Amount Of Glutathione Research Articles

Protective Effects of Apamin on Acetaminophen-Induced Hepatotoxicity in Mice

Acetaminophen (APAP) overdose can cause severe liver damage, but therapeutic options are limited. Apamin is a natural peptide present in bee venom and has antioxidant and anti-inflammatory properties. Accumulating evidence suggests that apamin has favorable actions in rodent models of inflammatory disorders. Here, we examined the effect of apamin on APAP-evoked hepatotoxicity. Intraperitoneal administration of apamin (0.1 mg/kg) alleviated histological abnormalities and reduced serum levels of liver enzymes in mice injected with APAP. Apamin inhibited oxidative stress through an increase in the amount of glutathione and activation of the antioxidant system. Apamin also attenuated apoptosis with inhibition of caspase-3 activation. Moreover, apamin reduced serum and hepatic levels of cytokines in APAP-injected mice. These effects were accompanied by suppression of NF-κB activation. Furthermore, apamin inhibited chemokine expression and inflammatory cell infiltration. Our results suggest that apamin dampens APAP-evoked hepatotoxicity through inhibiting oxidative stress, apoptosis, and inflammation.

A multi-omics investigation of tacrolimus off-target effects on a proximal tubule cell-line

IntroductionTacrolimus, an immunosuppressive drug prescribed to a majority of organ transplant recipients is nephrotoxic, through still unclear mechanisms. This study on a lineage of proximal tubular cells using a multi-omics approach aims to detect off-target pathways modulated by tacrolimus that can explain its nephrotoxicity. MethodsLLC-PK1 cells were exposed to 5 µM of tacrolimus for 24 h in order to saturate its therapeutic target FKBP12 and other high-affine FKBPs and favour its binding to less affine targets. Intracellular proteins and metabolites, and extracellular metabolites were extracted and analysed by LC-MS/MS. The transcriptional expression of the dysregulated proteins PCK-1, as well as of the other gluconeogenesis-limiting enzymes FBP1 and FBP2, was measured using RT-qPCR. Cell viability with this concentration of tacrolimus was further checked until 72 h. ResultsIn our cell model of acute exposure to a high concentration of tacrolimus, different metabolic pathways were impacted including those of arginine (e.g., citrulline, ornithine) (p < 0.0001), amino acids (e.g., valine, isoleucine, aspartic acid) (p < 0.0001) and pyrimidine (p < 0.01). In addition, it induced oxidative stress (p < 0.01) as shown by a decrease in total cell glutathione quantity. It impacted cell energy through an increase in Krebs cycle intermediates (e.g., citrate, aconitate, fumarate) (p < 0.01) and down-regulation of PCK-1 (p < 0.05) and FPB1 (p < 0.01), which are key enzymes in gluconeogenesis and acid-base balance control. DiscussionThe variations found using a multi-omics pharmacological approach clearly point towards a dysregulation of energy production and decreased gluconeogenesis, a hallmark of chronic kidney disease which may also be an important toxicity pathway of tacrolimus.

Metabolomic analysis reveals responses of Spirodela polyrhiza L. to salt stress

ABSTRACT Duckweeds are particularly well suited for studies needing high output because of their quick growth and reproduction. Due to their starches and flavonoids, the potential for using duckweed as a source of food, medicine or feed has been studied. Through LC-MS analysis, 195 differential metabolites, including organic acids, phenolics, and other categories, were screened in Spirodela polyrhiza L. exposed to 4 days of NaCl. S. polyrhiza contained higher amounts of oxidized glutathione, jasmonates, and phenolic compounds but lower amounts of citric acid and glutathione under salt stress. Additionally, after 4 days of salt stress, there was an increase in the relative expression levels of genes involved in the phenolic biosynthesis pathway. Based on metabolomics, this study provides insight into the mechanism of salt-tolerant by duckweeds, as well as useful information for plant breeders and molecular biologists developing duckweed cultivars with salt tolerance and high phenolic content. Key policy highlights A total of 195 differential metabolites were examined in S. polyrhiza under salt stress using LC‒MS analysis. The effects of salt stress on S. polyrhiza metabolic pathways were reported. Under salt stress, the expression of genes involved in the S. polyrhiza phenolic biosynthesis pathway was evaluated.

Appraising the Role of Astrocytes as Suppliers of Neuronal Glutathione Precursors.

The metabolism and intercellular transfer of glutathione or its precursors may play an important role in cellular defense against oxidative stress, a common hallmark of neurodegeneration. In the 1990s, several studies in the Neurobiology field led to the widely accepted notion that astrocytes produce large amounts of glutathione that serve to feed neurons with precursors for glutathione synthesis. This assumption has important implications for health and disease since a reduction in this supply from astrocytes could compromise the capacity of neurons to cope with oxidative stress. However, at first glance, this shuttling would imply a large energy expenditure to get to the same point in a nearby cell. Thus, are there additional underlying reasons for this expensive mechanism? Are neurons unable to import and/or synthesize the three non-essential amino acids that are the glutathione building blocks? The rather oxidizing extracellular environment favors the presence of cysteine (Cys) as cystine (Cis), less favorable for neuronal import. Therefore, it has also been proposed that astrocytic GSH efflux could induce a change in the redox status of the extracellular space nearby the neurons, locally lowering the Cis/Cys ratio. This astrocytic glutathione release would also increase their demand for precursors, stimulating Cis uptake, which these cells can import, further impacting the local decline of the Cis/Cys ratio, in turn, contributing to a more reduced extracellular environment and subsequently favoring neuronal Cys import. Here, we revisit the experimental evidence that led to the accepted hypothesis of astrocytes acting as suppliers of neuronal glutathione precursors, considering recent data from the Human Protein Atlas. In addition, we highlight some potential drawbacks of this hypothesis, mainly supported by heterogeneous cellular models. Finally, we outline additional and more cost-efficient possibilities by which astrocytes could support neuronal glutathione levels, including its shuttling in extracellular vesicles.

Salicylic acid treatment delayed the browning development in the pericarp of fresh longan by regulating the metabolisms of ROS and membrane lipid

Longans is popular among consumers because of its rich nutritional value, but it is prone to pericarp browning as it is harvested in the high-temperature season. This work was to investigate the effects of salicylic acid (SA) on the metabolisms of reactive oxygen species (ROS) and membrane lipid and their relationship with pericarp browning of postharvest longans. ‘Fuyan’ longans were soaked in the solution of 0.3 g L-1 SA for 5 min, then stockpiled at 28 °C. The results showed that, the pericarp browning index in SA-treated fruit was 42% lower than that in the control fruit at day 5 of storage. Meanwhile, SA treatment reduced the damage severity of cell membrane structure, and maintained a low level of cell membrane permeability, which was 25% lower than that in the control fruit at day 5 of storage. Additionally, compared to the control fruit, SA-treated longans displayed higher levels of pericarp L*, flavonoid, chlorophyll, carotenoid, total phenolics, and anthocyanin, higher activities of pericarp superoxide dismutase, catalase, and ascorbate peroxidase, higher values of pericarp reducing power and 1, 1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging ability, and higher amounts of pericarp ascorbic acid and glutathione, but lower levels of pericarp ROS and malondialdehyde. Moreover, SA-treated samples exhibited lower activities of pericarp phospholipase, lipase, and lipoxygenase, lower levels of pericarp phosphatidic acid and saturated fatty acids (SFA), but higher values of pericarp phosphatidylcholine, phosphatidylinositol, and unsaturated fatty acids (USFA), higher index of USFA, and higher ratio of USFA to SFA. These findings corroborated that SA delayed-browning occurrence in the pericarp of fresh longans was because SA enhanced the capacity to remove ROS, and reduced ROS accumulation and the membrane lipid degradation, thus maintaining the cellular membrane structure, reducing the degradation of pigments, and allowing the fresh longans to maintain a better appearance. Consequently, SA could be an effective means for suppressing pericarp browning and improving the commercial value of fresh longans.

Anti-epileptic Activity of Rosmarinus offi cinalis Extracts with Male Rats Experiment

Rosmarinus offi cialis L., Lamiaceae, has been used to treat a range of illnesses in Iraq for decades and is regarded as a desirable species due to its medicinal properties and antioxidant properties. Aim of study: The main aim of this study was to study more about how the R. offi cialis L plant may help to reduce the negative eff ects of epilepsy. Materials and methods: To estimate the alteration of antioxidant enzymes and lipid peroxidation. Fifty male rats were split into fi ve groups: control (no additions), FeCl3 group, and the rest of the groups were fed R. offi cialis L. components (fl avonoid, glycoside, and alkaloids). Results: β-asecretase, Na and K levels raised in FeCl3 and other R. offi cialis compounds groups while. In contrast to the FeCl3 group and FeCl3 groups containing R. offi cialis L. plant components reduced fucose, vit-C, and Zn levels. In compared to the control group, the activity of oxidant enzymes and lipid peroxidation resulted in a signifi cant amount of glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) in the FeCl3 group; however, R. offi cialis components increased the levels of MDA and SOD, whilst reducing GSH, and CAT. Conclusion: R. offi cinalis extraction components have an eff ects on -asecretase, fucose, and vit-C in male rats, in addition to antioxidant activity and may increase or decrease lipid peroxidation while also improving antioxidative enzymes significantly. The active components of the R. offi cinalis L. plant might be used as one of the next generation of anti-epileptic medications.

Mechanism of SOX10 in ferroptosis of hippocampal neurons after intracerebral hemorrhage via the miR-29a-3p/ACSL4 axis.

Intracerebral hemorrhage (ICH) is classified as a lethal neurological injury associated with cerebrovascular disorders. Ferroptosis is a unique form of cell death and participates in ICH pathogenesis. Herein, the role of SRY-box transcription factor 10 (SOX10) in ferroptosis of hippocampal neurons after ICH was investigated. The in vitro ICH models were established by treating immortalized mouse hippocampal cell line HT-22 with Hemin. Quantitative real-time polymerase chain reaction and Western blotting revealed that the transcription factor SOX10 and microRNA (miR)-29a-3p were decreased whilst acyl-CoA synthetase long chain family member 4 (ACSL4) was increased in the ICH cell models. Subsequently, the assays of the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, the commercial kits, and fluorescent labeling revealed that SOX10 overexpression improved cell viability, decreased the amount of reactive oxygen species (ROS) and Fe2+, and increased the amount of glutathione (GSH) and glutathione peroxidase 4 (GPX4) in ICH models. Thereafter, chromatin immunoprecipitation and dual-luciferase assays showed that SOX10 binding to the miR-29a-3p promoter region increased miR-29a-3p expression, and miR-29a-3p targeted and limited ACSL4 transcription. Rescue experiments showed that miR-29a-3p downregulation or ACSL4 overexpression expedited ferroptosis of Hemin-treated HT-22 cells. Taken together, SOX10 contributed to ferroptosis of hippocampal neurons after ICH via increasing miR-29a-3p to limit ACSL4 transcription.

Glutathione-Activated Emission of Ultrasmall Gold Nanoparticles in the Second Near-Infrared Window for Imaging of Early Kidney Injury.

Biomarker-activatable luminescent probes with high sensitivity and specificity show great promise in advanced bioimaging applications. However, the lack of stable biomarkers at an early stage is currently a major obstacle for sensitive early disease imaging. Herein, we develop a facile in vivo ligand exchange strategy to achieve renal-clearable activatable luminescent gold nanoparticles (AuNPs), which are independent of biomarkers for sensitive and long-time imaging of early kidney injury. Significantly activated emission in the second near-infrared region (∼1026 nm) is realized from the ligand exchange of triphenylphosphine-3,3',3″-trisulfonic acid (TPPTS)-coated AuNPs (∼1.4 nm, TPPTS-AuNPs) with quantitative amounts of glutathione (GSH). The abundant GSH in cells, particularly in liver sinusoids, is then demonstrated successfully to activate the emission of TPPTS-AuNPs with an extremely low background for both cell imaging and in vivo visualization of visceral organs (e.g., liver and kidneys). In addition, the in vivo GSH-exchanged TPPTS-AuNPs show enhanced interactions with acidic renal tubular epithelial cells, resulting in sensitive (contrast index, ∼3.9) and long-time (>6.5 h) noninvasive monitoring of acidosis-induced early kidney injury. This facile ligand exchange strategy opens new possibilities for designing activatable luminescent probes independent of biomarkers for earlier disease diagnosis and treatment.

Some Biochemical Parameters of Eggplant Species from Turkey and Nigeria

In this study, the amounts of vitamins, beta-carotene, lycopene, glutathione (GSH, GSSG), malondialdehyde (MDA), and hydroxyneoneal (4-HNE) in eggplant samples grown in Turkey (dark and light colored eggplant) and Nigeria (white garden egg, bitter apple and bitter tomato) were determined by HPLC. In addition, the total amount of phenolic, and flavonoid substances and antioxidant capacity (ABTS, IC50) were determined by a UV-Visible spectrophotometer. The amounts of vitamins A, E, β-carotene and lycopene were found to be in the ranged of 0.13 -3.63; 3.63-39.0; 1.87-30.5; 1.52-6.79 µg/g dw, respectively. The amounts of vitamin C, B1, B2, B3, B5, B6, B9 and B12 ranged 357-1136; 11.0-95.6; 1.9-5.4; 83-265; 30.16-65.43; 127-348; 24.74-78.6; 0.11-0.68 µg/g dw, respectively. GHS, GSSG, MDA and 4-HNE were found to be in between 364-1930; 225-962; 1.5-8.4; 24.57-38.25 µg/g dw, respectively. While the total phenolic substance was between 706-1260 µg GAE/g dw, the total amount of flavonoid substance was found to be in between 167-356 µg QE/g dw. ABTS values ranged between 365-692 µmol Troloxs/g dw, while IC50 values were in 65.1-99.3 µg/mL. It can be said that the differences observed in the parameters observed in eggplant varieties grown both in Turkey and Nigeria are due to genetic and geographical differences.

Comparative evaluation of the antioxidant potential of rainbow trout exposed to Yersiniosis vaccine and non-vaccinated fish

The antioxidant capacity of liver in fish is a major property which could prevent the diminished quality and safety of fish resulted from oxidation reactions. The aim of this study was to compare the antioxidant capacity of the liver of rainbow trout exposed to the yersiniosis vaccine and nonexposed fish. The amounts of carotenoids, glutathione, cupric assay, and lipid peroxidation levels of liver were determined. Then, the samples were normalized by Bradford test. The results showed that significant differences may exist in lipid peroxidation level (p&lt;0.05). The total antioxidant capacity, glutathione, and carotenoids content showed no significant difference in both group (p≥0.05). The use of vaccine, in addition to increasing resistance to yersiniosis, could prevent the lipid oxidation of fish liver.

Cytoprotective effects of low-frequency pulsed electromagnetic field against oxidative stress in glioblastoma cells.

The low-frequency pulsed electromagnetic field (PEMF) may have possible cytoprotective effects against the destructive effects of oxidative stress. The goal was to investigate if shortterm low-frequency PEMF has cytoprotective effects in glioblastoma cell line following high-dose hydrogen peroxide (H2O2) treatment. U87-MG cells were divided into four groups: Sham-control group; PEMF group (cells exposed to PEMF); H2O2 group (cells treated with H2O2 at time intervals 30 min and 48 h, respectively); H2O2+PEMF group (cells exposed to PEMF after H2O2 treatment at time intervals 30 min and 48 h, respectively). The cell viability, levels of reactive oxygen species, glutathione peroxidase activity, and the amount of glutathione were measured. The cytoprotective effect of PEMF against deleterious effects of oxidative stress triggered by different time interval of H2O2 treatment might be mediated by the increase in the cell viability, the elevation in the antioxidant enzyme activity/amount, and the decrease in the reactive oxygen species level. In addition, the cytoprotective effect of PEMF varies depending on different time intervals of H2O2 treatment. In the light of these findings, further in vivo and/or in vitro studies on neurophysiological effects of PEMFs and their underlying molecular mechanisms are needed to elucidate neurotoxic or neuroprotective role against antioxidant defense mechanisms.

Strategies to engineer various nanocarrier-based hybrid catalysts for enhanced chemodynamic cancer therapy.

Chemodynamic therapy (CDT) is a newly developed cancer-therapeutic modality that kills cancer cells by the highly toxic hydroxyl radical (˙OH) generated from the in situ triggered Fenton/Fenton-like reactions in an acidic and H2O2-overproduced tumor microenvironment (TME). By taking the advantage of the TME-activated catalytic reaction, CDT enables a highly specific and minimally-invasive cancer treatment without external energy input, whose efficiency mainly depends on the reactant concentrations of both the catalytic ions and H2O2, and the reaction conditions (including pH, temperature, and amount of glutathione). Unfortunately, it suffers from unsatisfactory therapy efficiency for clinical application because of the limited activators (i.e., mild acid pH and insufficient H2O2 content) and overexpressed reducing substance in TME. Currently, various synergistic strategies have been elaborately developed to increase the CDT efficiency by regulating the TME, enhancing the catalytic efficiency of catalysts, or combining with other therapeutic modalities. To realize these strategies, the construction of diverse nanocarriers to deliver Fenton catalysts and cooperatively therapeutic agents to tumors is the key prerequisite, which is now being studied but has not been thoroughly summarized. In particular, nanocarriers that can not only serve as carriers but are also active themselves for therapy are recently attracting increasing attention because of their less risk of toxicity and metabolic burden compared to nanocarriers without therapeutic capabilities. These therapy-active nanocarriers well meet the requirements of an ideal therapy system with maximum multifunctionality but minimal components. From this new perspective, in this review, we comprehensively summarize the very recent research progress on nanocarrier-based systems for enhanced CDT and the strategies of how to integrate various Fenton agents into the nanocarriers, with particular focus on the studies of therapy-active nanocarriers for the construction of CDT catalysts, aiming to guide the design of nanosystems with less components and more functionalities for enhanced CDT. Finally, the challenges and prospects of such a burgeoning cancer-theranostic modality are outlooked to provide inspirations for the further development and clinical translation of CDT.

Formation of Maillard Reaction Products in Aged Sorghum Vinegar during Ageing and Protective Effects of Pure Vinegar Melanoidin Against CCl4-Induced Rat Hepatic Damage.

The processing method generally affects the toxicity and biological activity of aged sorghum vinegar. This study investigates the changes in the intermediate Maillard reaction products of sorghum vinegar during ageing and the in vivo hepatoprotective effects of pure melanoidin obtained from it. High-performance liquid chromatography (HPLC) and fluorescence spectrophotometry were utilized to quantify intermediate Maillard reaction products. The CCl4-induced liver damage in rats was used to evaluate the protective role of pure melanoidin in rat liver. Compared with the initial concentration, the 18-month ageing process caused a 1.2- to 3.3-fold increase in the concentrations of intermediate Maillard reaction products, i.e. 5-hydroxymethylfurfural (HMF), 5-methylfurfural (MF), methyglyoxal (MGO), glyoxal (GO) and advanced glycation end products (AGEs). The concentrations of HMF in the aged sorghum vinegar were 6.1-fold higher than the 450 μM limit standard for honey, implying the need for shortening the ageing of the vinegar in practice for safety concerns. Pure melanoidin (Mr>3.5 kDa) demonstrated significant protective effects against CCl4-induced rat liver damage, as evidenced by normalized serum biochemical parameters (transaminases and total bilirubin), suppressing hepatic lipid peroxidation and reactive oxygen species, as well as increasing glutathione amount and restoring antioxidant enzyme activities. Histopathological analysis revealed that melanoidin in vinegar reduced cell infiltration and vacuolar hepatocyte necrosis in rat liver. The findings demonstrated that a shortened ageing process should be considered in practice to ensure the safety of aged sorghum vinegar. Vinegar melanoidin is a potential alternative for the prevention of hepatic oxidative damage. This study demonstrates that the manufacturing process had a profound influence on the generation of vinegar intermediate Maillard reaction products. In particular, it revealed the in vivo hepatoprotective effect of pure melanoidin from aged sorghum vinegar, and provides insight into the in vivo biological activity of melanoidin.

Effect of felodipine on indomethacin-induced gastric ulcers in rats.

Felodipine is a calcium channel blocker with antioxidant and anti-inflammatory properties. Researchers have stated that oxidative stress and inflammation also play a role in the pathophysiology of gastric ulcers caused by nonsteroidal anti-inflammatory drugs. The aim of this study was to investigate the antiulcer effect of felodipine on indomethacin-induced gastric ulcers in Wistar rats and compare it with that of famotidine. The antiulcer activities of felodipine (5 mg/kg) and famotidine were investigated biochemically and macroscopically in animals treated with felodipine (5 mg/kg) and famotidine in combination with indomethacin. The results were compared with those of the healthy control group and the group administered indomethacin alone. It was observed that felodipine suppressed the indomethacin-induced malondialdehyde increase (P<0.001); reduced the decrease in total glutathione amount (P<0.001), reduced the decrease superoxide dismutase (P<0.001), and catalase activities (P<0.001); and significantly inhibited ulcers (P<0.001) at the tested dose compared with indomethacin alone. Felodipine at a dose of 5 mg/kg reduced the indomethacin-induced decrease in cyclooxygenase-1 activity (P<0.001) but did not cause a significant reduction in the decrease in cyclooxygenase-2 activity. The antiulcer efficacy of felodipine was demonstrated in this experimental model. These data suggest that felodipine may be useful in the treatment of nonsteroidal anti-inflammatory drug-induced gastric injury.

Overexpression of auxin/indole-3-acetic acid gene MdIAA24 enhances Glomerella leaf spot resistance in apple (Malus domestica)

Auxin is throughout the entire life process of plants and is involved in the crosstalk with other hormones, yet its role in apple disease resistance remains unclear. In this study, we investigated the function of auxin/indole-3-acetic acid (IAA) gene MdIAA24 overexpression in enhancing apple resistance to Glomerella leaf spot (GLS) caused by Colletotrichum fructicola (Cf). Analysis revealed that, upon Cf infection, 35S::MdIAA24 plants exhibited enhanced superoxide dismutase (SOD) and peroxidase (POD) activity, as well as a greater amount of glutathione (reduced form) and ascorbic acid accumulation, resulting in less H2O2 and superoxide anion (O2.−) in apple leaves. Furthermore, 35S::MdIAA24 plants produced more protocatechuic acid, proanthocyanidins B1, proanthocyanidins B2 and chlorogenic acid when infected with Cf. Following Cf infection, 35S::MdIAA24 plants presented lower levels of IAA and jasmonic acid (JA), but higher levels of salicylic acid (SA), along with the expression of related genes. The overexpression of MdIAA24 was observed to enhance the activity of chitinase and β-1,3-glucanase in Cf-infected leaves. The results indicated the ability of MdIAA24 to regulate the crosstalk between IAA, JA and SA, and to improve reactive oxygen species (ROS) scavenging and defense-related enzymes activity. This jointly contributed to GLS resistance in apple.

Glutathione and Its Metabolic Enzymes in Gliomal Tumor Tissue and the Peritumoral Zone at Different Degrees of Anaplasia.

This research was aimed at investigating the features of free radical activity and the parameters of glutathione metabolism in tumor tissues and the peritumoral zone at different degrees of glial tumor anaplasia. We analyzed postoperative material from 20 patients with gliomas of different degrees of anaplasia. The greatest differences compared to adjacent noncancerous tissues were found in the tumor tissue: an increased amount of glutathione and glutathione-related enzymes at Grades I and II, and a decrease of these parameters at Grades III and IV. For the peritumoral zone of Grades I and II, the indices changed in different directions, while for Grades III and IV, they occurred synchronously with the tumor tissue changes. For Low Grade and High Grade gliomas, opposite trends were revealed regarding changes in the level of glutathione and the enzymes involved in its metabolism and in the free radical activity in the peritumoral zone. The content of glutathione and the enzymes involved in its metabolism decreased with the increasing degree of glioma anaplasia. In contrast, free radical activity increased. The glutathione system is an active participant in the antioxidant defense of the body and can be used to characterize the cell condition of gliomas at different stages of tumor development.

Effects of exogenous salicylic acid on alleviation of arsenic-induced oxidative damages in rice

Salicylic acid (SA) is a phenolic phytohormone that plays a vital role in plant development and mediates plant responses to plenty of adversity including arsenic (As) stress. The effects of exogenous addition of SA on As tolerance and As accumulation were assessed in two cultivars of rice (Oryza sativa L.) Nipponbare and Zhongzao 39, hydroponically grown with Kimura B nutrient solution under arsenite [As (III)] and dimethylarsonic acid (DMA) exposure. In the second ex-periment, the influence of soaking seed with SA on As uptake and As damages was investigated in rice (cv. Nipponbare) exposed to As (III) and DMA. The results showed that exogenous addition of SA significantly decreased the concentrations of hydrogen peroxide (H2O2) and malondialdehyde (MDA) in both As (III)- and DMA-stressed rice, indicating that SA alleviates As-induced oxidative damages in rice. SA increased the activity of antioxidant enzymes and, moreover, increased the relative amount of glutathione (GSH) and ascorbate (ASA) by accelerating the GSH-ASA circle system. Exogenous addition of SA significantly decreased the As concentration in both roots and shoots of rice under As(III) stress by influencing the expression of genes encoding As transporters, viz. OsLsi1, OsLsi2. The addition of SA significantly decreased the As content in shoots under DMA stress, which may be related to the expression of OsPTR7 involved in shoot xylem unloading. This finding may foster a novel perspective for reducing As accumulation in rice grains.

Investigating the protective effects of cinnamon bark hydroalcoholic extract on the inhibition of liver damage induced by rifampin in male Wistar rats

Introduction: Rifampin is one of the common drugs used to treat tuberculosis and is considered a strong toxic agent for the liver. The aim of this study is to investigate the effects of cinnamon extract administration on rifampin-induced hepatotoxicity in rats. Materials and methods: In this experimental study, 60 male Wistar rats were randomly divided into 6 groups. Liver damage and induction of oxidative stress were caused by administration of 80 mg/kg/day rifampin. Different doses of cinnamon extract (50, 100 and 200 mg/kg) were administered to sick mice by daily gavage in three experimental groups. Liver damage caused by rifampin was evaluated by examining serum biochemical factors as well as the amount of reactive oxygen species, glutathione, antioxidant capacity, lipid peroxidation and histopathological changes in liver tissue. Data analysis was done using Prism version 6 software and one-way analysis of variance and Tukey's post hoc test. Results: The administration of rifampin at the rate of 80 mg/kg for 21 consecutive days caused liver damage (P&lt;0.05). On the other hand, administration of different doses of cinnamon extract could significantly improve the liver damage caused by rifampin consumption (P&lt;0.05) Discussion and conclusion: According to the results of this study, cinnamon extract with antioxidant properties protects the liver against oxidative damage caused by rifampin. These healing effects were shown in the form of reduction of liver damage markers in serum, reduction of oxidative stress markers and improvement of liver tissue damage.

Veitti mataræði fyrr á öldum vernd gegn arfgengri heilablæðingu í arfberum cystatin L68Q stökkbreytingarinnar?

Hereditary cystatin C amyloid angiopathy (HCCAA) is a dominantly inherited disease caused by a mutation (L68Q) in the cystatin C gene, CST3. Mutant cystatin C protein accumulates as amyloid in arterioles in the brain leading to repeated brain hemorrhages and death of young carriers. Recently a possible treatment option was reported for HCCAA carriers involving an oral treatment with N-acetyl-cysteine in order to increase glutathione which was found to dissolve aggregates of mutant cystatin C. An earlier study described how the life span of carriers of the L68Q mutation shortened in the latter half of the 19th century. During the same decades a drastic change occured in the diet in Iceland. In the beginning of the century the diet was simple and low in carbohydrates, which mostly came from milk products. Import of grains and sugar was limited, but increased greatly according to import records. Due to lack of salt, food was preserved in acid whey, but gradually salt replaced whey as means of preserving food. This study aims to explore if changes in the diet of Icelanders during the same decades could possibly affect the amount of glutathione in people.

Protective effect of human amniotic membrane extract against hydrogen peroxide-induced oxidative damage in human dermal fibroblasts.

One of the main approaches to preventing skin ageing is to protect fibroblast cells from oxidative stress. The promoting effect of the human amniotic membrane extract (hAME) on re-epithelization, proliferation and migration of cells in wound healing has been already well studied. This experimental study aimed to investigate the antioxidant activity of hAME against hydrogen peroxide (H2 O2 )-induced dermal fibroblast damage. Here, to establish the ageing model, human foreskin fibroblasts (HFFs) were exposed to 200 μM H2 O2 for 2 h. HFFs were treated with 0.1mg/ml AME for 24 or 48h before or/and after H2 O2 exposure. A total of 48h following the H2 O2 treatment, we measured cell proliferation, viability, senescence-associated β-galactosidase (SA-β-Gal), antioxidants and preinflammatory cytokine (IL-6) levels, as well as the expression of senescence-associated genes (P53 and P21). The obtained results indicated that under oxidative stress, AME significantly increased cellular viability and not only promoted the cell proliferation rate but also attenuated apoptotic induction condition (p < 0.001). AME also significantly reversed the SA-β-Gal levels induced by H2 O2 (p < 0.001). Additionally, both pre- and post-treatment regimen by AME down-regulated the expression of senescence marker genes (p < 0.001). Moreover, AME declined different oxidative stress biomarkers such as superoxide dismutase and catalase and increased the glutathione amount. Altogether, our results indicated that AME had a remarkable antioxidant and antiageing activity as pre- and post-treatment regimen, pointing to this compound as a potential natural-based cosmeceutical agent to prevent and treat skin ageing conditions.