium levels is bimodal rather than linear, with higher levels of serum selenium linked to disturbances of glucose metabolism and high blood pressure, morbidities which are, in turn, substrates for stroke. Another such substrate is an infection, albeit forming a bidirectional relationship with both stroke and the consequences of impaired selenium metabolism. Perturbed selenium homeostasis leads to impaired immune fitness and antioxidant capacity, which both favor infection and inflammation; specific pathogens may also contend with the host for transcriptional control of the selenoproteome, adding a feed-forward loop to this described process. Broader consequences of infection such as endothelial dysfunction, hypercoagulation, and emergent cardiac dysfunction both provide stroke substrates and further feed-forward feedback to the consequences of deficient selenium metabolism. In this review, we provide a synthesis and interpretation of these outlined complex interrelationships that link selenium, stroke, and infection and attempt to decipher their potential impact on human health and disease. Selenium and the unique properties of its proteome could provide both biomarkers and treatment options in patients with stroke, infection, or both.

The protective role of vitamin C on intestinal damage induced by high-dose glycinin in juvenile Rhynchocypris lagowskii Dybowski

This study was to evaluate the mitigative effects of vitamin C (VC) on growth inhibition and intestinal damage induced by glycinin in juvenile Rhynchocypris lagowskii Dybowski. 270 healthy juvenile Rhynchocypris lagowskii Dybowski (4.65 ± 0.04 g) were randomly divided into 3 treatments, and fed with control diet, 80 g/kg glycinin diet and 80 g/kg glycinin+200 mg/kg VC diet respectively for 8 weeks. The results showed that glycinin significantly decreased the weight gain rate, specific growth rate, protein efficiency rate, feed efficiency rate and feeding rate of fish compared with the control group (P < 0.05), while VC supplementation improved the growth performance and feed utilization efficiency, and reached a level similar to the control group. Similarly, VC significantly increased the crude protein content of muscle and whole-body, and hepatopancreas and intestinal protease activities of fish fed with glycinin diet (P < 0.05). The distal intestine of fish in glycinin group showed typical damage characteristics, including breakage and atrophy of intestinal mucosal fold, and increased intestinal mucosal permeability. However, fish fed the glycinin + VC diet showed an unimpaired normal intestinal morphology. Usefully, VC supplementation could also restore impaired immune function and antioxidant capacity. VC down-regulated the mRNA levels of pro-inflammatory cytokines TNF‐α and IL-1β, and up-regulated the mRNA levels of anti-inflammatory cytokines IL-10 and TGF-β in the distal intestine of fish fed with glycinin. Furthermore, glycinin exposure could reduce the mRNA levels of HO-1, CAT and GPx by inhibiting the activation of Nrf2-Keap1 signaling pathway, while VC supplementation reversed this phenomenon and maintained the homeostasis of antioxidant defense system. Concluded, glycinin causes growth inhibition, digestive dysfunction and intestinal damage of Rhynchocypris lagowskii Dybowski, while sufficient VC intake is beneficial for fish to resist the adverse effects of glycinin.

Citric Acid and Magnolol Ameliorate Clostridium perfringens Challenge in Broiler Chickens.

Clostridium perfringens (C. perfringens) is a common pathogenic bacterium implicated in the enteric diseases of animals. Each year, the disease is responsible for billions of dollars of losses worldwide. The development of new phytomedicines as alternatives to antibiotics is becoming a new hotspot for treating such diseases. Citric acid (CA) and magnolol (MA) have been shown to have antibacterial, antioxidant, and growth-promoting properties. Here, the bacteriostatic effects of combinations of CA and MA against C. perfringens were investigated, together with their effects on yellow-hair chickens challenged with C. perfringens. It was found that the optimal CA:MA ratio was 50:3, with a dose of 265 μg/mL significantly inhibiting C. perfringens growth, and 530 μg/mL causing significant damage to the bacterial cell morphology. In animal experiments, C. perfringens challenge reduced the growth, damaged the intestinal structure, activated inflammatory signaling, impaired antioxidant capacity, and perturbed the intestinal flora. These effects were alleviated by combined CA-MA treatment. The CA-MA combination was found to inhibit the TLR/Myd88/NF-κB and Nrf-2/HO-1 signaling pathways. In conclusion, the results suggest the potential of combined CA-MA treatment in alleviating C. perfringens challenge by inhibiting the growth of C. perfringens and affecting the TLR/MyD88/NF-κB and Nrf-2/HO-1 signaling pathways.

Targeting ferroptosis in cardio-metabolic-diseases: Mechanisms and therapeutic prospects.

Cardio-metabolic-diseases (cardio-metabolic-diseases) are leading causes of death and disability worldwide and impose a tremendous burden on whole society as well as individuals. As a new type of regulated cell death (RCD), ferroptosis is distinct from several classical types of RCDs such as apoptosis and necroptosis in cell morphology, biochemistry, and genetics. The main molecular mechanisms of ferroptosis involve iron metabolism dysregulation, mitochondrial malfunction, impaired antioxidant capacity, accumulation of lipid-related peroxides and membrane disruption. Within the past few years, mounting evidence has shown that ferroptosis contributes to the pathophysiological process in cardio-metabolic-diseases. However, the exact roles and underlying molecular mechanisms have not been fully elucidated. This review comprehensively summarizes the mechanism of ferroptosis in the development and progression of cardio-metabolic-diseases, so as to provide new insights for cardio-metabolic-diseases pathophysiology. Moreover, we highlight potential druggable molecules in ferroptosis signaling pathway, and discuss recent advances in management strategies by targeting ferroptosis for prevention and treatment of cardio-metabolic-diseases.

Obesity Affects Maternal and Neonatal HDL Metabolism and Function.

Pregravid obesity is one of the major risk factors for pregnancy complications such as gestational diabetes mellitus (GDM) and an increased risk of cardiovascular events in children of affected mothers. However, the biological mechanisms that underpin these adverse outcomes are not well understood. High-density lipoproteins (HDLs) are antiatherogenic by promoting the efflux of cholesterol from macrophages and by suppression of inflammation. Functional impairment of HDLs in obese and GDM-complicated pregnancies may have long-term effects on maternal and offspring health. In the present study, we assessed metrics of HDL function in sera of pregnant women with overweight/obesity of the DALI lifestyle trial (prepregnancy BMI ≥ 29 kg/m2) and women with normal weight (prepregnancy BMI < 25 kg/m2), as well as HDL functionalities in cord blood at delivery. We observed that pregravid obesity was associated with impaired serum antioxidative capacity and lecithin−cholesterol acyltransferase activity in both mothers and offspring, whereas maternal HDL cholesterol efflux capacity was increased. Interestingly, functionalities of maternal and fetal HDL correlated robustly. GDM did not significantly further alter the parameters of HDL function and metabolism in women with obesity, so obesity itself appears to have a major impact on HDL functionality in mothers and their offspring.

Deciphering the disturbance mechanism of BaP on the symbiosis of Montipora digitata via 4D-Proteomics approach

The coral holobiont is mainly composed of coral polyps, zooxanthellae, and coral symbiotic microorganisms, which form the basis of coral reef ecosystems. In recent years, the severe degradation of coral reefs caused by climate warming and environmental pollution has aroused widespread concern. Benzo(a)pyrene (BaP) is a widely distributed pollutant in the environment. However, the underlying mechanisms of coral symbiosis destruction due to the stress of BaP are not well understood. In this study, diaPASEF proteomics and 16S rRNA amplicon pyrosequencing technology were used to reveal the effects of 50 μg/L BaP on Montipora digitate. Data analysis was performed from the perspective of the main symbionts of M. digitata (coral polyps, zooxanthellae, and coral symbiotic microorganisms). The results showed that BaP impaired cellular antioxidant capacity by disrupting the GSH/GSSG cycle, and sustained stress causes severe impairment of energy metabolism and protein degradation in coral polyps. In zooxanthellae, BaP downregulated the protein expression of SOD2 and mtHSP70, which then resulted in oxidative free radical accumulation and apoptosis. For coral symbiotic microorganisms, BaP altered the community structure of microorganisms and decreased immunity. Coral symbiotic microorganisms adapted to the stress of BaP by adjusting energy metabolism and enhancing extracellular electron transfer. BaP adversely affected the three main symbionts of M. digitata via different mechanisms. Decreased antioxidant capacity is a common cause of damages to coral polyps and zooxanthellae, whereas coral symbiotic microorganisms are able to appropriately adapt to oxidative stress. This study assessed the effects of BaP on corals from a symbiotic perspective, which is more comprehensive and reliable. At the same time, data from the study supports new directions for coral research and coral reef protection.

Dexmedetomidine attenuates airway inflammation and oxidative stress in asthma via the Nrf2 signaling pathway.

Allergic asthma is a chronic inflammatory disease in which oxidative stress serves a pivotal role. In clinical practice, dexmedetomidine (DEX), an α‑2‑adrenergic receptor agonist, is used as a sedative. DEX exhibits antioxidative and organ‑protective properties. In a murine model of asthma, DEX has a therapeutic effect via the toll like receptor 4/NF‑кB signaling pathway; however, whether DEX can exert an antioxidative effect on asthma has yet to be elucidated. In the present study, a T helper (Th)2‑dominant murine asthma model was established. DEX treatment significantly reduced eosinophilic airway inflammation, mucus overproduction and airway hyperresponsiveness, as well as the concentrations of Th2 cytokines. The lung tissues of mice with asthma were characterized by redox imbalance (increased oxidative stress and impaired antioxidant capacity). DEX treatment alleviated this imbalance by decreasing the levels of malondialdehyde and reactive oxygen species, and increasing the levels of glutathione. Furthermore, the nuclear factor erythroid 2‑related factor 2 (Nrf2) signaling pathway was inhibited in the lung tissues of asthmatic mice; these effects were noted in its downstream genes, heme oxygenase 1 and glutathione peroxidase 4. In mice with asthma, DEX treatment induced the expression of these antioxidant genes and the activation of Nrf2, whereas ML385 (an inhibitor of Nrf2) partially abrogated the antioxidative and therapeutic effects of DEX. To the best of our knowledge, the present study is the first to demonstrate the protective effect of DEX on Th2‑dominant asthma through the activation of the Nrf2 signaling pathway. The results suggested that the antioxidative properties of DEX could be beneficial in clinical application of DEX for the relief of asthmatic symptoms.

Protective effects of selenized yeast on the combination of cadmium-, lead-, mercury-, and chromium-induced toxicity in laying hens

The objective of this study was to investigate the toxic effects of a combination of cadmium (Cd), lead (Pb), mercury (Hg), and chromium (Cr) on laying performance, egg quality, serum biochemical parameters, and oxidative stress of laying hens, as well as the alleviating action of dietary supplementation of selenized yeast. A total of 160 Lohmann pink-shell laying hens (63-week-old) were randomly divided into four treatments with 10 replicates of four hens each. The treatments were the corn–soybean meal basal diet (control; CON), the CON diet supplemented with 0.4 mg selenium (Se)/kg from selenized yeast (Se); combined heavy metals group: the basal diet supplemented with 5 mg Cd/kg, 50 mg Pb/kg, 3 mg Hg/kg, and 5 mg Cr/kg (HEM), and the HEM diet supplemented with 0.4 mg Se/kg from selenized yeast (HEM+Se). The experimental period lasted for 12 weeks. The HEM diet decreased hen-day egg production, feed conversion ratio (FCR), and egg white quality (P < 0.05), but increased (P < 0.05) glutamic oxalacetic transaminase (AST) activity in the serum. HEM induced higher malondialdehyde (MDA) and reactive oxygen species (ROS) in the serum, liver, and ovary and significantly decreased (P < 0.05) the activity of total superoxide dismutase (SOD) and tended to decrease glutathione S-transferase (GST) (P = 0.09) in the serum. Meanwhile, HEM significantly decreased (P < 0.05) activity of SOD, GST, glutathione peroxidase (GPX), and glutathione (GSH) in the liver, and the activity of GPX and GSH in the ovary. Se addition of 0.4 mg/kg significantly (P < 0.05) improved hen-day egg production and FCR and decreased AST concentration and increased some enzyme activity in the serum, liver, and ovary. In conclusion, dietary HEM exposure depressed laying performance, and egg white quality was likely due to an impaired antioxidant capacity, disrupted hepatic function, and elevated HEM accumulation in the egg yolk and egg white of laying hens. Se addition of 0.4 mg/kg ameliorated toxic effects of HEM on laying performance, oxidative stress, and hepatic function.

Taurine can improve intestinal function and integrity in juvenile Rhynchocypris lagowskii Dybowski fed high-dose glycinin

The present study evaluated the protective effect and the regulatory mechanism of taurine on growth inhibition and intestinal damage induced by glycinin in juvenile Rhynchocypris lagowskii Dybowski. The control diets had no glycinin and taurine, the glycinin diets contained only 80 g/kg glycinin, and the glycinin + taurine diets contained 80 g/kg glycinin+10 g/kg taurine. Juvenile Rhynchocypris lagowskii Dybowski (4.65 ± 0.03 g/tail) were respectively fed with these 3 diets for 8 weeks. The results showed that glycinin significantly decreased the final body weight, weight gain rate, specific growth rate, protein efficiency rate, feed efficiency rate and feeding rate of fish compared with the control group (P < 0.05). While taurine supplementation improved the growth performance and feed efficiency, but final body weight, weight gain rate, specific growth rate of the glycinin + taurine group were still significantly lower than the control group (P < 0.05). Compared with the glycinin group, taurine supplementation significantly increased whole-body and muscle crude protein content, and hepatopancreas and intestinal protease activities (P < 0.05). Distal intestinal villous dysplasia and mucosal damage, and increased intestinal mucosal permeability were observed in the glycinin group, while taurine supplementation alleviated these adverse effects. Usefully, taurine supplementation could also partially restore the impaired immune function and antioxidant capacity of fish fed glycinin diets. Compared with the glycinin group, taurine supplementation down-regulated pro-inflammatory cytokines TNF‐α and IL-1β mRNA levels, and up-regulated anti-inflammatory cytokines IL-10 and TGF-β mRNA levels. Furthermore, taurine partially reversed the reduction of antioxidant genes Nrf2、HO-1, CAT and GPx mRNA levels in distal intestine induced by glycinin. Concluded, 80 g/kg glycinin led to intestinal damage, digestive dysfunction and increased intestinal mucosal permeability in juvenile Rhynchocypris lagowskii Dybowski, and these adverse effects were ultimately manifested in growth inhibition. But taurine supplementation could partially mitigate the negative effects induced by glycinin.

Autotoxicity effect of water extracts from rhizosphere soil of Elymus sibiricus in different planting years on seed germination, physiological characteristics and phytohormones of seedlings.

Elymus sibiricus is a highly valuable perennial forage that is widely planted in the Qinghai-Tibet Plateau (QTP) region. However, E. sibiricus artificial grasslands have a short utilization lifespan, and reach the highest yield in the 2nd and 3rd year of plantation, then rapidly drop its productivity. We hypothesized that autotoxicity is one of the mechanisms for the reduction of the productivity. To test this hypothesis, we prepared the water extract from rhizosphere soils of E. sibiricus planted for 3, 4, 5, and 8 years and examined the effects of the extract concentrations at 0.05, 0.1, 0.2, and 0.5 g/mL on seed germination, seedling growth, physiological characteristics and phytohormones in the aboveground and roots of E. sibiricus. The results showed that the soil extract concentration, planting years, and their interaction had significant influences on the most of these indices. The soil extract inhibited the seed germination and growth of seedlings, and the inhibitory effects appeared to be stronger at the 0.5 g/mL rhizosphere soil extract for 5 and 8 years. The superoxide dismultase and peroxide activities, the free proline concentration, soluble sugar concentration were altered. The malondialdehyde concentration was, in general, increased, especially in 8 years soil extract. The indole acetic acid and gibberellic acids concentrations were lowered, while the abscisic acid concentration varied. These changes were depending on the extract concentration and the years of planting, without clear patterns in some of them in response to the extract concentration and planting years. In summary, autotoxicity can be a contributor to the retardation of the growth and development of artificial E. sibiricus grasslands. The inhibitory effects could be attribute to impaired antioxidant capacity and disturbance of osmortic-regulatory substances and plant hormones, and are more profound on the root than on the aboveground part of the seedlings.

Hepatic Lipid Accumulation and Dysregulation Associate with Enhanced Reactive Oxygen Species and Pro-Inflammatory Cytokine in Low-Birth-Weight Goats.

Simple SummaryIn livestock, a low birth weight (LBW) has a broad impact on neonatal survival, growth performance, and metabolic health in adult life. The liver plays an important role to regulate lipid metabolism, but the development of hepatic dyslipidemia associated with LBW is still unknown in goats. Herein, we evaluated lipid and metabolic status of LBW livers in contrast to those of newborns with normal birth weight. RNA sequencing was used to screen potential dysregulated functional genes involved in hepatosteatosis. Results showed lower antioxidant capacity, enhanced pro-inflammatory cytokine, and increased hepatic lipid accumulation in LBW goats associated with impaired regulatory machineries. Understanding the knowledge of intrinsic mechanism underlying hepatic dyslipidemia in LBW goats could provide important implications for promoting efficiency of production and health in their later life.Occurrence of low birth weight (LBW) is a major concern in livestock production, resulting in poor postnatal growth, lowered efficiency of feed utilization, and impaired metabolic health in adult life. In the southwest region of China, birth weight of indigenous strains of goats varies seasonally with lower weights in summer and winter, but the metabolic regulation of the LBW offspring is still unknown. In this study, by comparing LBW goats to normal birth weight group, we examined hepatic lipid content in association with regulatory mechanisms. Histological studies showed higher microvesicular morphology in the liver of LBW goats in accompany with a significantly higher level of hepatic free fatty acids, total triglycerides, and cholesterols. Lipid metabolism impairment, increased oxidative stress, and inflammation were observed by transcriptome analysis. Meanwhile, Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation further demonstrated lipid peroxidation, antioxidant pathway, and pro-inflammatory response involved in the hepatic lipid dysregulation from LBW group. Therefore, dysregulations of hepatic lipid metabolism, including fatty acid biosynthesis and degradation, lipid transportation, and oxidative stress, played important roles to contribute the lipid accumulation in LBW goats. Moreover, due to impaired antioxidant capacity, the oxidative damage could interact with persisting pro-inflammatory responses, leading to a higher risk of liver injury and metabolic syndromes in their adult life.

Association of anti-oxidative capacity of HDL with subclinical atherosclerosis in subjects with and without non-alcoholic fatty liver disease

BackgroundNon-alcoholic fatty liver disease (NAFLD) patients are at a substantial risk for developing cardiovascular disease (CVD). High-density lipoprotein (HDL) is well known to have protective effects against the development of atherosclerotic CVD. One of the major antiatherogenic effects of HDL is its anti-oxidative function.ObjectivesThis study investigated the association of anti-oxidative capacity of HDL with subclinical atherosclerosis in NAFLD and non-NAFLD subjects.MethodsA total of 143 subjects including 51 NAFLD and 92 control subjects were included in this case–control study. HDL oxidative index (HOI) was determined spectrophotometrically using a cell-free method in the presence of a fluorescent substrate dichlorofluorescein diacetate (DCFDA). Paraoxonase 1 (PON1) activity, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) plasma levels were assessed in both groups.ResultsThe NAFLD patients with impaired HDL anti-oxidative function (HOI ≥ 1) had higher MDA levels, aspartate amino transferase (AST), liver stiffness (LS), and carotid intima-media thickness (cIMT) values compared to the controls. HDL oxidative index (HOI) was positively correlated with MDA levels and cIMT and negatively correlated with SOD activity.ConclusionsHigher circulating levels of MDA were associated with the impaired anti-oxidative function of HDL in NAFLD. The impaired anti-oxidative capacity of HDL might be related to NAFLD severity and subclinical atherosclerosis in NAFLD patients.