DOCSLIB.ORG

Effects of Testosterone and Evoked Resistance Exercise After Spinal

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Effects of Testosterone and Evoked Resistance Exercise After Spinal Open Access Protocol Effects of Testosterone and Evoked BMJ Open: first published as 10.1136/bmjopen-2016-014125 on 4 April 2017. Downloaded from Resistance Exercise after Spinal Cord Injury (TEREX-SCI): study protocol for a randomised controlled trial Ashraf S Gorgey,1,2 Refka E Khalil,1 Ranjodh Gill,3,4 Laura C O’Brien,1 Timothy Lavis,1,2 Teodoro Castillo,1 David X Cifu,1,2 Jeannie Savas,5 Rehan Khan,6 Christopher Cardozo,7,8 Edward J Lesnefsky,9,10 David R Gater,11 Robert A Adler3,4 To cite: Gorgey AS, ABSTRACT et al Strengths and limitations of this study Khalil RE, Gill R, . Effects Introduction: Individuals with spinal cord injury (SCI) of Testosterone and Evoked are at a lifelong risk of obesity and chronic metabolic ▪ Resistance Exercise after The trial will investigate the use of surface neuro- disorders including insulin resistance and Spinal Cord Injury (TEREX- muscular electrical stimulation-induced resist- SCI): study protocol for a dyslipidemia. Within a few weeks of injury, there is a ance training (NMES-RT) to restore muscle size randomised controlled trial. significant decline in whole body fat-free mass, after spinal cord injury (SCI). BMJ Open 2017;7:e014125. particularly lower extremity skeletal muscle mass, and ▪ The trial will provide evidence on the effective- doi:10.1136/bmjopen-2016- subsequent increase in fat mass (FM). This is ness of testosterone replacement therapy (TRT) 014125 accompanied by a decrease in anabolic hormones to restore muscle size and lean mass and serve including testosterone. Testosterone replacement as an alternative approach for those who cannot ▸ Prepublication history for therapy (TRT) has been shown to increase skeletal benefit from NMES. this paper is available online. muscle mass and improve metabolic profile. ▪ The trial will determine how restoring muscle To view these files please Additionally, resistance training (RT) has been shown size and lean mass by RT+TRT or TRT can visit the journal online to increase lean mass and reduce metabolic benefit the metabolic profile after SCI. (http://dx.doi.org/10.1136/ disturbances in SCI and other clinical populations. ▪ The study is only limited to men with complete bmjopen-2016-014125). Methods and analysis: 26 individuals with chronic, SCI. http://bmjopen.bmj.com/ motor complete SCI between 18 and 50 years old were ▪ Received 6 September 2016 Surface NMES may not benefit those with full Revised 17 January 2017 randomly assigned to a RT+TRT group (n=13) or a sensation or lower motor neuron denervation. Accepted 16 February 2017 TRT group (n=13). 22 participants completed the initial 16-week training phase of the study and 4 participants withdrew. 12 participants of the 22 completed 16 weeks of detraining. The TRT was provided via INTRODUCTION transdermal testosterone patches (4–6 mg/day). The There are ∼11 000–12 000 new cases of RT+TRT group had 16 weeks of supervised unilateral spinal cord injury (SCI) in the USA annually progressive RT using surface neuromuscular electrical with an overall prevalence of 250 000–400 on October 1, 2021 by guest. Protected copyright. stimulation with ankle weights. This study will 000.12Persons with motor complete injury investigate the effects of evoked RT+TRT or TRT alone have loss of sensation and motor function on body composition (muscle cross-sectional area, below the level of injury, while incomplete visceral adipose tissue, %FM) and metabolic profile injury is characterised by preserved motor or (glucose and lipid metabolism) in individuals with sensory function. Chronic SCI, defined as motor complete SCI. Findings from this study may 1 year postinjury, is associated with dramatic help in designing exercise therapies to alleviate the 3–5 deterioration in body composition after SCI and skeletal muscle atrophy, increase of fat 6–8 decrease the incidence of metabolic disorders in this mass (FM) and decrease of fat-free mass 67 clinical population. (FFM). Collectively, these factors put indi- Ethics and dissemination: The study is currently viduals with SCI at risk for metabolic disor- approved by the McGuire VA Medical Center and ders such as type II diabetes and For numbered affiliations see Virginia Commonwealth University. All participants read cardiovascular disease. end of article. and signed approved consent forms. Results will be Previous studies reveal that 60% of indivi- submitted to peer-reviewed journals and presented at duals with SCI in the USA are either over- – Correspondence to national and international conferences. weight or obese.2911 Despite a low body Dr Ashraf S Gorgey; Trial registration number: Pre-result, mass index (BMI) in 50% of the SCI popula- [email protected] NCT01652040. tion, individuals are likely to have more than Gorgey AS, et al. BMJ Open 2017;7:e014125. doi:10.1136/bmjopen-2016-014125 1 Open Access 30% of their body mass as FM. Furthermore, person decreased energy production and therefore play a signifi- BMJ Open: first published as 10.1136/bmjopen-2016-014125 on 4 April 2017. Downloaded from with SCI are 13% fatter per unit BMI than able-bodied cant role in the altered metabolic profile following SCI.44 individuals. Individuals with SCI also have a redistribu- Body composition and metabolic changes after SCI tion of adipose tissue, with greater trunk FM and visceral may be further exacerbated by reduced anabolic hor- adipose tissue (VAT) compared to age and waist circum- mones including testosterone (T), growth hormone and – ference matched able-bodied controls.12 14 Adipose the growth hormone second messenger insulin-like tissue, particularly VAT, secretes proinflammatory cyto- growth factor-1 (IGF-1).45 46 Previous studies have shown kines including interleukin-6 (IL-6) and tumour-necrosis that 60% of men with SCI have low T and that testoster- factor-α (TNF-α). Therefore, the increase in VAT after one replacement therapy (TRT) increases IGF-1 in – SCI may contribute to metabolic syndrome by stimulat- men.47 50 In rodent models of SCI, TRT attenuates the ing the hepatic production of C reactive protein (CRP), loss of muscle.51 52 TRT decreases total body fat, – which is tied to vascular inflammation.15 18 Another type increases lean mass53 54 and increases the number of of ectopic adipose tissue, intramuscular fat (IMF), is proliferating skeletal muscle satellite cells in men.55 increased after SCI and has been correlated with These findings suggest that TRT may provide metabolic reduced insulin sensitivity.19 20 benefits to individuals with SCI. Metabolic changes also accompany SCI, with previous Resistance training (RT) improves insulin sensitivity studies finding that more than 50% of individuals with and increases fatty acid and carbohydrate metabolism, as SCI are glucose intolerant, while one of five is dia- well as attenuates sarcopenia in the elderly and after – – betic.2911 21 Other studies report that 55% of indivi- SCI.56 63 Moreover, RT has been shown to influence duals with SCI are at risk of developing metabolic body composition by increasing lean mass, decreasing – syndrome.21 23 Individuals with complete tetraplegia are FM and reducing VAT, suggesting that the benefits of RT more likely to experience decreased glucose and carbo- could overcome the risk of developing insulin resist- – hydrate tolerance and have a higher prevalence of heart ance.56 59 Functional electrical stimulation (FES) has disease than those with incomplete injuries.24 25 been shown to improve fatty acid kinetics, carbohydrate – Likewise, depressed HDL-C (<35 mg/dL) and a higher metabolism and vascular health after SCI.60 63 total cholesterol/HDL-C ratio, predictors of coronary Electrically evoked RT using neuromuscular electrical heart disease, were noted in those with chronic SCI com- stimulation (NMES-RT) and ankle weights is another pared with able-bodied controls.24 26 These are not uni- form that has been shown to be effective in inducing versal findings, however, as a systematic review of muscle hypertrophy in individuals with chronic SCI.59 64 carbohydrate and lipid disorders in persons with SCI did One study showed a 40% increase in skeletal muscle size not find strong evidence of increased risk beyond that of and improved glucose tolerance after 12 weeks of train- the general population.27 ing.59 Another study showed that following 12 weeks of While previous studies have shown a link between NMES-RT, whole thigh, knee extensor and flexor cross- http://bmjopen.bmj.com/ body composition and metabolic profile after SCI, the sectional areas (CSAs) increased by 28%, 35% and 16%, cellular mechanisms remain unknown. Mitochondria respectively. Moreover, the ratio of leg FFM to whole are the site of oxygen consumption and energy produc- body FFM increased by 20% following intervention. tion from glucose and lipid metabolism. Unfortunately, There was 32% decrease in glucose area under the mitochondrial function is impaired in a number of dis- curve adjusted to muscle CSA following 12 weeks of eases including neurodegenerative disease, atheroscler- NMES-RT. However, there were only modest effects on – osis, hypertension and cancer.28 31 Fewer and smaller whole body composition, as well as a non-significant mitochondria are found in skeletal muscle of insulin decrease in VAT.64 It is possible that the limited effects on October 1, 2021 by guest. Protected copyright. resistant, obese and type II diabetic individuals.32 of NMES-RT on parameters of body composition and Previous studies found decreased muscle oxidative cap- VAT can be possibly explained by depressed T-level in acity and succinate dehydrogenase activity, complex II of persons with SCI. Supplementing exogenous T may opti- – the electron transport chain, after SCI.33 35 mise the outcomes of NMES-RT on parameters of body One hypothesis is that skeletal muscle mitochondrial composition and metabolic profile such as increased function is decreased in metabolic disorders, leading to basal metabolic rate (BMR).
Load more

Recommended publications
  • Mitochondrial Toxicity of Triclosan on Mammalian Cells
    Toxicology Reports 2 (2015) 624–637 Contents lists available at ScienceDirect Toxicology Reports j ournal homepage: www.elsevier.com/locate/toxrep Mitochondrial toxicity of triclosan on mammalian cells a,∗,1 a,1 b,1 c Charmaine Ajao , Maria A. Andersson , Vera V. Teplova , Szabolcs Nagy , d e f g Carl G. Gahmberg , Leif C. Andersson , Maria Hautaniemi , Balazs Kakasi , h a Merja Roivainen , Mirja Salkinoja-Salonen a Department of Food and Environmental Sciences, Haartman Institute, University of Helsinki, POB 56, FI-00014, Finland b Institute of Theoretical and Experimental Biophysics, RAS, Puschino, Moscow Region, Russia c Department of Animal Science and Animal Husbandry, University of Pannonia, Georgikon Faculty, Deak F. u.,16, H8360 Keszthely, Hungary d Dept. of Bio- and Environmental Sciences, Haartman Institute, University of Helsinki, FI-00014, Finland e Dept. of Pathology, Haartman Institute, University of Helsinki, FI-00014, Finland f Finnish Food Safety Authority (EVIRA), Research and Laboratory Department, Veterinary Virology Research Unit, Mustialankatu 3, FI 00790 Helsinki, Finland g Institute of Environmental Sciences, University of Pannonia, Egyetem u. 10, H-8200 Veszprem, Hungary h National Institute for Health and Welfare, Department of Virology, Mannerheimintie 166, 00300 Helsinki, Finland a r t a b i c s t l r e i n f o a c t Article history: Effects of triclosan (5-chloro-2 -(2,4-dichlorophenoxy)phenol) on mammalian cells were Received 28 January 2015 investigated using human peripheral blood mono nuclear cells (PBMC), keratinocytes Received in revised form 29 March 2015 (HaCaT), porcine spermatozoa and kidney tubular epithelial cells (PK-15), murine pan- Accepted 30 March 2015 creatic islets (MIN-6) and neuroblastoma cells (MNA) as targets.
    [Show full text]
  • Evaluation of Biorational and Natural Products for Vegetable Crop Management in Commercial Market Gardens and Home Gardens
    Report to the Ohio IPM Program on a Vegetable Team Project funded by the Ohio IPM Block Grant Program, 2005 Title: Evaluation of biorational and natural products for vegetable crop management in commercial market gardens and home gardens Investigators: Celeste Welty (entomologist), Sally Miller (plant pathologist), Doug Doohan (weed scientist); Mark Bennett, Matt Kleinhenz, Bob Precheur (horticulturists). Background: The insect pests and diseases that affect vegetable crops are the same whether grown on large farms for commercial production or on small diversified farms or home gardens, but the management tactics preferred by growers are often different for the different scale operations. Many market gardeners prefer to avoid using conventional pesticides because of concern about human safety and environmental contamination. During the past few years, many biorational crop protection products have become available. While it is known that biorational products are safer to humans than conventional pesticides, it is not known whether they are effective in controlling the target pests that they claim to control. In addition to products for insect and disease control, there are many products that promote plant growth, such as microbial soil inoculants. There is little to no unbiased data available on efficacy of these products. This deficit is a limiting factor in formulating up-to-date extension recommendations for market gardens and home gardens. This project was an important first step in the development of a set of recommended garden IPM tactics that will include cultural controls to prevent or delay pest problems, along with biological controls and selective chemical controls. Objective: To evaluate efficacy of biorational products that are available for vegetable crop management, in comparison with standard conventional materials.
    [Show full text]
  • Effect of Triclosan on the Functioning of Liver Mitochondria And
    The Journal of Membrane Biology https://doi.org/10.1007/s00232-019-00099-w Efect of Triclosan on the Functioning of Liver Mitochondria and Permeability of Erythrocyte Membranes of Marsh Frog (Pelophylax ridibundus (Pallas, 1771)) Mikhail V. Dubinin1 · Kirill S. Tenkov1 · Anton O. Svinin1 · Victor N. Samartsev1 · Konstantin N. Belosludtsev1,2 Received: 28 June 2019 / Accepted: 24 September 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract The paper examines the efects of the antimicrobial agent triclosan on the functioning of the liver mitochondria of marsh frog (Pelophylax ridibundus (Pallas, 1771)). It was established that triclosan inhibits DNP-stimulated respiration of mito- chondria and decreases respiratory control ratio. In addition, triclosan causes the collapse of the mitochondrial membrane potential on both types of substrates. Such an action of triclosan can be mediated by both a protonophore efect and suppres- sion of the activity of complex II and combined activity of complexes II + III (and, to a lesser degree, the combined activity of complexes I + III) of the mitochondrial respiratory chain. It is shown that high concentrations of triclosan enhance the production of hydrogen peroxide during the oxidation of substrates of the complex I by mitochondria, and decrease it in the case of succinate oxidation. It is found that triclosan is able to induce nonspecifc permeability of the liver mitochondria of these amphibians, as well as the plasma membrane of erythrocytes. The possible mechanisms of triclosan efect on marsh frog liver mitochondria and red blood cells are discussed. Graphic Abstract Keywords Triclosan · Toxicology · Mitochondria · Pelophylax ridibundus · Erythrocytes · Membrane permeability Abbreviations TCS Triclosan CsA Cyclosporine * Mikhail V.
    [Show full text]
  • Gas-Phase Chemical Reduction (GPCR)
    Gas-Phase Chemical Reduction (GPCR) Name of Process: Status: Gas-Phase Chemical Reduction (GPCR) A Commercial system operated in Australia for more than 5 years, treating Vendor: more than 2,500 tons of PCB’s, DDT and other POPs. In 1999 a full-scale test ELI Eco Logic International Inc. on HCB was conducted using the commercial plant. Web site: http://www.ecologic.ca Eco Logic’s partners in Japan have recently built a semi-mobile GPCR plant for Applicable Pesticides and related the treatment of PCB wastes, which will be operational in 2003. POPs wastes: Pesticides such as Hexachlorobenzene, In combination with Foster Wheeler and Kvaerner the company is DDT, Aldrin, Dieldrin, HCB’s, DDT, PCB’s, participating at present in the ACWA (Army Chemical Weapons Assessment) dioxins and furans and other POPs. Program for the destruction of chemical warfare agents. Eco Logic has partnered with Torftech Inc. for the treatment of soils and sediments at rates of up to 20 tons per hour. Eco Logic has also been selected by UNIDO for a pilot project for treatment of 1000 tons of PCB wastes in Slovakia. Additional approvals received: -for PCB and dioxin waste in Japan -for PCB’s TSCA permit in USA -for PCB’s and other toxic compounds in the Province of Ontario (Canada) Technology description: Eco Logic’s GPCR technology involves the gas-phase chemical reduction of organic compounds by hydrogen at a temperature of 850°C or higher. Chlorinated hydrocarbons, such as HCB, polychlorinated dibenzo-p-dioxins (dioxins) and other POPs, are chemically reduced to methane and hydrogen chloride (HCl).
    [Show full text]
  • Mitochondrial Complex I Inhibition Depletes Plasma Testosterone in the Rotenone Model of Parkinson’S Disease
    Physiology & Behavior 83 (2004) 395–400 Mitochondrial complex I inhibition depletes plasma testosterone in the rotenone model of Parkinson’s disease M. Alam, W.J Schmidt* Zoological Institute, Department of Neuropharmacology, Morgenstelle 28E, University of Tuebingen, 72076 Tuebingen, Germany Received 5 April 2004; received in revised form 29 July 2004; accepted 11 August 2004 Abstract Age-related depletion of testosterone may increase the brain’s vulnerability to parkinsonian- or Alzheimer’s-like neurodegenerative disorders. In rats, rotenone, a mitochondrial complex I inhibitor, causes specific nigral dopaminergic neurodegeneration producing parkinsonian symptoms. In this study, rotenone was administered on a daily basis (2 mg/kg i.p.) to two groups of rats, over a period of 30 and 60 days, respectively. In order to contribute towards the validation of the rotenone rat model, the changing level of the peripheral sex steroid hormone, testosterone, which would also mimic those found in Parkinson’s disease (PD) patients, was evaluated. Parallel to this, prolactin, luteinizing hormone (LH), the nonsexual steroid thyroid-stimulating hormone, and the corticosterone hormone levels in the peripheral blood plasma were measured to show whether other hormones have also been affected by complex I inhibition. The rotenone treatment caused a decrease of testosterone level in the peripheral blood plasma. There were no differences in the thyroid hormone and prolactin but increases in leutinizing hormone and corticosterone were observed. Data from this study indicate that rotenone depleted the sex steroid hormone which is preferentially produced in the periphery, e.g., adrenal gland and testis. In conclusion, because a decrease in testosterone levels is also one of the comorbidities which are found in male PD patients, our results indicate that the rotenone model mimics PD symptoms not only on a neuronal and behavioral level, but also on the testosterone levels.
    [Show full text]
  • Rotenone—A Review of Its Toxicity and Use for Fisheries Management
    Rotenone—a review of its toxicity and use for fisheries management SCIENCE FOR CONSERVATION 211 Nicholas Ling Published by Department of Conservation P.O. Box 10-420 Wellington, New Zealand While every care has been taken to ensure the accuracy of the information contained in this report, it is not intended as a substitute for specific specialist advice. The University of Waikato accepts no liability for any loss or damage suffered as a result of relying on the information, or applying it either directly or indirectly. Science for Conservation is a scientific monograph series presenting research funded by New Zealand Department of Conservation (DOC). Manuscripts are internally and externally peer-reviewed; resulting publications are considered part of the formal international scientific literature. Titles are listed in the DOC Science Publishing catalogue on the departmental website http:// www.doc.govt.nz and printed copies can be purchased from [email protected] © Copyright January 2003, New Zealand Department of Conservation ISSN 1173–2946 ISBN 0–478–22345–5 In the interest of forest conservation, DOC Science Publishing supports paperless electronic publishing. When printing, recycled paper is used wherever possible. This report (DOC science investigation no. 3414) was prepared for publication by DOC Science Publishing, Science & Research Unit; editing by Ian Mackenzie and layout by Ruth Munro. Publication was approved by the Manager, Science & Research Unit, Science Technology and Information Services, Department of Conservation, Wellington. CONTENTS Abstract 5 PART 1. A REVIEW OF THE USE AND TOXICITY OF ROTENONE FOR FISHERIES MANAGEMENT PURPOSES 1. Introduction 6 2. Use in fisheries management and research 9 3.
    [Show full text]
  • Role of Reactive Oxygen Species in the Neurotoxicity of Environmental Agents Implicated in Parkinson's Disease
    Free Radical Biology & Medicine 44 (2008) 1873–1886 Contents lists available at ScienceDirect Free Radical Biology & Medicine journal homepage: www.elsevier.com/locate/freeradbiomed Review Article Role of reactive oxygen species in the neurotoxicity of environmental agents implicated in Parkinson's disease Derek A. Drechsel, Manisha Patel ⁎ Department of Pharmaceutical Sciences, University of Colorado at Denver and Health Sciences Center, Denver, CO 80262, USA article info abstract Article history: Among age-related neurodegenerative diseases, Parkinson's disease (PD) represents the best example for which Received 11 October 2007 oxidative stress has been strongly implicated. The etiology of PD remains unknown, yet recent epidemiological Revised 19 February 2008 studies have linked exposure to environmental agents, including pesticides, with an increased risk of Accepted 19 February 2008 developing the disease. As a result, the environmental hypothesis of PD has developed, which speculates that Available online 4 March 2008 chemical agents in the environment are capable of producing selective dopaminergic cell death, thus contributing to disease development. The use of environmental agents such as 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine, rotenone, paraquat, dieldrin, and maneb in toxicant-based models of PD has become increasingly popular and provided valuable insight into the neurodegenerative process. Understanding the unique and shared mechanisms by which these environmental agents act as selective dopaminergic toxicants is critical in identifying pathways involved in PD pathogenesis. In this review, we discuss the neurotoxic properties of these compounds with specific focus on the induction of oxidative stress. We highlight landmark studies along with recent advances that support the role of reactive oxygen and reactive nitrogen species from a variety of cellular sources as potent contributors to the neurotoxicity of these environmental agents.
    [Show full text]
  • HHS Public Access Author Manuscript
    HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Toxicol Manuscript Author Sci. Author manuscript; Manuscript Author available in PMC 2020 July 17. Published in final edited form as: Toxicol Sci. 2020 July 01; 176(1): 147–161. doi:10.1093/toxsci/kfaa056. Topical Application of the Antimicrobial Agent Triclosan Induces NLRP3 Inflammasome Activation and Mitochondrial Dysfunction Lisa M. Weatherly*,1, Hillary L. Shane*, Sherri A. Friend†, Ewa Lukomska*, Rachel Baur*, Stacey E. Anderson* * Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505 † Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505 Abstract 5-Chloro-2-(2,4-dichlorophenoxy)phenol (triclosan) is an antimicrobial chemical widely used in consumer household and clinical healthcare products. Human and animal studies have associated triclosan exposure with allergic disease. Mechanistic studies have identified triclosan as a mitochondrial uncoupler; recent studies suggest that mitochondria play an important role in immune cell function and are involved in activation of the NLRP3 inflammasome. In this study, early immunological effects were evaluated via NLRP3 activation following dermal triclosan application in a BALB/c murine model. These investigations revealed rapid caspase-1 activation and mature IL-1β secretion in the skin and draining lymph nodes (dLNs) after 1.5% and 3% triclosan exposure. Correspondingly, pro-Il-1b and S100a8 gene expression increased along with extracellular ATP in the skin. Peak gene expression of chemokines associated with caspase-1 activation occurred after 2 days of exposure in both skin tissue and dLNs.
    [Show full text]
  • Long-Term Exposure to Bisphenol a Or S Promotes Glucose Intolerance and Changes Hepatic Mitochondrial Metabolism in Male Wistar Rats T
    Food and Chemical Toxicology 132 (2019) 110694 Contents lists available at ScienceDirect Food and Chemical Toxicology journal homepage: www.elsevier.com/locate/foodchemtox Long-term exposure to bisphenol A or S promotes glucose intolerance and changes hepatic mitochondrial metabolism in male Wistar rats T Lara Ferreira Azevedoa, Carlos Roberto Porto Dechandtb, Cecília Cristina de Souza Rochaa, Maria Fernanda Hornos Carneiroa, Luciane Carla Albericib,**, Fernando Barbosa Jr.a,* a Department of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo-USP, Ribeirão Preto, Brazil b Department of Physics and Chemistry, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo-USP, Ribeirão Preto, Brazil ARTICLE INFO ABSTRACT Keywords: The present study evaluates the effects of low-level long-term exposure to bisphenol A (BPA) and bisphenol S Mitochondria (BPS) on serum biochemical markers, glucose homeostasis, mitochondrial energy metabolism, biogenesis and Bisphenol A dynamics, and redox status in livers of Wistar rats. While only the exposure to BPS induces a significant body Bisphenol S mass gain after 21 weeks, both compounds alter serum lipid levels and lead to the development of glucose Reactive oxygen species intolerance. Regarding mitochondrial metabolism, both bisphenols augment the electron entry by complex II Mitochondrial dysfunction relative to complex I in the mitochondrial respiratory chain (MRC), and reduce mitochondrial content; BPA Toxicity reduces OXPHOS capacity and uncouples respiration (relative to maximal capacity of MRC) but promotes a significant increase in fatty acid oxidation. Either exposure to BPA or BPS leads to an increase in mitochondrial- derived reactive oxygen species, mainly at complex I.
    [Show full text]
  • Testosterone Protects Mitochondrial Function and Regulates Neuroglobin Expression in Astrocytic Cells Exposed to Glucose Deprivation
    ORIGINAL RESEARCH published: 27 June 2016 doi: 10.3389/fnagi.2016.00152 Testosterone Protects Mitochondrial Function and Regulates Neuroglobin Expression in Astrocytic Cells Exposed to Glucose Deprivation Nicolas Toro-Urrego 1, Luis M. Garcia-Segura 2*, Valentina Echeverria 3 and George E. Barreto 1, 4, 5* 1 Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, Colombia, 2 Instituto Cajal, Spanish National Research Council (CSIC), Madrid, Spain, 3 Facultad Ciencias de la Salud, Universidad San Sebastian, Concepción, Chile, 4 Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago, Chile, 5 Universidad Científica del Sur, Lima, Perú Testosterone is a hormone that has been shown to confer neuroprotection from different insults affecting the central nervous system (CNS). Testosterone induces this protection by different mechanisms that include the activation of anti-apoptotic pathways that are directly implicated in neuronal survival. However, little attention has been devoted to its actions on glial cells. In the present study, we have assessed whether testosterone exerts protection in a human astrocyte cell model, the T98G cells. Our results indicate that testosterone improves cell survival and mitochondrial membrane potential and reduces nuclear fragmentation and reactive oxygen species (ROS) generation. These effects were accompanied by a positive regulation of neuroglobin, an oxygen-binding and sensor Edited by: protein, which may serve as a regulator of ROS and nitrogen reactive species (NOS), Paula I. Moreira, and these protective effects of testosterone may be at least in part mediated by estradiol University of Coimbra, Portugal and DHT. In conclusion, these findings suggest that astroglia may mediate some of the Reviewed by: Anna Maria Colangelo, protective actions of testosterone in the brain upon pathological conditions.
    [Show full text]
  • Eb0825 1981.Pdf (1.214Mb)
    ;.--·- uI PEST CONTROL FOR HOME VEGETABLE GARDENS Common pests, Some registered Vegetable description, damage pesticides* Last use of pesticide before harvest How to apply, other remarks** General Pests Aphids. Small green, black, pink, or diazinon (Spectracide) Depends on vegetable; see product Apply to both tops and undersides of gray plant lice suck plant juices, malathion label. leaves. weaken plants. Sticky secretions lead endosulfan (Thiodan) ~ to sooty mold. j \ rtyl n"'ID Cutworms. Large caterpillars. Feed on carbaryl (Sevin) Depends on vegetable; see product Apply when cutworms are small. all parts of plants. label. Cutworms are nearly impossible to control when larger. Earwigs. Dark brown with pincers at carbaryl (Sevin) Depends on vegetable; see product Apply to soil surface as dust when rear end. Feed on many plant parts. chlordane*** label. earwigs are first seen. Grasshoppers. Large jumping insects. malathion Depends on vegetable; see product Not normally an important pest. Feed on leaves and blossoms. carbaryl (Sevin) label. I Mites. Tiny, spider-like mites on dicofol ( Kelthane) -mites Depends on vegetable; see product Good coverage needed, particularly on undersides of leaves. Suck plant juices, may be resistant to this label. undersides of leaves. cause leaves to yellow and die. Mites pesticide in some parts can seldom be seen with naked eye. of the state Slugs. Small to large, legless metaldehyde Depends on vegetable; see product Apply as bait to soil. Do not apply creatures. Feed on many plant parts, label. directly to plants. Stale beer in cans causing ragged holes. Leave slime trails. sunk to ground level can control slugs. The beer acts as a bait to which slugs are attracted and drown.
    [Show full text]
  • Poisons on Pets: Health Hazards from Flea and Tick Products (Pdf)
    POISONS ON PETS Health Hazards from Flea and Tick Products Authors David Wallinga, M.D., MPA Linda Greer, Ph.D. Natural Resources Defense Council November 2000 Acknowledgments This report was written by Dr. David Wallinga, M.D. and Dr. Linda Greer, Ph.D. Dr. Wallinga is a consultant to the Natural Resources Defense Council (NRDC); Dr. Greer is the Director of NRDC’s Health and Environment Program. The authors acknowledge the important contributions of their colleague Gina Solomon, M.D., M.P.H. The authors also extend their appreciation to Jill Stein, M.D., Greater Boston Physicians for Social Responsibility, for her scientific review. The authors also thank Michael Dryden, D.V.M. of Kansas State University for sharing his expertise about insecticides used to control fleas and ticks on pets, and Dianna Post, D.V.M. of the Rachel Carson Council for her earlier work drawing attention to the risks of pesti- cides in pet products. Finally, NRDC’s work on this report and on this issue more broadly is possible only because of the generous support of The Bauman Foundation, Richard and Rhoda Goldman Fund, W. Alton Jones Foundation, The Joyce Foundation, The McKnight Foundation, The Pew Charitable Trusts, Pond Foundation and The Streisand Foundation. About NRDC The Natural Resources Defense Council is a national nonprofit environmental organization with more than 400,000 contributing members. Since 1970, our scientists and lawyers have been working to protect the world’s natural resources and improve the quality of the human environment. NRDC has offices in New York City, Washington, DC, Los Angeles, and San Francisco.
    [Show full text]