Brassinosteroid Supplementation Alleviates Chromium Toxicity in Soybean (Glycine max L.) via Reducing Its Translocation.

Chromium (Cr) phytotoxicity severely inhibits plant growth and development which makes it a prerequisite to developing techniques that prevent Cr accumulation in food chains. However, little is explored related to the protective role of brassinosteroids (BRs) against Cr-induced stress in soybean plants. Herein, the morpho-physiological, biochemical, and molecular responses of soybean cultivars with/without foliar application of BRs under Cr toxicity were intensely investigated. Our outcomes deliberated that BRs application noticeably reduced Cr-induced phytotoxicity by lowering Cr uptake (37.7/43.63%), accumulation (63.92/81.73%), and translocation (26.23/38.14%) in XD-18/HD-19, plant tissues, respectively; besides, improved seed germination ratio, photosynthetic attributes, plant growth, and biomass, as well as prevented nutrient uptake inhibition under Cr stress, especially in HD-19 cultivar. Furthermore, BRs stimulated antioxidative defense systems, both enzymatic and non-enzymatic, the compartmentalization of ion chelation, diminished extra production of reactive oxygen species (ROS), and electrolyte leakage in response to Cr-induced toxicity, specifically in HD-19. In addition, BRs improved Cr stress tolerance in soybean seedlings by regulating the expression of stress-related genes involved in Cr accumulation, and translocation. Inclusively, by considering the above-mentioned biomarkers, foliar spray of BRs might be considered an effective inhibitor of Cr-induced damages in soybean cultivars, even in Cr polluted soil.

Protective Effect of Nanoselenium on Renal Oxidative Damage Induced by Mercury in Laying Hens.

This study investigated the effects of dietary nanoselenium (nano-Se) supplementation protecting from renal oxidative damages induced by mercury (Hg) exposure in laying hens. Furthermore, endoplasmic reticulum (ER) stress pathway was explored to reveal the protective mechanism of nano-Se. A total of 576 40-week-old Hyline-White laying hens were randomly allocated to 4 groups with 6 pens per group and 24 hens per pen. The experimental groups were as follows: control (basal diet), control + 27.0 mg/kg Hg, control + 5.0 mg/kg nano-Se, and Hg27.0 + 5.0 mg/kg nano-Se. The results revealed that dietary Hg exposure significantly reduced laying performance (P < 0.05) and egg quality (P < 0.05), whereas nano-Se supplementation partially reversed the reductions. Besides, dietary Hg exposure could induce histopathology damages and apoptosis in kidney, whereas nano-Se addition could alleviate these toxicities effectively. After Hg exposure, the activities and gene expressions of superoxidative dismutase (SOD) (P < 0.05), catalase (CAT) (P < 0.01), glutathione reductase (GR) (P < 0.05) and glutathione peroxidase (GSH-Px) (P < 0.05), and glutathione (GSH) content (P < 0.05) were significantly decreased, while the malondialdehyde (MDA) level was significantly increased (P < 0.05) in kidney. However, nano-Se supplementation partially reversed the levels and gene expressions of these antioxidant biomarkers in kidney. Furthermore, dietary Hg exposure significantly increased the gene expressions of PERK (P < 0.05), ATF4 (P < 0.05), CHOP (P < 0.05), IRE1α (P < 0.05), TRAF2 (P < 0.05), ASK1 (P < 0.05), Caspase-9 (P < 0.05), Caspase-8 (P < 0.05), Caspase-3 (P < 0.05), and Bax/Bcl-2 (P < 0.05), whereas nano-Se supplementation partially reversed these increases of gene expressions. In summary, this study provides evidence that dietary Hg exposure can induce renal oxidative damages, and elucidates an important role of ER stress pathway in nano-Se alleviating renal apoptosis in laying hens.

Potential Protective Role of Cyrtopodion Scabrum in Antioxidant Parameters in Serum and Liver of Rats with 5-FU-Induced Oxidative Damage.

Chemotherapy is the main approach for the treatment of cancer; however, it often causes unpleasant oxidative damages. Therefore, the development of an effective alternative/complementary therapy with improved tumor suppression efficiency and lower adverse effects is highly required. Recently, it has been shown that Cyrtopodion scabrum extract (CsE) is an effective and selective tumor suppressor medicine. The present study investigated the antioxidant activity of Cyrtopodion scabrum homogenate (CsH) and CsE and their effects on attenuating 5-fluorouracil (5-FU)-induced liver dysfunction in rats. A total of 60 male rats (weight: 200-220 g) were divided into six groups and treated for 14 days. The control (group I) and 5-FU (group II) groups received distilled water and 5-FU, respectively. The other four groups were orally administered with CsE, CsH, CsE+5-FU, and CsH+5-FU (groups III to VI), respectively by gavages based on a daily schedule. The 5-FU-induced oxidative damage was evaluated by changes in the weight and food and water intake during the treatment and antioxidant parameters in the liver and serum of the treated rats. The obtained data indicated that the administration of CsH and CsE significantly improved liver function and defense system of antioxidants by attenuating the levels or activities of malondialdehyde, superoxide anion, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase and decrease of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, total antioxidant capacity, glutathione, total protein, and albumin in the liver and serum, induced by 5-FU treatment. The obtained data of the current study suggested that CsH and CsE play a protective role in the imbalance elicited by 5-FU and can be used as alternative/complementary supplements with 5-FU to reduce oxidative damages which is the consequence of reactive oxygen species production in cancerous patients.

Jasmonic acid-mediated enhanced regulation of oxidative, glyoxalase defense system and reduced chromium uptake contributes to alleviation of chromium (VI) toxicity in choysum (Brassica parachinensis L.).

The cultivation of leafy vegetables on metal contaminated soil embodies a serious threat to yield and quality. In the present study, the potential role of exogenous jasmonic acid (JA; 0, 5, 10, and 20 µM) on mitigating chromium toxicity (Cr; 0, 150, and 300 µM) was investigated in choysum (Brassica parachinensis L.). With exposure to increasing Cr stress levels, a dose-dependent decline in growth, photosynthesis, and physio-biochemical attributes of choysum plants was observed. An increase in Cr levels also resulted in oxidative stress closely associated with higher lipoxygenase activity (LOX), hydrogen peroxide (H2O2) generation, lipid peroxidation (MDA), and methylglyoxal (MG) levels. Exogenous application of JA alleviated the Cr-induced phytotoxic effects on photosynthetic pigments, gas exchange parameters, and restored growth of choysum plants. While exposed to Cr stress, JA supplementation induced plant defense system via enhanced regulation of antioxidant enzymes, ascorbate and glutathione pool, and the glyoxalase system enzymes. The coordinated regulation of antioxidant and glyoxalase systems expressively suppressed the oxidative and carbonyl stress at both Cr stress levels. More importantly, JA restored the mineral nutrient contents, restricted Cr uptake, and accumulation in roots and shoots of choysum plants when compared to the only Cr-stressed plants. Overall, the application of JA2 treatment (10 µM JA) was more effective and counteracted the detrimental effects of 150 µM Cr stress by restoring the growth and physio-biochemical attributes to the level of control plants, while partially mitigated the detrimental effects of 300 µM Cr stress. Hence, JA application might be considered as an effective approach for minimizing Cr uptake and its detrimental effects in choysum plants grown on contaminated soils.

Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches.

Alzheimer's disease (AD) is an irreversible, age-related progressive neurological disorder, and the most common type of dementia in aged people. Neuropathological lesions of AD are neurofibrillary tangles (NFTs), and senile plaques comprise the accumulated amyloid-beta (Aß), loaded with metal ions including Cu, Fe, or Zn. Some reports have identified metal dyshomeostasis as a neurotoxic factor of AD, among which Cu ions seem to be a central cationic metal in the formation of plaque and soluble oligomers, and have an essential role in the AD pathology. Cu-Aß complex catalyzes the generation of reactive oxygen species (ROS) and results in oxidative damage. Several studies have indicated that oxidative stress plays a crucial role in the pathogenesis of AD. The connection of copper levels in AD is still ambiguous, as some researches indicate a Cu deficiency, while others show its higher content in AD, and therefore there is a need to increase and decrease its levels in animal models, respectively, to study which one is the cause. For more than twenty years, many in vitro studies have been devoted to identifying metals' roles in Aß accumulation, oxidative damage, and neurotoxicity. Towards the end, a short review of the modern therapeutic approach in chelation therapy, with the main focus on Cu ions, is discussed. Despite the lack of strong proofs of clinical advantage so far, the conjecture that using a therapeutic metal chelator is an effective strategy for AD remains popular. However, some recent reports of genetic-regulating copper transporters in AD models have shed light on treating this refractory disease. This review aims to succinctly present a better understanding of Cu ions' current status in several AD features, and some conflicting reports are present herein.

Urine Metabolites and Antioxidant Effect after Oral Intake of Date (Phoenix dactylifera L.) Seeds-Based Products (Powder, Bread and Extract) by Human.

A cross-over study was conducted in 16 healthy adult volunteers to describe the urinary excretion of polyphenols from date seeds and investigate the antioxidant effect after consumption of different doses of date seeds powder (DSP), bread (DSB) and extract (DSE). After 12 h of fasting, one of the six treatments (0.25 g and 0.5 g/kg bodyweight DSP, 360 g of 10% and 15% DSB, 30 mg and 60 mg/kg bodyweight DSE) was provided along with breakfast, with a two weeks wash-out period between 2 consecutive treatments. Blood was drawn at baseline, 1, 2, 8 and 24 h post intake. Urine was collected at baseline, 3, 8, and 24 h post intake. An abundant release of polyphenols was detected in urine within the 0-3 h post intake, reached a peak at 8 h, then decreased with polyphenols still being detected up to 24 h post intake. The antioxidant defence system, as measured by reduced glutathione (GSH), was strengthened as soon as 1 h and up to 8 h post intake. Markers of protein and lipid oxidative damages were reduced from 1 h and up to 8 and 24 h post intake, respectively. This supports an antioxidant effect of date seeds products in humans, most probably due to their polyphenols.

Fraxin Alleviates LPS-Induced ARDS by Downregulating Inflammatory Responses and Oxidative Damages and Reducing Pulmonary Vascular Permeability.

Acute respiratory distress syndrome (ARDS) is a severe acute disease that threatens human health, and few drugs that can effectively treat this disease are available. Fraxin, one of the main active ingredients of Cortex Fraxini, a Chinese herbal medicine, has presented various pharmacological and biological activities. However, the effects of fraxin on ARDS have yet to be reported. In the present study, the protective effect of fraxin in lipopolysaccharide (LPS)-induced ARDS in a mouse model was analyzed. Results from the hematoxylin and eosin staining showed that fraxin might alleviate pathological changes in the lung tissues of mice with ARDS. ELISA and Western blot results revealed that fraxin might inhibit the production of inflammatory factors, namely, IL-6, TNF-α, and IL-1ß, and the activation of NF-κB and MAPK signaling pathways in the lungs. Thus, the inflammatory responses were reduced. Fraxin might inhibit the increase in reactive oxygen species (ROS) and malondialdehyde (MDA), a product of lipid peroxidation in lung tissues. Fraxin might increase the superoxide dismutase (SOD) activity to avoid oxidative damage. Vascular permeability was also assessed through Evans blue dye tissue extravasation and fluorescein isothiocyanate-labeled albumin (FITC-albumin) leakage. Fraxin might inhibit the increase in pulmonary vascular permeability and relieve pulmonary edema. Fraxin was also related to the inhibition of the increase in matrix metalloproteinase-9, which is a glycocalyx-degrading enzyme, and the relief of damages to the endothelial glycocalyx. Thus, fraxin elicited protective effects on mice with LPS-induced ARDS and might be used as a drug to cure ARDS induced by Gram-negative bacterial infection.

Foraging in maize field areas: A risky business?

In Quebec, Canada, the cultivation of maize dominates the agricultural territory. This crop requires a sustained supply of fertilizers from different sources: chemical, natural or from residual materials (sludge). These amendments contain metallic trace elements, which may lead to metal-contaminated maize pollen, a possible source of prooxidants for the foraging bees. Our objective was to determine whether maize fields environment influences the oxidation processes and the accumulation of metals in bees. A few days prior to pollen shedding, beehives were installed in maize fields: one organically grown (site A) and three conventionally grown (sites B, C and D). Soil, maize pollen and bees were analyzed for metal content. Every 15days, bees were collected and analyzed for peroxidation of lipids, metallothionein-like proteins (MTLPs), proteins, retinoids and lipophilic antioxidants (carotenoids and α-tocopherol). The compound ß-carotene was the most abundant in bees from all sites, followed by α-carotene, ß-cryptoxanthin, α-cryptoxanthin, zeaxanthin and lutein. Retinaldehyde and retinol varied according to times and sites without demonstrating clear trends. However, significant differences between sites were noted in 13-cis-retinoic acid and two retinoic acid metabolites measured in bees, suggesting alteration in the reduction-oxidation processes. In line with these results, the level of lipid peroxidation was globally higher in sites B, C and D compared with the organic site. Higher concentrations of metals were observed in soil and pollen from the field A, but bees metal contents were equal or less than those measured in bees from other sites. Higher bee MTLP levels were measured in sites B, C and D. For most sampling times, the discriminant analysis revealed that the conditions were distinguished by the oxidation processes in bees. Our data suggest that bees foraging in conventionally grown maize fields are at risk of increased oxidative damages which can alter the fine regulation of retinoids.

Petroselinum Crispum is Effective in Reducing Stress-Induced Gastric Oxidative Damage.

BACKGROUND: Oxidative stress has been shown to play a principal role in the pathogenesis of stress-induced gastric injury. Parsley (Petroselinum crispum) contains many antioxidants such as flavanoids, carotenoids and ascorbic acid. AIMS: In this study, the histopathological and biochemical results of nutrition with a parsley-rich diet in terms of eliminating stress-induced oxidative gastric injury were evaluated. STUDY DESIGN: Animal experimentation. METHODS: Forty male Wistar albino rats were divided into five groups: control, stress, stress + standard diet, stress + parsley-added diet and stress + lansoprazole (LPZ) groups. Subjects were exposed to 72 hours of fasting and later immobilized and exposed to the cold at +4 degrees for 8 hours to create a severe stress condition. Samples from the animals' stomachs were arranged for microscopic and biochemical examinations. RESULTS: Gastric mucosal injury was obvious in rats exposed to stress. The histopathologic damage score of the stress group (7.00±0.57) was higher than that of the control group (1.50±0.22) (p<0.05). Significant differences in histopathologic damage score were found between the stress and stress + parsley-added diet groups (p<0.05), the stress and stress + standard diet groups (p<0.05), and the stress and stress + LPZ groups (p<0.05). The mean tissue malondialdehyde levels of the stress + parsley-added group and the stress + LPZ group were lower than that of the stress group (p<0.05). Parsley supported the cellular antioxidant system by increasing the mean tissue glutathione level (53.31±9.50) and superoxide dismutase (15.18±1.05) and catalase (16.68±2.29) activities. CONCLUSION: Oral administration of parsley is effective in reducing stress-induced gastric injury by supporting the cellular antioxidant defence system.

Sensitization of 5-Fluorouracil-Resistant SNUC5 Colon Cancer Cells to Apoptosis by α-Mangostin

5-fluorouracil (5-FU) is a chemotherapeutic agent commonly used for treatment of solid tumors, including colorectal cancer. However, chemoresistance against 5-fluorouracil (5-FU) often limits its success for chemotherapy and, therefore, finding out appropriate adjuvant(s) that might overcome chemoresistance against 5-FU bears a significant importance. In the present study, we have found that α-mangostin can sensitize 5-FU-resistant SNUC5/5-FUR colon cancer cells to apoptosis. Exposure of α-mangostin induced significant DNA damages and increased the intracellular 8-hydroxyguanosine (8-OH-G) and 4-hydroxynonenal (4-HNE) levels in SNUC5 and SNUC5/5-FUR cells. Western blot analysis illustrated that α-mangostin-induced apoptosis was mediated by the activation of the extrinsic and intrinsic pathways in SNUC5/5-FUR cells. In particular, we observed that Fas receptor (FasR) level was lower in SNUC5/5-FUR cells, compared with SNUC5 cells and that silencing FasR attenuated α-mangostin-mediated apoptosis in SNUC5/5-FUR cells. Together, our study illustrates that α-mangostin might be an efficient apoptosis sensitizer that can overcome chemoresistance against 5-FU by activating apoptosis pathway.

Selenium alleviates cadmium toxicity by preventing oxidative stress in sunflower (Helianthus annuus) seedlings.

The present study investigated the possible mediatory role of selenium (Se) in protecting plants from cadmium (Cd) toxicity. The exposure of sunflower seedlings to 20µM Cd inhibited biomass production, decreased chlorophyll and carotenoid concentrations and strongly increased accumulation of Cd in both roots and shoots. Similarly, Cd enhanced hydrogen peroxides content and lipid peroxidation as indicated by malondialdehyde accumulation. Pre-soaking seeds with Se (5, 10 and 20µM) alleviated the negative effect of Cd on growth and led to a decrease in oxidative injuries caused by Cd. Furthermore, Se enhanced the activities of catalase, ascorbate peroxidase and glutathione reductase, but lowered that of superoxide dismutase and guaiacol peroxidase. As important antioxidants, ascorbate and glutathione contents in sunflower leaves exposed to Cd were significantly decreased by Se treatment. The data suggest that the beneficial effect of Se during an earlier growth period could be related to avoidance of cumulative damage upon exposure to Cd, thus reducing the negative consequences of oxidative stress caused by heavy metal toxicity.

Molecular mechanisms of superoxide production by complex III: a bacterial versus human mitochondrial comparative case study.

In this mini review, we briefly survey the molecular processes that lead to reactive oxygen species (ROS) production by the respiratory complex III (CIII or cytochrome bc1). In particular, we discuss the "forward" and "reverse" electron transfer pathways that lead to superoxide generation at the quinol oxidation (Qo) site of CIII, and the components that affect these reactions. We then describe and compare the properties of a bacterial (Rhodobacter capsulatus) mutant enzyme producing ROS with its mitochondrial (human cybrids) counterpart associated with a disease. The mutation under study is located at a highly conserved tyrosine residue of cytochrome b (Y302C in R. capsulatus and Y278C in human mitochondria) that is at the heart of the quinol oxidation (Qo) site of CIII. Similarities of the major findings of bacterial and human mitochondrial cases, including decreased catalytic activity of CIII, enhanced ROS production and ensuing cellular responses and damages, are remarkable. This case illustrates the usefulness of undertaking parallel and complementary studies using biologically different yet evolutionarily related systems, such as α-proteobacteria and human mitochondria. It progresses our understanding of CIII mechanism of function and ROS production, and underlines the possible importance of supra-molecular organization of bacterial and mitochondrial respiratory chains (i.e., respirasomes) and their potential disease-associated protective roles. This article is part of a Special Issue entitled: Respiratory complex III and related bc complexes.