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Provedor de dados:  BJMBR
País:  Brazil
Título:  Oxidative stress in the latissimus dorsi muscle of diabetic rats
Autores:  De Angelis,K.L.D.
Cestari,I.A.
Barp,J.
Dall'Ago,P.
Fernandes,T.G.
Homem de Bittencourt,P.I.
Belló-Klein,A.
Belló,A.A.
Llesuy,S.
Irigoyen,M.C.
Data:  2000-11-01
Ano:  2000
Palavras-chave:  Streptozotocin-diabetes
Latissimus dorsi muscle
Oxidative stress
Catalase
Glutathione
Resumo:  The purpose of the present study was to investigate the effects of experimental diabetes on the oxidant and antioxidant status of latissimus dorsi (LD) muscles of male Wistar rats (220 ± 5 g, N = 11). Short-term (5 days) diabetes was induced by a single injection of streptozotocin (STZ, 50 mg/kg, iv; glycemia >300 mg/dl). LD muscle of STZ-diabetic rats presented higher levels of thiobarbituric acid reactive substances (TBARS) and chemiluminescence (0.36 ± 0.02 nmol/mg protein and 14706 ± 1581 cps/mg protein) than LD muscle of normal rats (0.23 ± 0.04 nmol/mg protein and 7389 ± 1355 cps/mg protein). Diabetes induced a 92% increase in catalase and a 27% increase in glutathione S-transferase activities in LD muscle. Glutathione peroxidase activity was reduced (58%) in STZ-diabetic rats and superoxide dismutase activity was similar in LD muscle of both groups. A positive correlation was obtained between catalase activity and the oxidative stress of LD, as evaluated in terms of TBARS (r = 0.78) and by chemiluminescence (r = 0.89). Catalase activity also correlated inversely with glutathione peroxidase activity (r = 0.79). These data suggest that an increased oxidative stress in LD muscle of diabetic rats may be related to skeletal muscle myopathy.
Tipo:  Info:eu-repo/semantics/other
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2000001100016
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X2000001100016
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.33 n.11 2000
Direitos:  info:eu-repo/semantics/openAccess
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