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dc.contributor.authorFernandes, Glaura S. A. [UNESP]
dc.contributor.authorFernandez, Carla D. B. [UNESP]
dc.contributor.authorCampos, Kleber E. [UNESP]
dc.contributor.authorDamasceno, Débora Cristina [UNESP]
dc.contributor.authorAnselmo-Franci, Janete A.
dc.contributor.authorKempinas, Wilma D. G. [UNESP]
dc.date.accessioned2014-05-20T13:35:36Z
dc.date.available2014-05-20T13:35:36Z
dc.date.issued2011-07-27
dc.identifierhttp://dx.doi.org/10.1186/1477-7827-9-100
dc.identifier.citationReproductive Biology and Endocrinology. London: Biomed Central Ltd., v. 9, p. 9, 2011.
dc.identifier.issn1477-7827
dc.identifier.urihttp://hdl.handle.net/11449/12262
dc.description.abstractBackground: Hyperglycemia can impair the male reproductive system in experimental animals and in men during reproductive age. Studies have shown that vitamin C has some good effects on male reproductive system, and therefore vitamin C treatment could attenuate the dysfunctions in this system caused by hyperglycemia. Thus, the objective of this work was to evaluate whether vitamin C treatment could attenuate reproductive dysfunctions in hyperglycemic male rats.Methods: Adult male rats were divided into 3 groups: a normoglycemic (n = 10) and two hyperglycemic (that received a single dose of streptozotocin -40 mg/kg BW). The two last groups (n = 10 per group) were divided into: hyperglycemic control (Hy) and hyperglycemic + 150 mg of vitamin C (HyC), by gavage during 30 consecutive days. The normoglycemic and hyperglycemic control groups received the vehicle (water). The first day after the treatment, the rats were anesthetized and killed to evaluate oxidative stress biomarkers (TBARS, SOD, GSHt and GSH-Px) in the erythrocytes, body and reproductive organ weights, sperm parameters, plasma hormone levels (FSH, LH and testosterone), testicular and epididymal histo-morphometry and histopathology.Results: Compared with the normoglycemic animals, hyperglycemic control rats showed reduced weight of the body and reproductive organ but testis weight was maintained. It was also observed reduction of testosterone and LH levels, seminiferous tubular diameter, sperm motility and sperm counts in the epididymis. In addition, there was an increase in morphological abnormalities on spermatozoa as well as in oxidative stress level. Vitamin C reduced the oxidative stress level, diminished the number of abnormal sperm, and increased testosterone and LH levels and seminiferous tubular diameter but did not show improvement of sperm motility in relation to the hyperglycemic control group. Hyperglycemia caused a rearrangement in the epididymal tissue components (stroma, ephitelium and lumen) as demonstrated by the stereological analysis results. However, this alteration was partially prevented by vitamin C treatment.Conclusions: We conclude that vitamin C partially attenuated some male reproductive system dysfunctions in hyperglycemic rats.en
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent9
dc.language.isoeng
dc.publisherBiomed Central Ltd.
dc.relation.ispartofReproductive Biology and Endocrinology
dc.sourceWeb of Science
dc.titleVitamin C partially attenuates male reproductive deficits in hyperglycemic ratsen
dc.typeArtigo
dcterms.licensehttp://www.biomedcentral.com/about/license
dcterms.rightsHolderBiomed Central Ltd.
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.description.affiliationUniv Campinas UNICAMP, Inst Biol, Grad Program Cell & Struct Biol, Campinas, SP, Brazil
dc.description.affiliationUNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Gynecol & Obstet, Botucatu, SP, Brazil
dc.description.affiliationUSP, Dent Sch Ribeirao Preto, Dept Morphol Stomatol & Physiol, Ribeirao Preto, SP, Brazil
dc.description.affiliationUNESP Univ Estadual Paulista, Inst Biosci, Dept Morphol, Botucatu, SP, Brazil
dc.description.affiliationUnespUNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Gynecol & Obstet, Botucatu, SP, Brazil
dc.description.affiliationUnespUNESP Univ Estadual Paulista, Inst Biosci, Dept Morphol, Botucatu, SP, Brazil
dc.identifier.doi10.1186/1477-7827-9-100
dc.identifier.wosWOS:000294539000001
dc.rights.accessRightsAcesso aberto
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
dc.identifier.fileWOS000294539000001.pdf
unesp.author.orcid0000-0002-7003-9643[4]
unesp.author.orcid0000-0002-0940-5894[2]
unesp.author.orcid0000-0002-6480-1187[5]
dc.relation.ispartofjcr2.852
dc.relation.ispartofsjr1,203
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