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Mitochondrial toxicity

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https://www.readbyqxmd.com/read/28220655/ppars-in-the-central-nervous-system-roles-in-neurodegeneration-and-neuroinflammation
#1
Juan M Zolezzi, Manuel J Santos, Sussy Bastías-Candia, Claudio Pinto, Juan A Godoy, Nibaldo C Inestrosa
Over 25 years have passed since peroxisome proliferators-activated receptors (PPARs), were first described. Like other members of the nuclear receptors superfamily, PPARs have been defined as critical sensors and master regulators of cellular metabolism. Recognized as ligand-activated transcription factors, they are involved in lipid, glucose and amino acid metabolism, taking part in different cellular processes, including cellular differentiation and apoptosis, inflammatory modulation and attenuation of acute and chronic neurological damage in vivo and in vitro...
February 20, 2017: Biological Reviews of the Cambridge Philosophical Society
https://www.readbyqxmd.com/read/28219713/effect-of-doxorubicin-induced-ovarian-toxicity-on-mouse-ovarian-granulosa-cells
#2
Ting Zhang, Wan Hong He, Ling Lin Feng, Hao Guang Huang
The objective of this study was to identify the effect of doxorubicin-induced ovarian toxicity on mouse ovarian granulosa cells. After granulosa cells were treated with doxorubicin at the final concentrations of 0, 0.4, 0.8, and 1.6 μg/ml for 24 h, cell apoptosis was detected by DAPI staining or caspase-3/7 fluorescence probe; ROS was determined by 2', 7'-dichlorodihydrofluorescin diacetate fluorescence probe; mitochondrial membrane potential was detected by rhodamine-123 fluorescence probe; and mRNA expression levels of Bax, Bcl-2, p53, FSHR, StAR, P450scc and P450arom were analyzed by RT-PCR...
February 17, 2017: Regulatory Toxicology and Pharmacology: RTP
https://www.readbyqxmd.com/read/28217951/cytotoxic-effect-of-zinc-oxide-nanoparticles-on-murine-photoreceptor-cells-via-potassium-channel-block-and-na-k-atpase-inhibition
#3
Chao Chen, Wenjuan Bu, Hongyan Ding, Qin Li, Dabo Wang, Hongsheng Bi, Dadong Guo
OBJECTIVE: Zinc oxide (ZnO) nanoparticles can exhibit toxicity towards organisms and oxidative stress is often hypothesized to be one of the most important factors. Nevertheless, the detailed mechanism of toxicity-induced by ZnO nanoparticles has not been completely addressed. The present study aimed to investigate the toxic effects of ZnO nanoparticles on the expression and activity of Na(+) /K(+) -ATPase and on potassium channel block. MATERIALS AND METHODS: In the present study, we explored the cytotoxic effect of ZnO nanoparticles on murine photoreceptor cells using lactate dehydrogenase (LDH) release assay, reactive oxygen species (ROS) determination, mitochondrial membrane potential (Δφm) measurement, delayed rectifier potassium current recordings and Na(+) /K(+) -ATPase expression and activity monitoring...
February 19, 2017: Cell Proliferation
https://www.readbyqxmd.com/read/28214890/a-new-perspective-for-osteosarcoma-therapy-proteasome-inhibition-by-mln9708-2238-successfully-induces-apoptosis-and-cell-cycle-arrest-and-attenuates-the-invasion-ability-of-osteosarcoma-cells-in-vitro
#4
Renhao Liu, Chunjiang Fu, Jiabing Sun, Xvming Wang, Shuo Geng, Xiaoyu Wang, Jilong Zou, Zhenggang Bi, Chenglin Yang
BACKGROUND: The proteasome exists in all eukaryotic cells and provides the main route of intracellular proteins degradation involved in cell growth and apoptosis. Proteasome inhibition could block protein degradation pathways and disturb regulatory networks, possibly leading to profound effects on cell growth, particularly in cancer cells. A proteasome inhibitor with an appropriate toxicity index for malignant cells rather than normal cells would be an attractive anticancer therapy. METHODS: The human osteosarcoma (OS) cell lines MG-63 and Saos-2 and normal osteoblast cells were used to study the antitumour activity of the proteasome inhibitor MLN9708/2238...
January 27, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28214842/inhibition-of-methylglyoxal-induced-ages-rage-expression-contributes-to-dermal-protection-by-n-acetyl-l-cysteine
#5
Chun-Tao Yang, Fu-Hui Meng, Li Chen, Xiang Li, Lai-Jian Cen, Yu-Hua Wen, Cai-Chen Li, Hui Zhang
BACKGROUND/AIM: Accumulation of advanced glycation end products (AGEs) is a major cause of diabetes mellitus (DM) skin complications. Methylglyoxal (MGO), a reactive dicarbonyl compound, is a crucial intermediate of AGEs generation. N-acetyl-L-cysteine (NAC), an active ingredient of some medicines, can induce endogenous GSH and hydrogen sulfide generation, and set off a condensation reaction with MGO. However, there is rare evidence to show NAC can alleviate DM-induced skin injury through inhibition of AGEs generation or toxicity...
13, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28214344/neferine-potentiates-the-antitumor-effect-of-cisplatin-in-human-lung-adenocarcinoma-cells-via-a-mitochondria-mediated-apoptosis-pathway
#6
Kalai Selvi Sivalingam, Poornima Paramasivan, Ching Feng Weng, Viswanadha Vijaya Padma
Cisplatin is one of the most potent chemotherapeutic agents for the treatment of many types of solid tumors but its efficacy is often limited by the development of resistance and dose limiting toxicity. Neferine is an alkaloid isolated from seed embryo of Nelumbo nucifera, it has recently been shown to have anticancer effects in various human cancer cell lines. The present investigation is designed to study the chemosensitizing ability of neferine with cisplatin in A549 cells. Neferine potentiates the cisplatin induced apoptosis through the exploration of characteristic apoptotic morphological changes, induced sub-G0/G1 cell cycle arrest, ROS hypergeneration, significant loss of cellular antioxidant enzymes as well as loss of mitochondrial membrane potential (ΔΨM)...
February 18, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28213526/structural-and-mechanistic-insights-into-hemoglobin-catalyzed-hydrogen-sulfide-oxidation-and-the-fate-of-polysulfide-products
#7
Victor Vitvitsky, Pramod K Yadav, Sojin An, Javier Seravalli, Uhn-Soo Cho, Ruma Banerjee
Hydrogen sulfide is a cardioprotective signaling molecule but is toxic at elevated concentrations. Red blood cells can synthesize H2S but lacking organelles, cannot dispose off H2S via the mitochondrial sulfide oxidation pathway. We have recently shown that at high sulfide concentrations, ferric hemoglobin oxidizes H2S to a mixture of thiosulfate and iron-bound polysulfides in which the latter species predominates. Here, we report the crystal structure of human hemoglobin containing low-spin ferric sulfide, the first intermediate in heme-catalyzed sulfide oxidation...
February 17, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28212723/redox-dynamics-of-manganese-as-a-mitochondrial-life-death-switch
#8
REVIEW
Matthew Ryan Smith, Jolyn Fernandes, Young-Mi Go, Dean P Jones
Sten Orrenius, M.D., Ph.D., pioneered many areas of cellular and molecular toxicology and made seminal contributions to our knowledge of oxidative stress and glutathione (GSH) metabolism, organellar functions and Ca(+2)-dependent mechanisms of cell death, and mechanisms of apoptosis. On the occasion of his 80(th) birthday, we summarize current knowledge on redox biology of manganese (Mn) and its role in mechanisms of cell death. Mn is found in all organisms and has critical roles in cell survival and death mechanisms by regulating Mn-containing enzymes such as manganese superoxide dismutase (SOD2) or affecting expression and activity of caspases...
January 15, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28211874/datf4-regulation-of-mitochondrial-folate-mediated-one-carbon-metabolism-is-neuroprotective
#9
Ivana Celardo, Susann Lehmann, Ana C Costa, Samantha Hy Loh, L Miguel Martins
Neurons rely on mitochondria as their preferred source of energy. Mutations in PINK1 and PARKIN cause neuronal death in early-onset Parkinson's disease (PD), thought to be due to mitochondrial dysfunction. In Drosophila pink1 and parkin mutants, mitochondrial defects lead to the compensatory upregulation of the mitochondrial one-carbon cycle metabolism genes by an unknown mechanism. Here we uncover that this branch is triggered by the activating transcription factor 4 (ATF4). We show that ATF4 regulates the expression of one-carbon metabolism genes SHMT2 and NMDMC as a protective response to mitochondrial toxicity...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28208701/excitotoxins-mitochondrial-and-redox-disturbances-in-multiple-sclerosis
#10
REVIEW
Cecilia Rajda, Dániel Pukoli, Zsuzsanna Bende, Zsófia Majláth, László Vécsei
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). There is increasing evidence that MS is not only characterized by immune mediated inflammatory reactions, but also by neurodegenerative processes. There is cumulating evidence that neurodegenerative processes, for example mitochondrial dysfunction, oxidative stress, and glutamate (Glu) excitotoxicity, seem to play an important role in the pathogenesis of MS. The alteration of mitochondrial homeostasis leads to the formation of excitotoxins and redox disturbances...
February 8, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28208301/biomolecular-interaction-assays-identified-dual-inhibitors-of-glutaminase-and-glutamate-dehydrogenase-that-disrupt-mitochondrial-function-and-prevent-growth-of-cancer-cells
#11
Min Zhu, Jinzhang Fang, Jingjing Zhang, Zheng Zhang, Jianhui Xie, Yan Yu, Jennifer Jin Ruan, Zhao Chen, Wei Hou, Gensheng Yang, Weike Su, Benfang Helen Ruan
Glutaminase (KGA/isoenzyme GAC) is an emerging and important drug target for cancer. Traditional methods for assaying glutaminase activity are coupled with several other enzymes. Such coupled assays do not permit the direct and stringent characterization of specific glutaminase inhibitors. Ebselen was identified as a potent 9 nM KGA inhibitor in the KGA/glutamate oxidase (GO)/horse radish peroxidase (HRP) coupled assay but showed very weak activity in inhibiting the growth of glutamine-dependent cancer cells...
February 7, 2017: Analytical Chemistry
https://www.readbyqxmd.com/read/28197542/the-proline-arginine-dipeptide-from-hexanucleotide-repeat-expanded-c9orf72-inhibits-the-proteasome
#12
Rahul Gupta, Matthews Lan, Jelena Mojsilovic-Petrovic, Won Hoon Choi, Nathaniel Safren, Sami Barmada, Min Jae Lee, Robert Kalb
An intronic hexanucleotide repeat expansion (HRE) mutation in the C9ORF72 gene is the most common cause of familial ALS and frontotemporal dementia (FTD) and is found in ∼7% of individuals with apparently sporadic disease. Several different diamino acid peptides can be generated from the HRE by noncanonical translation (repeat-associated non-ATG translation, or RAN translation), and some of these peptides can be toxic. Here, we studied the effects of two arginine containing RAN translation products [proline/arginine repeated 20 times (PR20) and glycine/arginine repeated 20 times (GR20)] in primary rat spinal cord neuron cultures grown on an astrocyte feeder layer...
January 2017: ENeuro
https://www.readbyqxmd.com/read/28196511/antiretroviral-therapy-related-adverse-effects-can-sub-saharan-africa-cope-with-the-new-test-and-treat-policy-of-the-world-health-organization
#13
Jobert Richie N Nansseu, Jean Joel R Bigna
BACKGROUND: Recent studies have shown that early antiretroviral therapy (ART) initiation results in significant HIV transmission reduction. This is the rationale behind the "test and treat" policy of the World Health Organization (WHO). Implementation of this policy will lead to an increased incidence of ART-related adverse effects, especially in sub-Saharan Africa (SSA). Is the region yet ready to cope with such a challenging issue? MAIN BODY: The introduction and widespread use of ART have drastically changed the natural history of HIV/AIDS, but exposure to ART leads to serious medication-related adverse effects mainly explained by mitochondrial toxicities, and the situation will get worse in the near future...
February 15, 2017: Infectious Diseases of Poverty
https://www.readbyqxmd.com/read/28194639/ultrafine-particulate-matter-increases-cardiac-ischemia-reperfusion-injury-via-mitochondrial-permeability-transition-pore
#14
Nathan A Holland, Chad R Fraiser, Ruben C Sloan, Robert B Devlin, David A Brown, Christopher J Wingard
Ultrafine particulate matter (UFP) has been associated with increased cardiovascular morbidity and mortality. However, the mechanisms that drive PM-associated cardiovascular disease and dysfunction remain unclear. We examined the impact of oropharyngeal aspiration of 100 μg UFP from the Chapel Hill, NC, air shed in Sprague-Dawley rats on cardiac function, arrhythmogenesis, and cardiac ischemia/reperfusion (I/R) injury using a Langendorff working heart model. We found that exposure to UFP was capable of significantly exacerbating cardiac I/R injury without changing overall cardiac function or major changes in arrhythmogenesis...
February 13, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28194437/mitochondrial-quality-control-dysregulation-in-conditional-ho-1-mice
#15
Hagir B Suliman, Jeffrey E Keenan, Claude A Piantadosi
The heme oxygenase-1 (Hmox1; HO-1) pathway was tested for defense of mitochondrial quality control in cardiomyocyte-specific Hmox1 KO mice (HO-1[CM](-/-)) exposed to oxidative stress (100% O2). After 48 hours of exposure, these mice showed persistent cardiac inflammation and oxidative tissue damage that caused sarcomeric disruption, cardiomyocyte death, left ventricular dysfunction, and cardiomyopathy, while control hearts showed minimal damage. After hyperoxia, HO-1(CM)(-/-) hearts showed suppression of the Pgc-1α/nuclear respiratory factor-1 (NRF-1) axis, swelling, low electron density mitochondria by electron microscopy (EM), increased cell death, and extensive collagen deposition...
February 9, 2017: JCI Insight
https://www.readbyqxmd.com/read/28193887/tmem175-deficiency-impairs-lysosomal-and-mitochondrial-function-and-increases-%C3%AE-synuclein-aggregation
#16
Sarah Jinn, Robert E Drolet, Paige E Cramer, Andus Hon-Kit Wong, Dawn M Toolan, Cheryl A Gretzula, Bhavya Voleti, Galya Vassileva, Jyoti Disa, Marija Tadin-Strapps, David J Stone
Parkinson disease (PD) is a neurodegenerative disorder pathologically characterized by nigrostriatal dopamine neuron loss and the postmortem presence of Lewy bodies, depositions of insoluble α-synuclein, and other proteins that likely contribute to cellular toxicity and death during the disease. Genetic and biochemical studies have implicated impaired lysosomal and mitochondrial function in the pathogenesis of PD. Transmembrane protein 175 (TMEM175), the lysosomal K(+) channel, is centered under a major genome-wide association studies peak for PD, making it a potential candidate risk factor for the disease...
February 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28193870/disruption-of-quercetin-metabolism-by-fungicide-affects-energy-production-in-honey-bees-apis-mellifera
#17
Wenfu Mao, Mary A Schuler, May R Berenbaum
Cytochrome P450 monooxygenases (P450) in the honey bee, Apis mellifera, detoxify phytochemicals in honey and pollen. The flavonol quercetin is found ubiquitously and abundantly in pollen and frequently at lower concentrations in honey. Worker jelly consumed during the first 3 d of larval development typically contains flavonols at very low levels, however. RNA-Seq analysis of gene expression in neonates reared for three days on diets with and without quercetin revealed that, in addition to up-regulating multiple detoxifying P450 genes, quercetin is a negative transcriptional regulator of mitochondrion-related nuclear genes and genes encoding subunits of complexes I, III, IV, and V in the oxidative phosphorylation pathway...
February 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28192797/aberrant-buildup-of-all-trans-retinal-dimer-a-nonpyridinium-bisretinoid-lipofuscin-fluorophore-contributes-to-the-degeneration-of-the-retinal-pigment-epithelium
#18
Junli Zhao, Yi Liao, Jingmeng Chen, Xinran Dong, Zhan Gao, Houjian Zhang, Xiaodan Wu, Zuguo Liu, Yalin Wu
Purpose: Nondegradable fluorophores that accumulate as deleterious lipofuscin of RPE are involved in pathological mechanisms leading to the degeneration of RPE in AMD. A2E, a major component of RPE lipofuscin, could cause damage to RPE cells. Nevertheless, all-trans-retinal dimer (atRAL dimer) was found to be much more abundant than that of A2E in eyes of Abca4-/-Rdh8-/- double-knockout (DKO) mice, a rodent model showing the typical characteristics of retinopathies in AMD patients. Our aim was to elucidate the effect and mechanism of atRAL dimer-induced RPE degeneration...
February 1, 2017: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/28192238/molecular-networks-related-to-the-immune-system-and-mitochondria-are-targets-for-the-pesticide-dieldrin-in-the-zebrafish-danio-rerio-central-nervous-system
#19
Andrew M Cowie, Kathleena I Sarty, Angella Mercer, Jin Koh, Karen A Kidd, Christopher J Martyniuk
: The objectives of this study were to determine the behavioral and molecular responses in the adult zebrafish (Danio rerio) central nervous system (CNS) following a dietary exposure to the pesticide dieldrin. Zebrafish were fed pellets spiked with 0.03, 0.15, or 1.8μg/g dieldrin for 21days. Behavioral analysis revealed no difference in exploratory behaviors or those related to anxiety. Transcriptional networks for T-cell aggregation and selection were decreased in expression suggesting an immunosuppressive effect of dieldrin, consistent with other studies investigating organochlorine pesticides...
February 9, 2017: Journal of Proteomics
https://www.readbyqxmd.com/read/28190920/acute-alloxan-renal-toxicity-in-the-rat-initially-causes-degeneration-of-thick-ascending-limbs-of-henle
#20
Yui Terayama, Yasushi Kodama, Tetsuro Matsuura, Kiyokazu Ozaki
Alloxan (AL) is a material well-known to induce diabetes. Prior to inducing a prolonged diabetic state, AL causes acute tubulointerstitial nephritis. However, the precise primary target site and mechanism of its nephrotoxicity remain unclear. The objective of this study was to evaluate the morphological characteristics relevant to acute renal toxicity following AL administration. Rats were intravenously treated with AL. Eight hours after AL treatment, aquaporin 1-negative and Na/K pump-positive thick ascending limbs of Henle (TAL) were degenerated in the outer medulla...
January 2017: Journal of Toxicologic Pathology
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