Pretreatment with egg white hydrolysate protects resistance arteries from damage induced after treatment with accidental cadmium exposure values

We investigated whether pretreatment with an egg white hydrolysate (EWH) protects the cardiovascular system, especially the resistance vessels, from damage promoted by Cd exposure at high levels. Male Wistar rats, divided into groups: 1) Control – tap water by gavage + distilled water i.p. (28 days)...

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Detalles Bibliográficos
Autores: Piagette, Janaína Trindade, Gomes Pinheiro Júnior, José Eudes, Kanaan, Samia Hassan Husein, Teixeira Herrera, Camila, Ortiz Bastilhos, Leandro, Peçanha, Franck Maciel, Vassallo, Dalton Valentim, Miguel, Marta, Wiggers, Giulia Alessandra
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2023
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:dnet:digitalcsic_::621effc263d1e61609221c4a7b9bc603
Acceso en línea:http://hdl.handle.net/10261/334109
Access Level:acceso abierto
Palabra clave:Egg white hydrolysate
Cadmium
Vascular dysfunction
Oxidative stress
Inflammation
Apoptosis
Descripción
Sumario:We investigated whether pretreatment with an egg white hydrolysate (EWH) protects the cardiovascular system, especially the resistance vessels, from damage promoted by Cd exposure at high levels. Male Wistar rats, divided into groups: 1) Control – tap water by gavage + distilled water i.p. (28 days); 2) Cd – tap water (28 days) + CdCl2 1 mg/kg i.p. (last 14 days); 3) EWH 1 mg/kg/day by gavage + distilled water i.p. (28 days); 4) EWHCd – EWH (first 14 days) and CdCl2 i.p. + EWH (last 14 days). EWH pretreatment protected against vascular damage occurring in mesenteric resistance arteries (MRA) after exposure to elevated Cd levels by reducing the increased vascular contractile response. Pretreatment with EWH maintained SBP at control levels, protected against increased oxidative stress through NOX1 pathway, prevented triggering of inflammatory cascades (COX-2, TNFα, NF-κB), and protected MRA from Caspase-3 activation induced by Cd, an important apoptotic protease.