Total Glutathione Content Research Articles

In vitro airway models from mice, rhesus macaques, and humans maintain species differences in xenobiotic metabolism and cellular responses to naphthalene.

The translational value of high-throughput toxicity testing will depend on pharmacokinetic validation. Yet, popular in vitro airway epithelia models were optimized for structure and mucociliary function without considering the bioactivation or detoxification capabilities of lung-specific enzymes. This study evaluated xenobiotic metabolism maintenance within differentiated air-liquid interface (ALI) airway epithelial cell cultures (human bronchial; human, rhesus, and mouse tracheal), isolated airway epithelial cells (human, rhesus, and mouse tracheal; rhesus bronchial), and ex vivo microdissected airways (rhesus and mouse) by measuring gene expression, glutathione content, and naphthalene metabolism. Glutathione levels and detoxification gene transcripts were measured after 1-h exposure to 80 µM naphthalene (a bioactivated toxicant) or reactive naphthoquinone metabolites. Glutathione and glutathione-related enzyme transcript levels were maintained in ALI cultures from all species relative to source tissues, while cytochrome P450 monooxygenase gene expression declined. Notable species differences among the models included a 40-fold lower total glutathione content for mouse ALI trachea cells relative to human and rhesus; a higher rate of naphthalene metabolism in mouse ALI cultures for naphthalene-glutathione formation (100-fold over rhesus) and naphthalene-dihydrodiol production (10-fold over human); and opposite effects of 1,2-naphthoquinone exposure in some models-glutathione was depleted in rhesus tissue but rose in mouse ALI samples. The responses of an immortalized bronchial cell line to naphthalene and naphthoquinones were inconsistent with those of human ALI cultures. These findings of preserved species differences and the altered balance of phase I and phase II xenobiotic metabolism among the characterized in vitro models should be considered for future pulmonary toxicity testing.

Level of oxidative stress for the land snail Cepaea nemoralis from aged and bioremediated soil contaminated with petroleum products.

Here, we investigated whether the widely distributed snail Cepaea nemoralis could be used as a suitable sentinel animal for assessing the effects of soil contaminants-petroleum oil derivatives-after years of soil ageing and treatment with a bacterial formulation. Oxidative stress was assessed in the foot and hepatopancreas of C. nemoralis L. exposed to soil contaminated with unleaded petrol, spent engine oil or diesel oil and bioremediated with a bacterial formulation (soil was used 2years after contamination and bioremediation process). We measured total antioxidant capacity, catalase and glutathione transferase activity and concentrations of superoxide anions, hydrogen peroxide and protein carbonyls in the foot and hepatopancreas of snails after 2 and 4weeks of treatment. The studied antioxidant responses appeared largely to be tissue and remediation process specific, while the concentrations of superoxide anions, hydrogen peroxide and protein carbonyls depended on time of exposure, tissue type and the type of contaminants, but mostly not on the remediation process. Generally, changes in the concentrations of superoxide anions, hydrogen peroxide and protein carbonyls in the hepatopancreas of snails seemed to be a suitable measure to assess the risk of animals exposed to soil contaminated with petroleum substances and used after many years of ageing and treatment with a microbial formulation.

Understanding the Behaviour of Human Cell Types under Simulated Microgravity Conditions: The Case of Erythrocytes.

Erythrocytes are highly specialized cells in human body, and their main function is to ensure the gas exchanges, O2 and CO2, within the body. The exposure to microgravity environment leads to several health risks such as those affecting red blood cells. In this work, we investigated the changes that occur in the structure and function of red blood cells under simulated microgravity, compared to terrestrial conditions, at different time points using biochemical and biophysical techniques. Erythrocytes exposed to simulated microgravity showed morphological changes, a constant increase in reactive oxygen species (ROS), a significant reduction in total antioxidant capacity (TAC), a remarkable and constant decrease in total glutathione (GSH) concentration, and an augmentation in malondialdehyde (MDA) at increasing times. Moreover, experiments were performed to evaluate the lipid profile of erythrocyte membranes which showed an upregulation in the following membrane phosphocholines (PC): PC16:0_16:0, PC 33:5, PC18:2_18:2, PC 15:1_20:4 and SM d42:1. Thus, remarkable changes in erythrocyte cytoskeletal architecture and membrane stiffness due to oxidative damage have been found under microgravity conditions, in addition to factors that contribute to the plasticity of the red blood cells (RBCs) including shape, size, cell viscosity and membrane rigidity. This study represents our first investigation into the effects of microgravity on erythrocytes and will be followed by other experiments towards understanding the behaviour of different human cell types in microgravity.

Zinc Oxide Nanoparticle Improves the Intestinal Function of Intrauterine Growth Retardation Finishing Pigs via Regulating Intestinal Morphology, Inflammation, Antioxidant Status and Autophagy.

This study was to investigate effects of zinc oxide nanoparticle (Nano-ZnO) on growth, immunity, intestinal morphology and function of intrauterine growth retardation (IUGR) finishing pigs. Six normal birth weight (NBW) and 12 IUGR male piglets were obtained and weaned at 21 d. NBW-weaned piglets fed basal diets (NBW group), IUGR-weaned piglets allocated to two groups fed basal diets (IUGR group) and basal diets further supplemented 600 mg Zn/kg from Nano-ZnO (IUGR+Zn group), respectively. All pigs were slaughtered at 163 d. Results showed: (1) IUGR pigs showed no difference in body weight at 77d and 163d (P > 0.05), while had increased villus height (VH) and villus surface area in jejunum (P < 0.05) and enhanced interleukin-6, TNF-α and NF-κB mRNA expression (P < 0.05) as compared to NBW group; Compared with IUGR group, dietary Nano-ZnO did not affect the body weight (P > 0.05), but increased VH to crypt depth ratio and IgA concentration (P < 0.05) and decreased TNF-α and NF-κB mRNA expression in jejunum (P < 0.05). (2) IUGR increased the number of swollen mitochondria and autolysosomes, and protein expressions of sequestosome-1 (P62) and microtubule-associated protein light chain 3 B/A (LC3B/A) in jejunum as compared to NBW group (P < 0.05); Compared with IUGR group, Nano-ZnO decreased the number of swollen mitochondria and autolysosomes, and P62 and LC3B/A protein expression (P < 0.05). (3) IUGR increased mucosal contents of malondialdehyde and protein carbonyl (PC) and Keap1 protein expression (P < 0.05) as compared to NBW group; Compared with IUGR group, dietary Nano-ZnO increased activities of total antioxidant capacity, catalase, glutathione peroxidase, and glutathione content (P < 0.05), and enhanced nuclear respiratory factor 2 (Nrf2), glutamate-cysteine ligase modifier subunit and glutathione peroxidase 1 mRNA expression, and increased total and nuclear Nrf2 protein expression (P < 0.05), and decreased malondialdehyde and PC content, and Keap1 protein expression (P < 0.05) in jejunum. Results suggested that IUGR pigs showed postnatal catch-up growth and improved intestinal morphology, and dietary Nano-ZnO may further improve intestinal morphology, reduce inflammation, decrease autophagy and alleviate oxidative stress via Nrf2/Keap1 pathway in jejunum of IUGR pigs.

Assessment of diphenhydramine toxicity - Is its mode of action conserved between human and zebrafish?

The main aim of the study is to evaluate the effects of the pharmaceutical diphenhydramine (DPH) on embryo-larvae Danio rerio across distinct levels of organization - individual and subcellular - and correlate those effects with the DPH mode of action (MoA) assessed by in silico analysis. An embryos heartbeat rate reduction was observed at 10mg/L DPH, but 0.001 to 10mg/L did not significantly affect the zebrafish survival, hatching and morphology. Larvae swimming distance decreased (hypoactivity) at 1 and 10mg/L DPH. Moreover, the straightforward movements decrease and the increase in the zigzag movements or movements with direction changes, shown an erratic swimming behavior. Energy budgets decreased for lipid (0.01mg/L DPH) and carbohydrate (10mg/L DPH) contents. Cholinesterase (neural function) and glutathione S-transferase (Phase II biotransformation/antioxidant processes) increased their activities at 10mg/L DPH, where a decrease in the total glutathione content (antioxidant system) was observed. DNA damage was found at 0.01 and 10mg/L DPH. However, a DNA repair occurred after subsequent 72h in clean media. The in silico study revealed a relevant conservation between human and zebrafish DPH target molecules. These data provide a valuable ecotoxicological information about the DPH effects and MoA to non-target organisms.

Enhanced Cd-Accumulation in Typha latifolia by Interaction with Pseudomonas rhodesiae GRC140 under Axenic Hydroponic Conditions.

The Typha genus comprises plant species extensively studied for phytoremediation processes. Recently, Pseudomonas rhodesiae GRC140, an IAA-producing bacterium, was isolated from Typha latifolia roots. This bacterium stimulates the emergence of lateral roots of Arabidopsis thaliana in the presence and absence of cadmium. However, the bacterial influence on cadmium accumulation by the plant has not been determined. Moreover, the P. rhodesiae GRC140 effect in Cd phytoextraction by T. latifolia remains poorly understood. In this work, an axenic hydroponic culture of T. latifolia was established. The plants were used to evaluate the effects of cadmium stress in axenic plants and determine the effects of P. rhodesiae GRC140 and exogenous indole acetic acid (IAA) on Cd tolerance and Cd uptake by T. latifolia. Biomass production, total chlorophyll content, root electrolyte leakage, catalase activity, total glutathione, and Cd content were determined. The results showed that Cd reduces shoot biomass and increases total glutathione and Cd content in a dose-dependent manner in root tissues. Furthermore, P. rhodesiae GRC140 increased Cd translocation to the shoots, while IAA increased the Cd accumulation in plant roots, indicating that both treatments increase Cd removal by T. latifolia plants. These results indicate that axenic plants in hydroponic systems are adequate to evaluate the Cd effects in plants and suggest that T. latifolia phytoextraction abilities could be improved by P. rhodesiae GRC140 and exogenous IAA application.

Case-control exercise challenge study on the pathogenesis of high serum gamma-glutamyl transferase activity in racehorses.

High serum γ-glutamyl-transferase (GGT) activity syndrome in racehorses has been associated with maladaption to exercise. Investigation of affected horses before and immediately after standard exercise may provide critical insight into the syndrome's pathophysiology. To investigate blood biomarker changes in actively competing racehorses with high GGT activity associated with an exercise challenge. Case-control study. High GGT case (age: 2-3 years) and normal GGT control (age: 2-7 years) pairs (3 Thoroughbred, 4 Standardbred pairs) at least 3months into their training/racing season were included. Horses with a recent history of high GGT activity (≥50 IU/L) without additional biochemical evidence of liver disease were identified by veterinarians. Horses were tested again in the week prior to a planned exercise challenge to confirm persistent increases in GGT activity. Controls from the same stable with similar training/racing intensity and serum GGT activity ≤36 IU/L were matched with each case. Blood samples were obtained immediately before, 15 and 120 min after exercise. Pre-exercise serum samples were analysed for baseline select serum chemistries, selenium and vitamin E concentrations. Cortisol concentration and markers of oxidative status were measured in serum or plasma for all time points. Individual serum bile acid and coenzyme Q10 concentrations, plasma lipid mediator (fatty acids, oxylipids, isoprostanes) concentrations and targeted metabolomics analyses were performed using liquid chromatography-mass spectrometry. Serum viral PCR for equine hepaci- and parvovirus was performed in each animal. Cases had higher baseline concentrations of total glutathione, taurocholic acid, cortisol and cholesterol concentrations and higher or lower concentrations of specific oxylipid and isoprostane mediators, but there were no case-dependent changes after exercise. Small sample size. Results indicated that glutathione metabolism was altered in high GGT horses. Enhanced glutathione recycling and mild cholestasis are possible explanations for the observed differences.

HMGCS2 silencing attenuates high glucose-induced in vitro diabetic cardiomyopathy by increasing cell viability, and inhibiting apoptosis, inflammation, and oxidative stress

ABSTRACT Diabetic cardiomyopathy (DCM) is a diabetic mellitus-related complications and progression of DCM may eventually lead to heart failure, while mechanisms related to DCM pathophysiology remain unclear. The study was undertaken to identify possible hub genes associated with DCM progression through bioinformatics analysis and to validate the role of 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) in DCM progression using a cellular model of high glucose (HG)-induced DCM. The common differentially expressed genes (DEGs) between GSE173884 and GSE161827 were used for PPI network analysis. Our results identified 17 common DEGs between GSE173384 and GSE161827. Further analysis of the protein–protein interaction network identified nine hub genes and HMGCS2. The in vitro functional assays showed that HG induced up-regulation of HMGCS2, suppressed cardiomyocyte viability, enhanced apoptosis, inflammation, and oxidative stress of cardiomyocytes. Gain-of-function assays showed that HMGCS2 overexpression reduced cell viability, increased apoptosis, caspase-3/-9 activity, up-regulated interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) expression, decreased superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase expression, increased malondialdehyde (MDA) content, and reactive oxygen species (ROS) level but inhibited total antioxidant activity, SOD activity, CAT activity, and glutathione content in cardiomyocytes. Rescue experiments demonstrated HMGCS2 silence attenuated HG-induced decrease in cardiomyocyte viability and increase in cardiomyocyte apoptosis, inflammation, and oxidative stress. All in all, our study identified HMGCS2 as a hub gene in DCM pathophysiology and further functional studies indicated that HMGCS2 may aggravate DCM progression by reducing cardiomyocyte viability, increasing cardiomyocyte apoptosis, and promoting inflammation and oxidative stress in cardiomyocytes.

Agmatine Mitigates Inflammation-Related Oxidative Stress in BV-2 Cells by Inducing a Pre-Adaptive Response

Neuroinflammation and microglial activation, common components of most neurodegenerative diseases, can be imitated in vitro by challenging microglia cells with Lps. We here aimed to evaluate the effects of agmatine pretreatment on Lps-induced oxidative stress in a mouse microglial BV-2 cell line. Our findings show that agmatine suppresses nitrosative and oxidative burst in Lps-stimulated microglia by reducing iNOS and XO activity and decreasing O2− levels, arresting lipid peroxidation, increasing total glutathione content, and preserving GR and CAT activity. In accordance with these results, agmatine suppresses inflammatory NF-kB, and stimulates antioxidant Nrf2 pathway, resulting in decreased TNF, IL-1 beta, and IL-6 release, and reduced iNOS and COX-2 levels. Together with increased ARG1, CD206 and HO-1 levels, our results imply that, in inflammatory conditions, agmatine pushes microglia towards an anti-inflammatory phenotype. Interestingly, we also discovered that agmatine alone increases lipid peroxidation end product levels, induces Nrf2 activation, increases total glutathione content, and GPx activity. Thus, we hypothesize that some of the effects of agmatine, observed in activated microglia, may be mediated by induced oxidative stress and adaptive response, prior to Lps stimulation.

Postharvest 24-epibrassinolide treatment alleviates pomegranate fruit chilling injury by regulating proline metabolism and antioxidant activities

Pomegranate fruit is susceptible to chilling injury (CI) during long term cold storage. In the current work, we studied the impact of pre-storage 24-epibrassinolide (24-EBL) application for CI amelioration of pomegranate during cold storage. The fruit were treated with 0, 5, 10 and 15 µmol L−1 24-EBL and stored for 84 d at 5 ± 1 ºC. Results showed that 15 µmol L−1 24-EBL treatment markedly alleviated CI, suppressed weight loss and reduced decay. Similarly, 15 µmol L−1 24-EBL application stimulated the activity of ornithine-δ-aminotransferase (OAT) and Δ1-pyrroline-5-carboxylate synthetase (P5CS) along with suppressed increase in proline dehydrogenase (PDH) enzyme which subsequently resulted in increased proline accumulation. The 15 µmol L−1 24-EBL treated pomegranate fruit had substantially lower activity of lipoxygenase (LOX) enzyme along with reduced concentrations of malondialdehyde (MDA), electrolyte leakage (EL), hydrogen peroxide (H2O2) and superoxide anion (O2•−) contents. In addition, 15 µmol L−1 24-EBL treated pomegranate fruit showed significantly higher activity of catalase (CAT), ascorbate peroxidase (APX), peroxidase (POD) and superoxide dismutase (SOD) enzyme in contrast with control. The 15 µmol L−1 24-EBL treated pomegranate fruit showed higher phenylalanine ammonia lyase (PAL) and had lower polyphenol oxidase (PPO) activity that subsequently resulted in conserved total phenols content. In the same way, pomegranate fruit treated with 15 µmol L−1 24-EBL had markedly higher total anthocyanins content, ascorbic acid and glutathione content as compared with control. It was also observed that 15 µmol L−1 24-EBL treated pomegranate fruit showed lower juice pH, higher titratable acidity (TA) and relatively lower soluble solids content (SSC) in contrast with control. In conclusion, 15 µmol L−1 24-EBL could be considered suitable for CI alleviation and quality maintenance of pomegranate fruit under cold storage.

Andrological Aspects of Exercise: Moderate Swimming Protects against Isoproterenol Induced Testis and Semen Abnormalities in Rats

The development and progression of male infertility are closely linked to a sedentary lifestyle; however, its underlying mechanisms are not fully elucidated. Our aim was to assess the protective effects of moderate swimming exercise on the male reproductive system in isoproterenol-treated rats. Male Wistar rats were divided into five groups as follows: (1) non-interventional controls (CTRL), (2) isoproterenol-treated (ISO), (3) pre-treatment swimming training + ISO (PRE + ISO), (4) ISO + post-treatment swimming training (ISO+POST), (5) pre-treatment swimming training + ISO + post-treatment swimming training (PRE + ISO + POST) groups. Testicular oxidative stress was induced by ISO injection (1.0 mg/kg). Rats in the pre- or post-training groups were trained five days a week. At the end of the experimental period, serum testosterone levels, sperms’ hyaluronan binding, and total glutathione (GSH) content, as well as myeloperoxidase activity (MPO), TNF alpha and IL6 concentrations in the testis and semen, were measured. Serum testosterone levels, sperms’ hyaluronan binding, and GSH content were found to be significantly reduced, while MPO, TNF alpha and IL6 concentrations in the testis and semen were elevated after the ISO treatment compared to the CTRL group. Moderate-intensity swimming exercise effectively alleviated the negative effects of high oxidative stress. Our findings provide the first evidence that moderate-intensity swimming exercise confers sustained protection from isoproterenol-induced adverse effects on testicular inflammation.

Arsenic intake-induced gastric toxicity is blocked by grape skin extract by modulating inflammation and oxidative stress in a mouse model

Arsenic (As) is known to induce toxic responses in many organs of human beings and animals. However, research concerning toxicity in the stomach is limited. In this study, arsenic-induced gastric toxicity was investigated in a mouse model, and grape skin extract (GSE) was confirmed to have protective effects against arsenic toxicity. Our experimental results showed that exposure to 10 mg/l arsenic via drinking water for 56 days caused oxidative damage and inflammatory responses. The H2O2 and malondialdehyde (MDA) contents were significantly increased, accompanied by significant decreases in total superoxide dismutase (T-SOD) activity and glutathione (GSH) content in the gastric tissue of arsenic-treated mice. Two inflammatory signalling pathways, i.e., TLR2/MyD88/NF-κB and IL-6/STAT-3, were activated, along with inflammatory cell infiltration and the elevated mRNA expression of pro-inflammatory cytokines (TNF-α, IL-1β and IFN-γ) and myeloperoxidase (MPO) in the gastric tissue of mice exposed to arsenic. Meanwhile, the mRNA levels of the ZO-1, ZO-2 and occludin genes, which encode the key components of tight junction (TJ) complexes, were downregulated. However, the application of GSE (300 mg/kg bw) significantly inhibited the arsenic-induced increases in H2O2 and MDA contents and the decreases in T-SOD activity and GSH content. The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-α, IL-1β and IFN-γ), MPO and IL-6/STAT3 and TLR2/MyD88/NF-κB pathways was found down-regulated. Moreover, the arsenic-induced inflammatory cell infiltration and inhibition of TJ genes transcription were markedly attenuated in the As+GSE (300 mg/kg bw) group. Based on the present findings, arsenic intake appears to cause gastric toxicity via oxidative stress and inflammation, and the application of GSE offers significant protection against arsenic toxicity in a mouse model by attenuating the oxidative stress and inflammatory response. Our results suggest that GSE by oral administration might function as a candidate therapeutic supplement to antagonize arsenic toxicity.

Supplementation of freezing medium with encapsulated or free glutathione during cryopreservation of bull sperm

AbstractThe objective was to compare effects of encapsulated or free glutathione (GSH) on the quality of frozen‐thawed bull sperm. Ejaculates were collected via artificial vagina from six mature Holstein bulls once weekly for 6 weeks. All ejaculates had motility ≥70%, sperm concentration ≥1.0 × 109/ml and ≤15% morphologically abnormal sperm. Each week, semen was pooled and diluted with lecithin‐based extenders containing various concentrations of encapsulated (E0, E1, E2.5 and E5 mM) or free (F0, F1, F2.5 and F5 mM) GSH, with total glutathione content determined before and after cryopreservation. Total GSH in fresh semen was (mean+SEM) 4.8 ± 0.2 nmol/108 sperm, whereas in frozen‐thawed semen of group F0 (control), it decreased to 1.4 ± 0.2 nmol/108 sperm, a 70.8% reduction (p &lt; .05). In addition, total GSH in frozen‐thawed semen from groups E2.5, E5 and F5 were 2.4 ± 0.2, 2.8 ± 0.2 and 1.8 ± 0.2 nmol/108 sperm, respectively (E5 versus. F0, p &lt; .05). Compared to group F0, frozen‐thawed sperm from group E2.5 had greater (p &lt; .05) percentages of sperm that were viable (Annexin‐V) (61.1 ± 1.8 versus. 71.1 ± 1.8) and that had cell membrane integrity (eosin‐nigrosin) (64.5 ± 3.1 versus. 80.0 ± 3.1). Furthermore, frozen‐thawed sperm from group E2.5 had the numerically highest total and progressive motility (CASA) and cell membrane functionality (HOS) and the lowest percentage of early apoptotic sperm (Annexin‐V). However, acrosome membrane integrity (PSA) of E5 had the lowest mean (p &lt; .05), whereas E2.5 caused a small nonsignificant decrease (69.1 ± 1.4%) compared to E0 and F0. In conclusion, 2.5 mM encapsulated GSH in semen extender significantly improved the quality of frozen‐thawed bull sperm.

Milk performance and oxidative status responses to rumen protected methionine supplementation in genotyped α-S1 casein lactating dairy goats fed two levels of metabolizable protein diets

In dairy goats, responses to rumen-protected Methionine (RPM) supplementation on milk performance and milk protein synthesis were inconsistent. The objective of the study was to evaluate the effects of supplemental RPM in diets differing in CP content on milk performance, milk composition, plasma concentration of amino-acids (AA) and parameters of oxidative status in goats genotyped for their genetic variant for alpha-S1 casein (CNS1). Sixteen goats (Body weight = 66.6 ± 8.5 kg, days in milk = 89 ± 5) were grouped into 2 blocks (High vs Low) according to their secretion of CNS1 in milk, and within each CNS1 block, goats were selected to make blocks comparable for milk yield, milk protein content, body weight and days in milk. Goats within CNS1 blocks were allotted to 2 periods cross-over (4 wks for each period with one washout week) nested in 2 × 2 factorial design with dietary CP (LP vs HP, 14 vs 16 % CP in TMR fed ad libitum) and RPM supplementation (CTL vs RPM, 0 vs 4 g/d). Dry matter intake and milk yield were individually recorded daily, whereas milk samples for milk composition determination, and blood samples were obtained individually twice weekly, and once weekly, respectively. Blood was sampled for glucose, NEFA, BHB, urea, insulin, total or oxidized glutathion, superoxide dismutase, catalase, malondialdehyde, and protein carbonyl. At the end of each period, blood was sampled during two consecutive wks to determine plasma AA profile. Goats fed HP diet had higher CP, PDIE, and LysDi (lysine digestible in intestine) intake than those fed LP diet, whereas goats supplemented with RPM had higher MetDi (methionine digestible in intestine) intake (P < 0.001) than those fed the CTL diet. Goats fed HP diet had similar milk performance, milk composition and yields, and similar feed, energy and PDI efficiencies, but higher milk urea concentration than those fed LP diet. Goats supplemented with RPM had higher milk yield only when fed the LP diet (RPM x dietary CP: P < 0.02). Compared to goats fed CTL diet, those supplemented with RPM had higher milk protein content, but this was observed only in those fed HP diet (RPM x dietary CP: P < 0.008), especially for Low CNS1 goats (RPM x CNS1: P < 0.05; RPM x dietary CP x CNS1: P < 0.11). Efficiencies of PDI, feed and energy were not altered by RPM supplementation, but CNS1 x dietary CP x RPM interaction was significant for these efficiencies. Goats supplemented with RPM tended to have higher plasma MDA (P < 0.07) and total glutathione concentrations (P < 0.09). In conclusion, increasing dietary CP failed to improve DMI, milk performance, milk protein content and protein yield, which suggest that Net Energy for lactation was a limiting factor of our experimental diets. With RPM supplementation, increase in milk production in the low CP group, and increase in milk protein content in the high CP group suggests that changes in metabolic partition of nutrients between milk secretion vs milk protein synthesis occurs according to the level of limitation of methionine in diet, which may affect the methionine requirement for goat milk production.

Biochemical indicators of woody plants in the diagnosis of air condition

It is found that anthropogenic pollution has a significant effect on the change in the content of total nitrogen, glutathione and vitamin E, which increases the resistance of woody plants to stress. A series of woody plants with regard to their sensitivity to aerosol pollution has been compiled: according to the degree of decrease in total nitrogen – Picea abies > Thuja occidentalis > Syringa vulgaris > Acer platanoides > Tilia cordata > Sorbus aucuparia; the degree of decrease in glutathione content – Picea abies > Thuja occidentalis > Syringa vulgaris > Acer platanoides > Tilia cordata > Sorbus aucuparia; the degree of decrease in the content of vitamin E – Picea abies > Thuja occidentalis > Sorbus aucuparia > Tilia cordata > Syringa vulgaris > Acer platanoides. A positive correlation was revealed between the biochemical parameters of woody plants and the monitoring complex indices proposed by the Russian meteorological service. A close direct regression dependence of the air pollution index and the average stability coefficient for the content of total nitrogen, vitamin E and glutathione in the biomass of model woody plants was revealed: with an increase in the degree of air pollution, the average stability coefficient for certain biochemical indicators increases.

Cytoprotective effect of taurine against sodium chlorate-induced oxidative damage in human red blood cells: an ex vivo study.

Sodium chlorate (NaClO3) is a common non-selective herbicide that is also used in paper and pulp mills and is produced as a by-product during drinking water disinfection by chlorine dioxide. Here, we report the effect of dietary antioxidant taurine on NaClO3-induced cytotoxicity in human red blood cells (RBC). RBC were treated with 5mM NaClO3, either alone or in presence of 1, 2.5 and 5.0mM taurine. Incubation of RBC with NaClO3 alone caused hemolysis, increased oxidation of lipids and proteins, methemogobin level and decreased total sulfhydryl and glutathione content. It lowered the activities of antioxidant enzymes thioredoxin reductase, glutathione peroxidase, catalase and glutathione reductase, while Cu-Zn superoxide dismutase activity was increased. The antioxidant capacity of RBC was impaired. This strongly suggests that NaClO3 causes the induction of oxidative stress condition in RBC. The specific activities of lactate dehydrogenase, glucose 6-phosphate dehydrogenase and plasma membrane bound enzymes, were also greatly altered. However, prior treatment of RBC with taurine conferred significant protection against NaClO3-induced oxidative damage and also improved the antioxidant defence system of cells. These results were supported by electron microscopy images of RBC. Treatment with NaClO3 alone converted the normal biconcave discoidal RBC to acanthocytes and echinocytes but this transformation was greatly prevented in the presence of taurine. Thus, taurine mitigates the cytotoxicity of NaClO3 in human RBC and can function as an effective chemoprotectant.

Increased selenium concentration in the synthesis of CdSe magic-sized quantum dots affects how the brain responds to oxidative stress.

CdSe magic-sized quantum dots (MSQDs) have been widely used as fluorescent probes in biological systems due to their excellent optical properties with a broader fluorescence spectrum and stable luminescence in biological media. However, they can be cytotoxic and alter the redox balance depending on the amounts of Cd2+ adsorbed on their surface. Thus, the present study aimed to evaluate whether increases in selenium concentration in the synthesis of CdSe-MSQDs decrease the oxidative stress caused by Cd2+ -based quantum dots. CdSe-MSQDs synthesized with different concentrations of selenium were investigated against oxidative stress in the brain of chicken embryos by examining total antioxidant capacity, lipid peroxidation, thiol, and glutathione contents, as well as the activities of glutathione peroxidase, superoxide dismutase (SOD), catalase (CAT), and glutathione reductase. In addition, the vascularization of the chorioallantoic membrane (CAM) analysis was performed. Higher selenium concentrations alter the surface defect levels (decrease free Cd2+ ) and controlled the oxidative effects of CdSe-MSQDs by reducing the lipid peroxidation, restoring the glutathione defense system and the antioxidant enzymes SOD and CAT, and maintaining the vascular density of the CAM. The current findings reinforce the study of the effects of the presence of Cd2+ ions on the surface of quantum dots, changing toxicity, and aiming interesting strategies of nanomaterials in biological systems.

Mitochondria damage and ferroptosis involved in Ni-induced hepatotoxicity in mice

Nickel (Ni) is an environmental toxicant that can cause toxic damage to humans and animals. Although the hepatotoxicity of Ni has been confirmed, its precise mechanism is still unclear. In this study, the results showed that nickel chloride (NiCl2)-treatment could induce mice hepatotoxicity including hepatic histopathological alterations and up-regulation of serum AST and ALT. According to the results, NiCl2 increased malondialdehyde (MDA) production while reducing total antioxidant capacity (T-AOC) activity and glutathione (GSH) content. Additionally, NiCl2 induced mitochondrial damage which was featured by increase in mitochondrial ROS (mt-ROS) and mitochondrial membrane potential (MMP) depolarization. The mitochondrial respiratory chain complexes I-IV and ATP content were decreased in the liver of NiCl2-treated mice. Meanwhile, NiCl2 caused hepatic ferroptosis accompanied by increased iron content in the liver and up-regulation of cyclooxygenase 2 (COX-2) protein and mRNA expression levels, down-regulation of glutathione eroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1) and nuclear receptor coactivator 4 (NCOA4) protein and mRNA expression levels. Altogether, the above mentioned results indicate that NiCl2 treatment may induce hepatic damage through mitochondrial damage and ferroptosis.

Exposure to aerosol extract from heated tobacco products causes a drastic decrease of glutathione and protein carbonylation in human lung epithelial cells

Heated tobacco products (HTPs) are an emerging class of tobacco goods that claim to have lower health risks than those of smoking combustible tobacco products. In this study, we exposed human lung epithelial cell lines to extracts prepared from HTP aerosols and combustible cigarette smoke to compare cytotoxicity. We focused on the effects of aldehydes present in the aerosols of HTPs at levels close to those in combustible cigarette smoke. Significant toxicity was confirmed for the HTP extract, albeit to a lesser extent than that with the combustible cigarette extract. When redox balance was evaluated by the oxidative loss of low-molecular-weight thiols in the cells, we found that total glutathione (GSH) contents and low-molecular-weight thiol levels were significantly decreased after exposure to the aerosol extract of HTPs. These results indicated that GSH is rapidly consumed during the detoxification of xenobiotics, such as aldehydes from tobacco extracts. Accordingly, exposure to the aerosol extract of HTPs resulted in the enhanced carbonylation of many proteins. In a simple comparison, the results for HTPs were significantly different from those obtained with combustible cigarette smoke, suggesting reduced toxicity of HTPs. However, we found significant and harmful effects after exposing lung epithelial cells to the aerosol extract of HTPs. Thus, a further comprehensive study is needed to clarify the lung damage induced via the long-term inhalation of aerosols from HTPs.

N-Acetylcysteine Reverses the Mitochondrial Dysfunction Induced by Very Long-Chain Fatty Acids in Murine Oligodendrocyte Model of Adrenoleukodystrophy.

The accumulation of saturated very long-chain fatty acids (VLCFA, ≥C22:0) due to peroxisomal impairment leads to oxidative stress and neurodegeneration in X-linked adrenoleukodystrophy (ALD). Among the neural supporting cells, myelin-producing oligodendrocytes are the most sensitive to the detrimental effect of VLCFA. Here, we characterized the mitochondrial dysfunction and cell death induced by VLFCA, and examined whether N-acetylcysteine (NAC), an antioxidant, prevents the cytotoxicity. We exposed murine oligodendrocytes (158 N) to hexacosanoic acid (C26:0, 1–100 µM) for 24 h and measured reactive oxygen species (ROS) and cell death. Low concentrations of C26:0 (≤25 µM) induced a mild effect on cell survival with no alterations in ROS or total glutathione (GSH) concentrations. However, analysis of the mitochondrial status of cells treated with C26:0 (25 µM) revealed depletion in mitochondrial GSH (mtGSH) and a decrease in the inner membrane potential. These results indicate that VLCFA disturbs the mitochondrial membrane potential causing ROS accumulation, oxidative stress, and cell death. We further tested whether NAC (500 µM) can prevent the mitochondria-specific effects of VLCFA in C26:0-treated oligodendrocytes. Our results demonstrate that NAC improves mtGSH levels and mitochondrial function in oligodendrocytes, indicating that it has potential use in the treatment of ALD and related disorders.