scholarly journals Climate change affects seed aging? Initiation mechanism and consequences of loss of forest tree seed viability

Trees ◽  
2021 ◽  
Author(s):  
Joanna Kijowska-Oberc ◽  
Aleksandra M. Staszak ◽  
Ewelina Ratajczak
Keyword(s):  
Oxidative Stress ◽  
Aging Process ◽  
Climate Changes ◽  
Germination Rate ◽  
Initiation Mechanism ◽  
Seed Aging ◽  
Forest Reproductive Material ◽  
Storage Methods ◽  
Tree Seed

Abstract Key message Environmental stress resulting from rapid climate changes leads to the initiation of the seed aging process in mitochondria and peroxisomes. Seed storage methods limiting germinability loss are fundamental for forest future. Abstract Seed aging is a natural process. It decreases the seed germination rate, i.e. the process is essential for the plant’s life cycle. Aging involves a progressive accumulation of oxidative damage over time. One of the main plant responses to stress is an excessive production of reactive oxygen species (ROS), such as O 2 −• , H2O2 and •OH. If the concentration of ROS is too high, it causes damage of the structure of lipid membranes, proteins, carbohydrates, and DNA. Climate changes affect tree reproduction and may have long-term consequences in the form of reduced species dispersal and acquisition of new habitats. High temperatures accelerate the aging of seeds and decrease their viability. There is, therefore, an indisputable need to store forest reproductive material to maintain continuity of regeneration in farm forests. The quality of seeds subjected to long-term storage correlates negatively with ROS concentration, as ROS accumulation typically occurs in tissues experiencing oxidative stress. Therefore, to preserve forest genetic resources, it is particularly important to know the causes and sites of initiation of the aging process in seed cells, as well as to prevent the germination rate decrease by developing appropriate storage methods. The main organelles responsible for intracellular ROS production are mitochondria and peroxisomes. This article aims at verifying the causes of seed aging and determining its consequences for future forest regeneration due to climate changes. We review the literature on oxidative stress, as well as the sites where the tree seed aging process originates, such as mitochondria and peroxisomes.

scholarly journals Effect of Natural Seed Aging on Root and Shoot Traits in Bread Wheat (Triticum aestivum L.) Cultivars

2021 ◽  
Vol 9 (4) ◽  
pp. 759-763
Author(s):  
Hayati Akman
Keyword(s):  
Bread Wheat ◽  
Germination Rate ◽  
Seedling Emergence ◽  
Seed Storage ◽  
Wheat Cultivars ◽  
Coleoptile Length ◽  
Seed Aging ◽  
Long Term Storage ◽  
Term Storage

This study targeted to elucidate the effect of seed aging on germination and emergence rates with and shoot characteristics in wheat cultivars. For this purpose, different bread wheat cultivars stored for 7 years and non-stored were compared for coleoptile length, root mass, shoot mass, root length as well as germination and seedling emergence rates. Here, the evidence suggested that seed storage over a prolonged period affected root and Shoot growth, coleoptile length, seed germination, and seedling emergence rates adversely. By linking germination and emergence rates, the data presented here indicated that a reduction in emergence rate in long-term storage was higher than that in the germination rate. It was also found that there were significant variations among the wheat cultivars about investigated traits during long-term storage. However, the emergence rates of Kate A1 and Flamura 85 were not affected substantially by long-term storage. The study suggested future studies to focus on clarification of the process controlling natural seed aging as such knowledge allows clue the eventual consequences of long-term storage.

scholarly journals Oxidative stress: Its role in regulating aging and longevity

2015 ◽  
Vol 37 (4) ◽  
pp. 16-19
Author(s):  
Catherine E. Aiken ◽  
Jane L. Tarry-Adkins ◽  
Susan E. Ozanne
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Aging Process ◽  
Cellular Level ◽  
Cellular Aging ◽  
Free Radical Damage ◽  
Early Life Environment ◽  
Cellular Components ◽  
Radical Damage

Although aging is ubiquitous across organisms, the rate at which it occurs varies considerably between species and individuals. The initial links between oxidative stress and rates of cellular aging were postulated over 50 years ago by Harman, who published a theory connecting free radical damage with the aging process in 19561. Since then a wide body of literature has accumulated demonstrating the links between oxidative damage to various cellular components and cellular senescence2. Oxidative stress is known to contribute to the aetiology of a wide variety of pathological processes including metabolic, cardiovascular and neoplastic diseases, all of which can shorten lifespan. Macromolecules such as proteins, lipids and particularly DNA can be irreversibly damaged by oxidative stress, leading to a decline in cellular function and apoptosis. This leads to aging, initially at a cellular level, then of the tissues and organs, culminating in whole organism pathology and eventually death. This article explores the various processes by which cells accrue oxidative damage and how such long-term damage leads to senescence. In particular, we focus on how the early-life environment influences the accumulation of oxidative stress over the entire life-course of an individual and how this may accelerate the normal aging process.

scholarly journals Blood–brain barrier disruption and ventricular enlargement are the earliest neuropathological changes in rats with repeated sub-concussive impacts over 2 weeks

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bailey Hiles-Murison ◽  
Andrew P. Lavender ◽  
Mark J. Hackett ◽  
Joshua J. Armstrong ◽  
Michael Nesbit ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Brain Barrier ◽  
Hippocampal Formation ◽  
Brain Barrier ◽  
Lateral Ventricles ◽  
Blood Brain Barrier Disruption ◽  
Blood Brain ◽  
Brain Barrier Disruption ◽  
Underlying Mechanisms

AbstractRepeated sub-concussive impact (e.g. soccer ball heading), a significantly lighter form of mild traumatic brain injury, is increasingly suggested to cumulatively alter brain structure and compromise neurobehavioural function in the long-term. However, the underlying mechanisms whereby repeated long-term sub-concussion induces cerebral structural and neurobehavioural changes are currently unknown. Here, we utilised an established rat model to investigate the effects of repeated sub-concussion on size of lateral ventricles, cerebrovascular blood–brain barrier (BBB) integrity, neuroinflammation, oxidative stress, and biochemical distribution. Following repeated sub-concussion 3 days per week for 2 weeks, the rats showed significantly enlarged lateral ventricles compared with the rats receiving sham-only procedure. The sub-concussive rats also presented significant BBB dysfunction in the cerebral cortex and hippocampal formation, whilst neuromotor function assessed by beamwalk and rotarod tests were comparable to the sham rats. Immunofluorescent and spectroscopic microscopy analyses revealed no significant changes in neuroinflammation, oxidative stress, lipid distribution or protein aggregation, within the hippocampus and cortex. These data collectively indicate that repeated sub-concussion for 2 weeks induce significant ventriculomegaly and BBB disruption, preceding neuromotor deficits.

scholarly journals Crosstalk between Long-Term Sublethal Oxidative Stress and Detrimental Inflammation as Potential Drivers for Age-Related Retinal Degeneration

Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 25
Author(s):  
Lara Macchioni ◽  
Davide Chiasserini ◽  
Letizia Mezzasoma ◽  
Magdalena Davidescu ◽  
Pier Luigi Orvietani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Age Related Macular Degeneration ◽  
Inflammasome Activation ◽  
Related Factor ◽  
Nuclear Factor ◽  
Rpe Cells ◽  
Age Related ◽  
Oxidative Insult

Age-related retinal degenerations, including age-related macular degeneration (AMD), are caused by the loss of retinal pigmented epithelial (RPE) cells and photoreceptors. The pathogenesis of AMD, deeply linked to the aging process, also involves oxidative stress and inflammatory responses. However, the molecular mechanisms contributing to the shift from healthy aging to AMD are still poorly understood. Since RPE cells in the retina are chronically exposed to a pro-oxidant microenvironment throughout life, we simulated in vivo conditions by growing ARPE-19 cells in the presence of 10 μM H2O2 for several passages. This long-term oxidative insult induced senescence in ARPE-19 cells without affecting cell proliferation. Global proteomic analysis revealed a dysregulated expression in proteins involved in antioxidant response, mitochondrial homeostasis, and extracellular matrix organization. The analyses of mitochondrial functionality showed increased mitochondrial biogenesis and ATP generation and improved response to oxidative stress. The latter, however, was linked to nuclear factor-κB (NF-κB) rather than nuclear factor erythroid 2–related factor 2 (Nrf2) activation. NF-κB hyperactivation also resulted in increased pro-inflammatory cytokines expression and inflammasome activation. Moreover, in response to additional pro-inflammatory insults, senescent ARPE-19 cells underwent an exaggerated inflammatory reaction. Our results indicate senescence as an important link between chronic oxidative insult and detrimental chronic inflammation, with possible future repercussions for therapeutic interventions.

scholarly journals Barley Seeds miRNome Stability during Long-Term Storage and Aging

2021 ◽  
Vol 22 (9) ◽  
pp. 4315
Author(s):  
Marta Puchta ◽  
Jolanta Groszyk ◽  
Magdalena Małecka ◽  
Marek D. Koter ◽  
Maciej Niedzielski ◽  
...  
Keyword(s):  
Seed Viability ◽  
Small Rna Sequencing ◽  
The Novel ◽  
Seed Aging ◽  
Long Term Storage ◽  
Novel Mirna ◽  
Complex Biological Process ◽  
Almost All ◽  
Term Storage

Seed aging is a complex biological process that has been attracting scientists’ attention for many years. High-throughput small RNA sequencing was applied to examine microRNAs contribution in barley seeds senescence. Unique samples of seeds that, despite having the same genetic makeup, differed in viability after over 45 years of storage in a dry state were investigated. In total, 61 known and 81 novel miRNA were identified in dry seeds. The highest level of expression was found in four conserved miRNA families, i.e., miR159, miR156, miR166, and miR168. However, the most astonishing result was the lack of significant differences in the level of almost all miRNAs in seed samples with significantly different viability. This result reveals that miRNAs in dry seeds are extremely stable. This is also the first identified RNA fraction that is not deteriorating along with the loss of seed viability. Moreover, the novel miRNA hvu-new41, with higher expression in seeds with the lowest viability as detected by RT-qPCR, has the potential to become an indicator of the decreasing viability of seeds during storage in a dry state.

scholarly journals Nicotinamide Nucleotide Transhydrogenase as a Novel Treatment Target in Adrenocortical Carcinoma

Endocrinology ◽  
2018 ◽  
Vol 159 (8) ◽  
pp. 2836-2849 ◽  
Author(s):  
Vasileios Chortis ◽  
Angela E Taylor ◽  
Craig L Doig ◽  
Mark D Walsh ◽  
Eirini Meimaridou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adrenocortical Carcinoma ◽  
Reduced Form ◽  
Polyamine Metabolism ◽  
Metabolome Analysis ◽  
Nucleotide Synthesis ◽  
Treatment Target ◽  
Nicotinamide Nucleotide Transhydrogenase ◽  
Response To Chemotherapy

Abstract Adrenocortical carcinoma (ACC) is an aggressive malignancy with poor response to chemotherapy. In this study, we evaluated a potential new treatment target for ACC, focusing on the mitochondrial reduced form of NAD phosphate (NADPH) generator nicotinamide nucleotide transhydrogenase (NNT). NNT has a central role within mitochondrial antioxidant pathways, protecting cells from oxidative stress. Inactivating human NNT mutations result in congenital adrenal insufficiency. We hypothesized that NNT silencing in ACC cells will induce toxic levels of oxidative stress. To explore this, we transiently knocked down NNT in NCI-H295R ACC cells. As predicted, this manipulation increased intracellular levels of oxidative stress; this resulted in a pronounced suppression of cell proliferation and higher apoptotic rates, as well as sensitization of cells to chemically induced oxidative stress. Steroidogenesis was paradoxically stimulated by NNT loss, as demonstrated by mass spectrometry–based steroid profiling. Next, we generated a stable NNT knockdown model in the same cell line to investigate the longer lasting effects of NNT silencing. After long-term culture, cells adapted metabolically to chronic NNT knockdown, restoring their redox balance and resilience to oxidative stress, although their proliferation remained suppressed. This was associated with higher rates of oxygen consumption. The molecular pathways underpinning these responses were explored in detail by RNA sequencing and nontargeted metabolome analysis, revealing major alterations in nucleotide synthesis, protein folding, and polyamine metabolism. This study provides preclinical evidence of the therapeutic merit of antioxidant targeting in ACC as well as illuminating the long-term adaptive response of cells to oxidative stress.

Immunolocalization of antioxidant enzymes in testis of rams submitted to long-term heat stress

Zygote ◽  
2019 ◽  
Vol 27 (6) ◽  
pp. 432-435
Author(s):  
Thais Rose dos Santos Hamilton ◽  
Gabriela Esteves Duarte ◽  
José Antonio Visintin ◽  
Mayra Elena Ortiz D’Ávila Assumpção
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Heat Stress ◽  
Glutathione Peroxidase ◽  
Cell Types ◽  
Treated Group ◽  
Oxidative Balance ◽  
Testicular Cells

SummaryLong-term heat stress (HS) induced by testicular insulation generates oxidative stress (OS) on the testicular environment; consequently activating antioxidant enzymes such as superoxide dismutase (SOD), glutathione reductase (GR) and glutathione peroxidase (GPx). The aim of this work was to immunolocalize antioxidant enzymes present in different cells within the seminiferous tubule when rams were submitted to HS. Rams were divided into control (n = 6) and treated group (n = 6), comprising rams subjected to testicular insulation for 240 h. After the testicular insulation period, rams were subjected to orchiectomy. Testicular fragments were submitted to immunohistochemistry for staining against SOD, GR and GPx enzymes. We observed immunolocalization of GPx in more cell types of the testis after HS and when compared with other enzymes. In conclusion, GPx is the main antioxidant enzyme identified in testicular cells in an attempt to maintain oxidative balance when HS occurs.

scholarly journals Cellular stress signaling activates type-I IFN response through FOXO3-regulated lamin posttranslational modification

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Inah Hwang ◽  
Hiroki Uchida ◽  
Ziwei Dai ◽  
Fei Li ◽  
Teresa Sanchez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Environmental Changes ◽  
Type I ◽  
Neurogenic Differentiation ◽  
Forkhead Box ◽  
Nuclear Lamin ◽  
Neural Stem Progenitor Cells ◽  
Subsequent Activation ◽  
Methyl Group Transfer

AbstractNeural stem/progenitor cells (NSPCs) persist over the lifespan while encountering constant challenges from age or injury related brain environmental changes like elevated oxidative stress. But how oxidative stress regulates NSPC and its neurogenic differentiation is less clear. Here we report that acutely elevated cellular oxidative stress in NSPCs modulates neurogenic differentiation through induction of Forkhead box protein O3 (FOXO3)-mediated cGAS/STING and type I interferon (IFN-I) responses. We show that oxidative stress activates FOXO3 and its transcriptional target glycine-N-methyltransferase (GNMT) whose upregulation triggers depletion of s-adenosylmethionine (SAM), a key co-substrate involved in methyl group transfer reactions. Mechanistically, we demonstrate that reduced intracellular SAM availability disrupts carboxymethylation and maturation of nuclear lamin, which induce cytosolic release of chromatin fragments and subsequent activation of the cGAS/STING-IFN-I cascade to suppress neurogenic differentiation. Together, our findings suggest the FOXO3-GNMT/SAM-lamin-cGAS/STING-IFN-I signaling cascade as a critical stress response program that regulates long-term regenerative potential.

scholarly journals Changes in surface characteristics and adsorption properties of 2,4,6-trichlorophenol following Fenton-like aging of biochar

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Liqiang Cui ◽  
Qinya Fan ◽  
Jianxiong Sun ◽  
Guixiang Quan ◽  
Jinlong Yan ◽  
...  
Keyword(s):  
Adsorption Capacity ◽  
Surface Properties ◽  
Aging Process ◽  
Surface Characteristics ◽  
Natural Soil ◽  
Peanut Shell ◽  
Soil Environment ◽  
Polluted Soils ◽  
Physico Chemical

AbstractFenton-like system formed in a natural soil environment deemed to be significant in the aging process of biochar. Aged biochars have distinct physico-chemical and surface properties compared to non-aged biochar. The aged biochar proved to be useful soil amendment due to its improved elements contents and surface properties. The biochar aging process resulted in increased surface area and pore volume, as well as carbon and oxygen-containing functional groups (such as C=O, –COOH, O–C=O etc.) on its surface, which were also associated with the adsorption behavior of 2,4,6-trichlorophenol (2,4,6-TCP). The biochar aging increased the adsorption capacity of 2,4,6-TCP, which was maximum at pH 3.0. The 2,4,6-TCP adsorption capacity of aged-bush biochar (ABB) and aged-peanut shell biochar (APB) was increased by 1.0–11.0% and 7.4–38.8%, respectively compared with bush biochar (BB) and peanut shell biochar (PB) at the same initial concentration of 2,4,6-TCP. All biochars had similar 2,4,6-TCP desorption rates ranging from 33.2 to 73.3% at different sorption temperatures and times. The desorbed components were mainly 2,4,6-TCP and other degraded components, which were low in concentration with small molecule substance. The results indicated that the aged-biochar could be effective for the long-term remediation of naturally organic polluted soils.

scholarly journals Hypermetabolism of glutathione, glutamate and ornithine via redox imbalance in methylglyoxal-induced peritoneal injury rats

2019 ◽  
Author(s):  
Ichiro Hirahara ◽  
Eiji Kusano ◽  
Denan Jin ◽  
Shinji Takai
Keyword(s):  
Oxidative Stress ◽  
Intraperitoneal Administration ◽  
Methionine Sulfoxide ◽  
Mesenchymal Cell ◽  
Oxidative Stress Marker ◽  
Peritoneal Fibrosis ◽  
Metabolome Analysis ◽  
Glycation End Products ◽  
Excessive Proliferation

Abstract Peritoneal dialysis (PD) is a blood purification treatment for patients with reduced renal function. However, the peritoneum is exposed to oxidative stress during PD and long-term PD results in peritoneal damage, leading to the termination of PD. Methylglyoxal (MGO) contained in commercial PD fluids is a source of strong oxidative stress. The aim of this study was to clarify the mechanism of MGO-induced peritoneal injury using metabolome analysis in rats. We prepared peritoneal fibrosis rats by intraperitoneal administration of PD fluids containing MGO for 21 days. As a result, MGO-induced excessive proliferation of mesenchymal cells with an accumulation of advanced glycation end-products (AGEs) at the surface of the thickened peritoneum in rats. The effluent levels of methionine sulfoxide, an oxidative stress marker and glutathione peroxidase activity were increased in the MGO-treated rats. The levels of glutathione, glutamate, aspartate, ornithine and AGEs were also increased in these rats. MGO upregulated the gene expression of transporters and enzymes related to the metabolism of glutathione, glutamate and ornithine in the peritoneum. These results suggest that MGO may induce peritoneal injury with mesenchymal cell proliferation via increased redox metabolism, directly or through the formation of AGEs during PD.

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