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https://www.readbyqxmd.com/read/28801545/cardiotoxicity-and-mechanism-of-particulate-matter-2-5-pm2-5-exposure-in-offspring-rats-during-pregnancy
#1
Hongling Wang, Xiangwen Peng, Fenglin Cao, Ying Wang, Huijie Shi, Shuai Lin, Weijie Zhong, Jingxia Sun
BACKGROUND The aim of this study was to investigate the cardiotoxicity and mechanism of particulate matter 2.5 (PM2.5) exposure on offspring rats during pregnancy. MATERIAL AND METHODS Wistar rats were used to establish a PM2.5 exposure animal model during pregnancy, and they were divided into a control group, a low-dose group, a middle-dose group, and a high-dose group according to PM2.5 exposure dose. The pathological changes of heart tissue, the rate of myocardial cell apoptosis, the levels of LDH, AST, and CM-KB in serum, and the difference in mitochondrial fusion genes (OPA1 and Mfn1) and mitochondrial genes (Drp1 and Fis1) were compared among groups...
August 12, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28801211/parkin-clearance-of-dysfunctional-mitochondria-regulates-ros-levels-and-increases-survival-of-human-chondrocytes
#2
Mohammad Y Ansari, Nazir M Khan, Imran Ahmad, Tariq M Haqqi
OBJECTIVE: Mitochondrial dysfunction, oxidative stress and chondrocyte death are important contributors to the development and pathogenesis of osteoarthritis (OA). In this study, we determined the expression and role of Parkin in the clearance of damaged/dysfunctional mitochondria, regulation of ROS levels and chondrocyte survival under pathological conditions. METHODS: Human chondrocytes were from the unaffected area of knee OA cartilage (n=12) and were stimulated with IL-1β to mimic pathological conditions...
August 8, 2017: Osteoarthritis and Cartilage
https://www.readbyqxmd.com/read/28797885/mitophagy-in-neurodegenerative-diseases
#3
REVIEW
Carlo Rodolfo, Silvia Campello, Francesco Cecconi
Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and Amyotrophic Lateral Sclerosis (ALS), are a complex "family" of pathologies, characterised by the progressive loss of neurons and/or neuronal functions, leading to severe physical and cognitive inabilities in affected patients. These syndromes, despite differences in the causative events, the onset, and the progression of the disease, share as common features the presence of aggregate-prone neuro-toxic proteins, in the form of aggresomes and/or inclusion bodies, perturbing cellular homeostasis and neuronal function (Popovic et al...
August 7, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28796242/the-triterpenoid-cddo-imidazolide-ameliorates-mouse-liver-ischemia-reperfusion-injury-through-activating-the-nrf2-ho-1-pathway-enhanced-autophagy
#4
Dongwei Xu, Lili Chen, Xiaosong Chen, Yankai Wen, Chang Yu, Jufang Yao, Hailong Wu, Xin Wang, Qiang Xia, Xiaoni Kong
Nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated induction of antioxidants has been implicated to have protective roles in ischemia-reperfusion (I/R) injury in many animal models. However, the in vivo effects of CDDO-imidazole (CDDO-Im) (1-[2-cyano-3-,12-dioxooleana-1,9(11)-dien-28-oyl] imidazole), a Nrf2 activator, in hepatic I/R injury is lacking and its exact molecular mechanisms are still not very clear. The goals of this study were to determine whether CDDO-Im can prevent liver injury induced by I/R in the mouse, and to elucidate the molecular target of drug action...
August 10, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28796154/the-ability-of-exercise-associated-oxidative-stress-to-trigger-redox-sensitive-signalling-responses
#5
REVIEW
Richard Webb, Michael G Hughes, Andrew W Thomas, Keith Morris
In this review, we discuss exercise as an oxidative stressor, and elucidate the mechanisms and downstream consequences of exercise-induced oxidative stress. Reactive oxygen species (ROS) are generated in the mitochondria of contracting skeletal myocytes; also, their diffusion across the myocyte membrane allows their transport to neighbouring muscle tissue and to other regions of the body. Although very intense exercise can induce oxidative damage within myocytes, the magnitudes of moderate-intensity exercise-associated increases in ROS are quite modest (~two-fold increases in intracellular and extracellular ROS concentrations during exercise), and so the effects of such increases are likely to involve redox-sensitive signalling effects rather than oxidative damage...
August 10, 2017: Antioxidants (Basel, Switzerland)
https://www.readbyqxmd.com/read/28795394/mitophagy-in-maintaining-skeletal-muscle-mitochondrial-proteostasis-and-metabolic-health-with-aging
#6
Joshua C Drake, Zhen Yan
Skeletal muscle is important for overall functionality and health. Aging is associated with an accumulation of damage to mitochondria DNA and proteins. In particular, damage to mitochondrial proteins in skeletal muscle, which is a loss of mitochondrial proteostasis, contributes to tissue dysfunction and negatively impacts systemic health. Therefore, understanding the mechanisms underlying the regulation of mitochondrial proteostasis and how those mechanisms change with age is important for the development of interventions to promote healthy aging...
August 10, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28795098/data-on-administration-of-cyclosporine-nicorandil-metoprolol-on-reperfusion-related-outcomes-in-st-segment-elevation-myocardial-infarction-treated-with-percutaneous-coronary-intervention
#7
Gianluca Campo, Rita Pavasini, Giampaolo Morciano, Michael A Lincoff, Michael C Gibson, Masafumi Kitakaze, Jacob Lonborg, Amrita Ahluwalia, Hideki Ishii, Michael Frenneaux, Michel Ovize, Marcello Galvani, Dan Atar, Borja Ibanez, Giampaolo Cerisano, Simone Biscaglia, Brandon J Neil, Masanori Asakura, Thomas Engstrom, Daniel A Jones, Dana Dawson, Roberto Ferrari, Paolo Pinton, Filippo Ottani
Mortality and morbidity in patients with ST elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) are still high [1]. A huge amount of the myocardial damage is related to the mitochondrial events happening during reperfusion [2]. Several drugs directly and indirectly targeting mitochondria have been administered at the time of the PCI and their effect on fatal (all-cause mortality, cardiovascular (CV) death) and non fatal (hospital readmission for heart failure (HF)) outcomes have been tested showing conflicting results [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16]...
October 2017: Data in Brief
https://www.readbyqxmd.com/read/28793917/molluscicidal-activity-and-mechanism-of-toxicity-of-a-novel-salicylanilide-ester-derivative-against-biomphalaria-species
#8
Ping He, Weisi Wang, Benjamin Sanogo, Xin Zeng, Xi Sun, Zhiyue Lv, Dongjuan Yuan, Liping Duan, Zhongdao Wu
BACKGROUND: Schistosomiasis mansoni is one of the most important, but often neglected, tropical diseases transmitted by snails of the genus Biomphalaria. Control of the intermediate host snail plays a crucial role in preventing the spread of schistosomiasis. However, there is only one molluscicide, niclosamide, recommended by the World Health Organization. Niclosamide has been used for several decades but is toxic to non-target organisms. Therefore, it is necessary to optimize the scaffold of niclosamide and develop novel molluscicides with enhanced potency and decreased toxicity to non-target organisms...
August 10, 2017: Parasites & Vectors
https://www.readbyqxmd.com/read/28790886/molecular-bases-of-brain-preconditioning
#9
Oleg G Deryagin, Svetlana A Gavrilova, Khalil L Gainutdinov, Anna V Golubeva, Vyatcheslav V Andrianov, Guzel G Yafarova, Sergey V Buravkov, Vladimir B Koshelev
Preconditioning of the brain induces tolerance to the damaging effects of ischemia and prevents cell death in ischemic penumbra. The development of this phenomenon is mediated by mitochondrial adenosine triphosphate-sensitive potassium ([Formula: see text]) channels and nitric oxide signaling (NO). The aim of this study was to investigate the dynamics of molecular changes in mitochondria after ischemic preconditioning (IP) and the effect of pharmacological preconditioning (PhP) with the [Formula: see text]-channels opener diazoxide on NO levels after ischemic stroke in rats...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28790012/mdivi-1-ameliorates-early-brain-injury-after-subarachnoid-hemorrhage-via-the-suppression-of-inflammation-related-blood-brain-barrier-disruption-and-endoplasmic-reticulum-stress-based-apoptosis
#10
Lin-Feng Fan, Ping-You He, Yu-Cong Peng, Qing-Hua Du, Yi-Jun Ma, Jian-Xiang Jin, Hang-Zhe Xu, Jian-Ru Li, Zhi-Jiang Wang, Sheng-Long Cao, Tao Li, Feng Yan, Chi Gu, Lin Wang, Gao Chen
Aberrant modulation of mitochondrial dynamic network, which shifts the balance of fusion and fission towards fission, is involved in brain damage of various neurodegenerative diseases including Parkinson's disease, Huntington's disease and Alzheimer's disease. A recent research has shown that the inhibition of mitochondrial fission alleviates early brain injury after experimental subarachnoid hemorrhage, however, the underlying molecular mechanisms have remained to be elucidated. This study was undertaken to characterize the effects of the inhibition of dynamin-related protein-1 (Drp1, a dominator of mitochondrial fission) on blood-brain barrier (BBB) disruption and neuronal apoptosis following SAH and the potential mechanisms...
August 5, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28789970/mitochondrial-fusion-fission-and-mitochondrial-toxicity
#11
Joel N Meyer, Tess C Leuthner, Anthony L Luz
Mitochondrial dynamics are regulated by two sets of opposed processes: mitochondrial fusion and fission, and mitochondrial biogenesis and degradation (including mitophagy), as well as processes such as intracellular transport. These processes maintain mitochondrial homeostasis, regulate mitochondrial form, volume and function, and are increasingly understood to be critical components of the cellular stress response. Mitochondrial dynamics vary based on developmental stage and age, cell type, environmental factors, and genetic background...
August 5, 2017: Toxicology
https://www.readbyqxmd.com/read/28780470/acrylamide-induces-immunotoxicity-through-reactive-oxygen-species-production-and-caspase-dependent-apoptosis-in-mice-splenocytes-via-the-mitochondria-dependent-signaling-pathways
#12
Ehsan Zamani, Fatemeh Shaki, Saeid AbedianKenari, Mohammad Shokrzadeh
INTRODUCTION: Acrylamide (AA), a well-known food neo-contamination, can be produced during food preparing at high temperature. The immunotoxicity of AA have been revealed in the experimental animals. In this study, we explored the molecular mechanism responsible for the immunotoxicity of AA. METHODS: The mice splenocytes exposed to AA concentrations (0,5,10 and 25 mM) and apoptosis cell death was measured through Annexin V/Propidium Iodide staining by flow cytometry method...
August 3, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28780379/proinflammatory-cytokine-mif-plays-a-role-in-the-pathogenesis-of-type-2-diabetes-mellitus-but-does-not-affect-hepatic-mitochondrial-function
#13
Miriam Rodriguez-Sosa, Tecilli Cabellos-Avelar, Yuriko Sanchez-Zamora, Imelda Juárez-Avelar, Esperanza García-Reyes, Alejandra Lira-León, José Del Carmen Benítez-Flores, Thalia Pacheco-Fernández, Marcia Hiriart, Emma Berta Gutiérrez-Cirlos
BACKGROUND: Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that plays an important role in the pathogenesis of type 2 diabetes mellitus (T2DM). Although the effect of high glucose on liver function has been described, the role of MIF in hepatic mitochondrial function during T2DM has not been studied. OBJECTIVE: We examine the influence of MIF to hepatic mitochondrial function in T2DM mouse model. METHODS: WT and Mif(-/-) BALB/c mice were treated with a single dose of streptozotocin (STZ)...
August 2, 2017: Cytokine
https://www.readbyqxmd.com/read/28775302/deoxyarbutin-displays-antitumour-activity-against-melanoma-in-vitro-and-in-vivo-through-a-p38-mediated-mitochondria-associated-apoptotic-pathway
#14
Limei Ma, Yao Xu, Zeliang Wei, Guang Xin, Zhihua Xing, Hai Niu, Wen Huang
Deoxyarbutin (DeoxyArbutin, dA), a natural compound widely used in skin lighting, displayed selectively cytotoxicity in vitro. In the study, we found that dA significantly inhibited viability/proliferation of B16F10 melanoma cells, induced tumour cell arrest and apoptosis. Furthermore, dA triggered its pro-apoptosis through damaging the mitochondrial function (membrane potential loss, ATP depletion and ROS overload generation etc.) and activating caspase-9, PARP, caspase-3 and the phosphorylation of p38. Treatment with p38 agonist confirmed the involvement of p38 pathway triggered by dA in B16F10 cells...
August 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28774709/treatment-with-antioxidants-ameliorates-oxidative-damage-in-a-mouse-model-of-propionic-acidemia
#15
Ana Rivera-Barahona, Esmeralda Alonso-Barroso, Belén Pérez, Michael P Murphy, Eva Richard, Lourdes R Desviat
Oxidative stress contributes to the pathogenesis of propionic acidemia (PA), a life threatening disease caused by the deficiency of propionyl CoA-carboxylase, in the catabolic pathway of branched-chain amino acids, odd-number chain fatty acids and cholesterol. Patients develop multisystemic complications including seizures, extrapyramidal symptoms, basal ganglia deterioration, pancreatitis and cardiomyopathy. The accumulation of toxic metabolites results in mitochondrial dysfunction, increased reactive oxygen species and oxidative damage, all of which have been documented in patients' samples and in a hypomorphic mouse model...
July 25, 2017: Molecular Genetics and Metabolism
https://www.readbyqxmd.com/read/28774157/the-potential-liver-brain-and-embryo-toxicity-of-titanium-dioxide-nanoparticles-on-mice
#16
Xiaochuan Jia, Shuo Wang, Lei Zhou, Li Sun
Nanoscale titanium dioxide (nano-TiO2) has been widely used in industry and medicine. However, the safety of nano-TiO2 exposure remains unclear. In this study, we evaluated the liver, brain, and embryo toxicity and the underlying mechanism of nano-TiO2 using mice models. The results showed that titanium was distributed to and accumulated in the heart, brain, spleen, lung, and kidney of mice after intraperitoneal (i.p.) nano-TiO2 exposure, in a dose-dependent manner. The organ/body weight ratios of the heart, spleen, and kidney were significantly increased, and those of the brain and lung were decreased...
December 2017: Nanoscale Research Letters
https://www.readbyqxmd.com/read/28769076/connexin-43-is-required-for-the-maintenance-of-mitochondrial-integrity-in-brown-adipose-tissue
#17
Sang-Nam Kim, Hyun-Jung Kwon, Seo-Woo Im, Yeon-Ho Son, Seun Akindehin, Young-Suk Jung, Se Jeong Lee, Im Joo Rhyu, Il Yong Kim, Je-Kyoung Seong, Jinu Lee, Hee-Chan Yoo, James G Granneman, Yun-Hee Lee
We investigated the role of connexin 43 (Cx43) in maintaining the integrity of mitochondria in brown adipose tissue (BAT). The functional effects of Cx43 were evaluated using inducible, adipocyte-specific Cx43 knockout in mice (Gja1 (adipoq) KO) and by overexpression and knockdown of Cx43 in cultured adipocytes. Mitochondrial morphology was evaluated by electron microscopy and mitochondrial function and autophagy were assessed by immunoblotting, immunohistochemistry, and qPCR. The metabolic effects of adipocyte-specific knockout of Cx43 were assessed during cold stress and following high fat diet feeding...
August 2, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28768445/single-walled-carbon-nanotube-multi-walled-carbon-nanotube-and-fe2o3-nanoparticles-induced-mitochondria-mediated-apoptosis-in-melanoma-cells
#18
Parvaneh Naserzadeh, Fatemeh Ansari Esfeh, Mahboubeh Kaviani, Khadigeh Ashtari, Raheleh Kheirbakhsh, Ahmad Salimi, Jalal Pourahmad
PURPOSE: Nanomaterials (NM) exhibit novel anticancer properties. MATERIALS AND METHODS: The toxicity of three nanoparticles that are currently being produced in high tonnage including single-walled carbon nanotube (SWCNT), multi-walled carbon nanotube (MWCNT) and Fe2O3 nanoparticles, were compared with normal and melanoma cells. RESULTS: All tested nanoparticles induced selective toxicity and caspase 3 activation through mitochondria pathway in melanoma cells and mitochondria cause the generating of reactive oxygen species (ROS), mitochondrial membrane potential decline (MMP collapse), mitochondria swelling and cytochrome c release...
August 2, 2017: Cutaneous and Ocular Toxicology
https://www.readbyqxmd.com/read/28766251/melatonin-alleviates-intracerebral-hemorrhage-induced-secondary-brain-injury-in-rats-via-suppressing-apoptosis-inflammation-oxidative-stress-dna-damage-and-mitochondria-injury
#19
Zhong Wang, Feng Zhou, Yang Dou, Xiaodi Tian, Chenglin Liu, Haiying Li, Haitao Shen, Gang Chen
Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity, and the effective treatment is still lacking. We designed this study to investigate the therapeutic effects and mechanisms of melatonin on the secondary brain injury (SBI) after ICH. An in vivo ICH model was induced via autologous whole blood injection into the right basal ganglia in Sprague-Dawley (SD) rats. Primary rat cortical neurons were treated with oxygen hemoglobin (OxyHb) as an in vitro ICH model. The results of the in vivo study showed that melatonin alleviated severe brain edema and behavior disorders induced by ICH...
August 1, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/28766175/backbone-and-side-chain-resonance-assignments-for-a-structured-domain-within-atg32
#20
Xue Xia, Maria Pellegrini, Michael J Ragusa
Autophagy is a catabolic cellular process that targets cytosolic material, including mitochondria, to the vacuole or lysosomes for degradation. The selective degradation of mitochondria by autophagy is termed mitophagy. Dysfunctional mitophagy, which leads to the accumulation of damaged mitochondria, has been implicated in Parkinson's disease, cancer, cardiac disease and metabolic disease. In Saccharomyces cerevisiae, mitophagy is initiated by the autophagy receptor Atg32, an outer mitochondrial membrane protein...
August 1, 2017: Biomolecular NMR Assignments
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