About: Protective effect of sildenafil on the genotoxicity and cytotoxicity in apolipoprotein E-deficient mice bone marrow cells

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About: Protective effect of sildenafil on the genotoxicity and cytotoxicity in apolipoprotein E-deficient mice bone marrow cells Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Protective effect of sildenafil on the genotoxicity and cytotoxicity in apolipoprotein E-deficient mice bone marrow cells
Creator	Batista, Alan Bernardes, Franciane Campagnaro, Bianca Meyrelles, Silvana Porto, Marcella Vasquez, Elisardo
topic	covid:3f8d3e900290496401f7a6557a64255fdb3ebf0e#this
source	Medline; PMC
abstract	BACKGROUND: The pharmacological inhibitor of phosphodiesterase 5 (PDE5), sildenafil, is a promising candidate for antioxidant therapy that can result in cardiovascular protection. In addition to its known effects on the cardiovascular system, hypercholesterolemia leads to increased oxidative stress and DNA damage in the bone marrow, which is a non-classical target organ of atherosclerosis. In the present study, we evaluate oxidative stress and assess the effect of genomic instability on cell cycle kinetics in atherosclerotic animals and determine if sildenafil reverses these detrimental effects in bone marrow cells. METHODS: Experiments were performed in male wild-type (WT) and apolipoprotein E knockout mice (apoE(−/−)) (9 weeks of age). apoE(−/−) mice were randomly distributed into the following 2 groups: sildenafil-treated (40 mg/kg/day for 3 weeks, n = 8) and vehicle-treated (n = 8), by oral gavage. After treatment, bone marrow cells were isolated to assess the production of superoxide anions and hydrogen peroxide, determine cell cycle kinetics and evaluate the presence of micronucleated cells. RESULTS: Sildenafil treatment reduced the cytoplasmic levels of superoxide anion (~95 % decrease, p < 0.05) and decreased hydrogen peroxide (~30 % decrease, p < 0.05). Moreover, we observed protective effects on the DNA of bone marrow cells, including normal cell cycling, decreased DNA fragmentation and a diminished frequency of micronucleated cells. CONCLUSION: Our data reveal that the excessive production of ROS in atherosclerotic mice overcome the DNA repair pathways in bone marrow cells. The novelty of the present study is that the administration of sildenafil reduced ROS to baseline levels and, consequently, reverted the DNA damage and its outcomes in bone marrow cells.
has issue date	2016-05-27(xsd:dateTime)
bibo:doi	10.1186/s12944-016-0268-6
bibo:pmid	27229150
has license	cc-by
sha1sum (hex)	3f8d3e900290496401f7a6557a64255fdb3ebf0e
schema:url	https://doi.org/10.1186/s12944-016-0268-6
resource representing a document's title	Protective effect of sildenafil on the genotoxicity and cytotoxicity in apolipoprotein E-deficient mice bone marrow cells
has PubMed Central identifier	PMC4882816
has PubMed identifier	27229150
schema:publication	Lipids Health Dis
resource representing a document's body	covid:3f8d3e900290496401f7a6557a64255fdb3ebf0e#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/3f8d3e900290496401f7a6557a64255fdb3ebf0e
is schema:about of	named entity 'levels' named entity 'oxidative stress' named entity 'Experiments' named entity 'apolipoprotein' named entity 'atherosclerotic' named entity 'addition' named entity 'administration' named entity 'wild-type' named entity 'isolated' named entity 'bone marrow' named entity 'genotoxicity' named entity 'apolipoprotein' named entity 'EFFECT' named entity 'DNA DAMAGE' named entity '0.05' named entity 'RESULT' named entity 'SILDENAFIL' named entity 'MICRONUCLEATED CELLS' named entity 'BASELINE' named entity 'DISTRIBUTED' named entity 'GROUPS' named entity 'EFFECTS' named entity 'PRODUCTION' named entity 'MICE' named entity 'HYDROGEN PEROXIDE' named entity 'SUPEROXIDE' named entity 'APOE' named entity 'EXCESSIVE' named entity 'ITS' named entity 'PRESENT' named entity 'LEVELS' named entity 'DIMINISHED' named entity 'METHODS' named entity 'RESULTS' named entity 'MALE' named entity 'TREATED' named entity 'REDUCED' named entity 'TREATMENT' named entity 'ATHEROSCLEROTIC' named entity 'DNA REPAIR' named entity 'WEEKS' named entity 'ANIONS' named entity 'ANTIOXIDANT THERAPY' named entity 'OVERCOME' named entity 'MG%' named entity 'OXIDATIVE STRESS' named entity 'PHARMACOLOGICAL' named entity 'REVEAL' named entity 'THESE' named entity 'EXPERIMENTS' named entity 'KNOCKOUT MICE' named entity 'DETERMINE' named entity 'REVERSES' named entity 'CARDIOVASCULAR PROTECTION' named entity 'DNA' named entity 'CELL CYCLING' named entity 'DNA FRAGMENTATION' named entity 'AGE' named entity 'IS A' named entity 'AFTER TREATMENT' named entity 'CONCLUSION' named entity 'OUTCOMES' named entity 'ON CELL' named entity 'GENOMIC INSTABILITY' named entity 'NORMAL CELL' named entity 'ROS' named entity 'CARDIOVASCULAR SYSTEM' named entity 'INHIBITOR' named entity 'HYPERCHOLESTEROLEMIA' named entity 'DEFICIENT' named entity 'MICE' named entity 'PROTECTIVE EFFECT' named entity 'ATHEROSCLEROSIS' named entity 'CANDIDATE'

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