Asunto(s)
Metabolismo de los Lípidos/efectos de los fármacos , Hígado/efectos de los fármacos , Ácidos Ftálicos/toxicidad , Alanina Transaminasa/sangre , Animales , Aspartato Aminotransferasas/sangre , Colesterol/sangre , Cromatografía Liquida , Lipoproteínas HDL/sangre , Hígado/enzimología , Masculino , Espectrometría de Masas , Metabolómica , Distribución Aleatoria , Ratas , Ratas Wistar , Triglicéridos/sangreRESUMEN
OBJECTIVE: Di-(2-ethylhexyl) phthalate (DEHP) is a ubiquitous environmental contaminant. As an endocrine disruptor, it seriously threatens human health and ecological environmental safety. This study examines the impact of intervention with soybean isoflavones (SIF) on DEHP-induced toxicity using a metabonomics approach. METHODS: Rats were randomly divided into control (H), SIF-treated (A, 86 mg/kg body weight), DEHP-treated (B, 68 mg/kg), and SIF plus DEHP-treated (D) groups. Rats were given SIF and DEHP daily through diet and gavage, respectively. After 30 d of treatment, rat urine was tested using UPLC/MS with multivariate analysis. Metabolic changes were also evaluated using biochemical assays. RESULTS: Metabolomics analyses revealed that p-cresol glucuronide, methyl hippuric acid, N1-methyl-2-pyridone-5-carboxamide, lysophosphatidycholine [18:2 (9Z, 12Z)] {lysoPC [18:2 (9Z, 12Z)]}, lysoPC (16:0), xanthosine, undecanedioic acid, and N6-acetyl-l-lysine were present at significantly different levels in control and treatment groups. CONCLUSION: SIF supplementation partially protects rats from DEHP-induced metabolic abnormalities by regulating fatty acid metabolism, antioxidant defense system, amino acid metabolism, and is also involved in the protection of mitochondria.
Asunto(s)
Dietilhexil Ftalato/toxicidad , Disruptores Endocrinos/toxicidad , Contaminantes Ambientales/toxicidad , Glycine max/química , Isoflavonas/orina , Metaboloma , Sustancias Protectoras/metabolismo , Animales , Femenino , Plastificantes/toxicidad , Ratas , Ratas Wistar , UrinálisisRESUMEN
Galectin-3, a unique chimera-type member of the ß-galactoside-binding soluble lectin family, is present in both normal and cancer cells and plays a crucial role in the regulation of cell adhesion. It is involved both in accelerating detachment of cells from primary tumor sites and promoting cancer cell adhesion and survival to anoikis in the blood stream. Cell adhesion molecules (CAMs) are membrane receptors that mediate cell-cell and cell-matrix interactions, and are essential for transducing intracellular signals responsible for adhesion, migration, invasion, angiogenesis, and organ-specific metastasis. This review will discuss the recent advances in our understanding the biological functions, mechanism and therapeutic implication of the interaction between galectin-3 and CAMs in cancer metastasis.
