scholarly journals Short Duration Exposure of 3 µm Polystyrene Microplastics Affected Morphology and Physiology of Watermilfoil (sp. Roraima)

2021 ◽  
Author(s):  
Mudalige Don Hiranya Jayasanka Senavirathna ◽  
Liu Zhaozhi ◽  
Takeshi Fujino
Keyword(s):  
Oxidative Stress ◽  
Catalase Activity ◽  
Growth Parameters ◽  
Environmental Issues ◽  
Antioxidant Response ◽  
Anthocyanin Content ◽  
Exposure Concentration ◽  
Polystyrene Microspheres ◽  
Freshwater Macrophytes ◽  
Order Polynomial

Abstract Microplastics are one of the most widely discussed environmental issues worldwide. Several studies have shown the effect of microplastic exposure on the marine environment; however, studies on freshwater systems are lacking. This study was conducted to investigate the effect of microplastics on hydroponically growing emergent freshwater macrophytes, Watermilfoil (sp. Roraima) under controlled environmental conditions. Plants were exposed to 0 mg L− 1 (control), 0.05 mg L− 1, 0.25 mg L− 1, 1.25 mg L− 1, and 6 mg L− 1 of 3 µm polystyrene microspheres for seven days. The oxidative stress, antioxidant response, pigmentations, Fv/Fm, and growth parameters in above-water and below-water parts were analyzed separately. Microscopic observations were performed to confirm the tissue absorbance of the microplastics. Exposure to microplastics altered some parameters; however, growth was not affected. The effect of microplastics was not linear with the exposure concentration for most of the parameters and between 1.25 mg L− 1 and 6 mg L− 1 concentrations. The response trends mostly followed the second-order polynomial distributions. Under the 1.25 mg L− 1 exposure, there were significant changes in root length, H2O2 content, catalase activity, anthocyanin content, and Fv/Fm. There were differences in parameters between the above-water and below-water parts, and the responses of the microplastics followed different trends. Microscopic observations confirmed the attachment of microplastic particles onto newly formed roots, except for older roots or shoot tissues.

Targeting PPARalpha in Alzheimer's Disease

2018 ◽  
Vol 15 (4) ◽  
pp. 345-354 ◽  
Author(s):  
Barbara D'Orio ◽  
Anna Fracassi ◽  
Maria Paola Cerù ◽  
Sandra Moreno
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Antioxidant Response ◽  
Peroxisome Proliferator ◽  
Prevailing Paradigm

Background: The molecular mechanisms underlying Alzheimer's disease (AD) are yet to be fully elucidated. The so-called “amyloid cascade hypothesis” has long been the prevailing paradigm for causation of disease, and is today being revisited in relation to other pathogenic pathways, such as oxidative stress, neuroinflammation and energy dysmetabolism. The peroxisome proliferator-activated receptors (PPARs) are expressed in the central nervous system (CNS) and regulate many physiological processes, such as energy metabolism, neurotransmission, redox homeostasis, autophagy and cell cycle. Among the three isotypes (α, β/δ, γ), PPARγ role is the most extensively studied, while information on α and β/δ are still scanty. However, recent in vitro and in vivo evidence point to PPARα as a promising therapeutic target in AD. Conclusion: This review provides an update on this topic, focussing on the effects of natural or synthetic agonists in modulating pathogenetic mechanisms at AD onset and during its progression. Ligandactivated PPARα inihibits amyloidogenic pathway, Tau hyperphosphorylation and neuroinflammation. Concomitantly, the receptor elicits an enzymatic antioxidant response to oxidative stress, ameliorates glucose and lipid dysmetabolism, and stimulates autophagy.

scholarly journals Role of hepcidin in oxidative stress and cell death of cultured mouse renal collecting duct cells: protection against iron and sensitization to cadmium

2021 ◽  
Author(s):  
Stephanie Probst ◽  
Johannes Fels ◽  
Bettina Scharner ◽  
Natascha A. Wolff ◽  
Eleni Roussa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Fate ◽  
Catalase Activity ◽  
Metal Ion ◽  
Iron Homeostasis ◽  
Collecting Duct ◽  
Duct Cell ◽  
Plasmid Transfection

AbstractThe liver hormone hepcidin regulates systemic iron homeostasis. Hepcidin is also expressed by the kidney, but exclusively in distal nephron segments. Several studies suggest hepcidin protects against kidney damage involving Fe2+ overload. The nephrotoxic non-essential metal ion Cd2+ can displace Fe2+ from cellular biomolecules, causing oxidative stress and cell death. The role of hepcidin in Fe2+ and Cd2+ toxicity was assessed in mouse renal cortical [mCCD(cl.1)] and inner medullary [mIMCD3] collecting duct cell lines. Cells were exposed to equipotent Cd2+ (0.5–5 μmol/l) and/or Fe2+ (50–100 μmol/l) for 4–24 h. Hepcidin (Hamp1) was transiently silenced by RNAi or overexpressed by plasmid transfection. Hepcidin or catalase expression were evaluated by RT-PCR, qPCR, immunoblotting or immunofluorescence microscopy, and cell fate by MTT, apoptosis and necrosis assays. Reactive oxygen species (ROS) were detected using CellROX™ Green and catalase activity by fluorometry. Hepcidin upregulation protected against Fe2+-induced mIMCD3 cell death by increasing catalase activity and reducing ROS, but exacerbated Cd2+-induced catalase dysfunction, increasing ROS and cell death. Opposite effects were observed with Hamp1 siRNA. Similar to Hamp1 silencing, increased intracellular Fe2+ prevented Cd2+ damage, ROS formation and catalase disruption whereas chelation of intracellular Fe2+ with desferrioxamine augmented Cd2+ damage, corresponding to hepcidin upregulation. Comparable effects were observed in mCCD(cl.1) cells, indicating equivalent functions of renal hepcidin in different collecting duct segments. In conclusion, hepcidin likely binds Fe2+, but not Cd2+. Because Fe2+ and Cd2+ compete for functional binding sites in proteins, hepcidin affects their free metal ion pools and differentially impacts downstream processes and cell fate.

scholarly journals Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 630 ◽  
Author(s):  
Donald G Matthews ◽  
Maya Caruso ◽  
Charles F Murchison ◽  
Jennifer Y Zhu ◽  
Kirsten M Wright ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyloid Β ◽  
Water Extract ◽  
Centella Asiatica ◽  
Antioxidant Response ◽  
Plaque Burden ◽  
Heme Oxygenase 1 ◽  
Synaptic Density ◽  
Cognitive Benefits ◽  
5Xfad Mice

Centella asiatica (CA) herb is a traditional medicine, long reputed to provide cognitive benefits. We have reported that CA water extract (CAW) treatment improves cognitive function of aged Alzheimer’s disease (AD) model Tg2576 and wild-type (WT) mice, and induces an NRF2-regulated antioxidant response in aged WT mice. Here, CAW was administered to AD model 5XFAD female and male mice and WT littermates (age: 7.6 +/ − 0.6 months), and object recall and contextual fear memory were tested after three weeks treatment. CAW’s impact on amyloid-β plaque burden, and markers of neuronal oxidative stress and synaptic density, was assessed after five weeks treatment. CAW antioxidant activity was evaluated via nuclear transcription factor (erythroid-derived 2)-like 2 (NRF2) and NRF2-regulated antioxidant response element gene expression. Memory improvement in both genders and genotypes was associated with dose-dependent CAW treatment without affecting plaque burden, and marginally increased synaptic density markers in the hippocampus and prefrontal cortex. CAW treatment increased Nrf2 in hippocampus and other NRF2 targets (heme oxygenase-1, NAD(P)H quinone dehydrogenase 1, glutamate-cysteine ligase catalytic subunit). Reduced plaque-associated SOD1, an indicator of oxidative stress, was observed in the hippocampi and cortices of CAW-treated 5XFAD mice. We postulate that CAW treatment leads to reduced oxidative stress, contributing to improved neuronal health and cognition.

Antioxidant response to oxidative stress in zooplankton thrived in wastewater-fed ponds in East Calcutta Wetland Ecosystem, a Ramsar site

2013 ◽  
Vol 95 (4) ◽  
pp. 627-634 ◽  
Author(s):  
Abhishek Roy Goswami ◽  
Anulipi Aich ◽  
Sudin Pal ◽  
Buddhadeb Chattopadhyay ◽  
Siddhartha Datta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Response ◽  
Ramsar Site ◽  
Wetland Ecosystem

scholarly journals RBM45 Modulates the Antioxidant Response in Amyotrophic Lateral Sclerosis through Interactions with KEAP1

2015 ◽  
Vol 35 (14) ◽  
pp. 2385-2399 ◽  
Author(s):  
Nadine Bakkar ◽  
Arianna Kousari ◽  
Tina Kovalik ◽  
Yang Li ◽  
Robert Bowser
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Amyotrophic Lateral Sclerosis ◽  
Motor Neurons ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Antioxidant Response ◽  
Cytoplasmic Inclusions ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective loss of motor neurons. Various factors contribute to the disease, including RNA binding protein dysregulation and oxidative stress, but their exact role in pathogenic mechanisms remains unclear. We have recently linked another RNA binding protein, RBM45, to ALS via increased levels of protein in the cerebrospinal fluid of ALS patients and its localization to cytoplasmic inclusions in ALS motor neurons. Here we show RBM45 nuclear exit in ALS spinal cord motor neurons compared to controls, a phenotype recapitulatedin vitroin motor neurons treated with oxidative stressors. We find that RBM45 binds and stabilizes KEAP1, the inhibitor of the antioxidant response transcription factor NRF2. ALS lumbar spinal cord lysates similarly show increased cytoplasmic binding of KEAP1 and RBM45. Binding of RBM45 to KEAP1 impedes the protective antioxidant response, thus contributing to oxidative stress-induced cellular toxicity. Our findings thus describe a novel link between a mislocalized RNA binding protein implicated in ALS (RBM45) and dysregulation of the neuroprotective antioxidant response seen in the disease.

Ageing in embryos from wheat grains stored at different temperatures: oxidative stress and antioxidant response

2011 ◽  
Vol 38 (7) ◽  
pp. 624 ◽  
Author(s):  
Carmelina Spanò ◽  
Stefania Bottega ◽  
Roberto Lorenzi ◽  
Isa Grilli
Keyword(s):  
Oxidative Stress ◽  
Low Temperature ◽  
Seed Viability ◽  
Storage Period ◽  
Antioxidant Response ◽  
Protective Role ◽  
Native Page ◽  
Wheat Grains ◽  
Different Temperatures ◽  
Enzymatic Machinery

In the present work we studied oxidative stress as an important cause of seed deterioration during ageing in embryos from durum wheat grains stored at room temperature and at low temperature (10°C). The protective role of low temperature on seed viability was confirmed. The increase of hydrogen peroxide content during dry storage was strongly correlated with the decrease of germinability. Ascorbate and glutathione showed a good correlation with grain germinability and significantly increased upon imbibition, in particular in embryos from viable grains. Ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), glutathione reductase (GR), glutathione peroxidase (GPX) and catalase (CAT) were studied quantitatively (enzymatic assays). APX, GR, and GPX were also studied qualitatively by native PAGE. The enzymes were active in dry, still viable, embryos whereas no activity was detected in non-viable embryos. With the exception of APX, all enzymatic activities decreased upon imbibition. The study of grains stored in different conditions indicated a negative correlation between the efficiency of the antioxidant enzymatic machinery and the age of the grain. The differences detected in differently stored materials confirmed that both germination parameters and the length of storage period are important in determining grain condition.

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