Efeito protetor do ácido elágico sobre a reatividade vascular e parâmetros morfofuncionais da aorta de ratos expostos por trinta dias ao cloreto de cádmio

• Ano de defesa: 2025
• Autor(a) principal: Simões, Rakel Passos
• Orientador(a): Padilha, Alessandra Simão
• Banca de defesa: Nunes, Karolini Zuqui , Batista, Priscila Rossi de , Pereira, Camila Almenara Cruz , Abreu, Glaucia Rodrigues de
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal do Espírito Santo; Doutorado em Ciências Fisiológicas
• Programa de Pós-Graduação: Programa de Pós-Graduação em Ciências Fisiológicas
• Departamento: Centro de Ciências da Saúde
• País: BR
• Palavras-chave em Português: Ácido elágico; Cádmio; Reatividade vascular; Disfunção endotelial; Estresse oxidativo; Ellagic acid; Cadmium; Vascular reactivity; Endothelial dysfunction; Oxidative stress
• Área do conhecimento CNPq: Fisiologia
• Link de acesso: http://repositorio.ufes.br/handle/10/20712

Cadmium (Cd) is a toxic heavy metal widely present in the environment, and its chronic exposure is associated with several deleterious effects on the cardiovascular system, including arterial hypertension and endothelial dysfunction. Ellagic acid (EA), a natural polyphenol with antioxidant, anti inflammatory, and chelating properties, has been proposed as a potential vascular protective agent. This study investigated the effects of EA on cardiovascular alterations induced by subchronic exposure to CdCl₂ (100 ppm for 30 days) in Wistar rats. Animals were divided into four experimental groups: Control (Ct), Cd, EA, and Cd+EA. Cd was administered via drinking water, and EA was given by gavage (30 mg/kg/day). Systolic blood pressure (SBP) was monitored weekly using tail-cuff plethysmography. At the end of the protocol, blood Cd concentration was consistent with levels observed in human occupational exposure (31.15 ± 2.8 µg/L). To assess vascular function, thoracic aortic rings were mounted in organ baths and subjected to protocols with phenylephrine, acetylcholine (ACh), and sodium nitroprusside (SNP), with or without endothelium, and in the presence of inhibitors (L-NAME, apocynin, catalase, allopurinol, and SOD). Cd exposure reduced body weight, increased SBP, enhanced vascular reactivity to phenylephrine, and impaired endothelium dependent relaxation, effects associated with reduced nitric oxide (NO) bioavailability and increased reactive oxygen species (ROS) production. Increased collagen deposition and endothelial cell damage were also observed. EA treatment prevented these changes, restoring endothelial function, normalizing vascular tone, and preserving collagen content and endothelial cell integrity. These findings indicate that EA exerts a significant protective effect against Cd-induced vascular toxicity and appears promising as a functional agent for the prevention of cardiovascular diseases