RESUMO
In this work, we aim to provide evidence for the protective effect of a copper chelator, neocuproine (NeoCu), against the oxidative stress in NSC34 cells, which inhibits biomolecule oxidation and cell death. Results obtained with the comet assay allowed to determine the increase in oxidized purines and pyrimidines by H2O2 exposure, and their changes after the addition of NeoCu. We also observed a higher ATP7b activity in nuclei and a higher Cu concentration inside the cells, proving that the NeoCu acts directly in DNA to promote cell recovery in oxidative stress conditions, also observed in Reactive Oxygen Species (ROS) detection assay by Flow Cytometry. Based on these results, we propose that NeoCu is a promising drug for the protection of motor neuron cells during oxidative stress caused by neurodegenerative diseases in this system.
Assuntos
Quelantes/farmacologia , Dano ao DNA , Peróxido de Hidrogênio/toxicidade , Neuroblastoma/prevenção & controle , Estresse Oxidativo/efeitos dos fármacos , Fenantrolinas/farmacologia , Substâncias Protetoras/farmacologia , Cobre/metabolismo , ATPases Transportadoras de Cobre/metabolismo , Humanos , Neuroblastoma/patologia , Oxidantes/toxicidade , Espécies Reativas de Oxigênio/metabolismo , Células Tumorais CultivadasRESUMO
Methylmercury (MeHg) is an environmental pollutant that is highly toxic to the central nervous system. As its effects on male reproductive system are poorly understood, this study was carried out to analyse the effects of MeHg on the rat prostate. To evaluate the MeHg toxicity on ventral prostate, three groups of adult male Wistar rats received oral doses of 0.5, 1.0 and 3.0 mg/kg MeHg, respectively, on a daily basis for 14 days. A fourth group was used as a control. The prostate weight was decreased in rats treated orally with 0.5 mg/kg MeHg compared to controls. Also, Hg concentration increased significantly in the prostate after treatments. There were reductions in serum testosterone levels and androgen receptor immunoreactivity in animals receiving 3.0 mg MeHg/kg. The stereological data showed changes in the prostatic epithelial, stromal and luminal compartments which varied according to the different doses. Histopathological alterations, such as chronic inflammation, stratified epithelial hyperplasia and epithelial inflammatory reactive atypia, were observed in the 0.5 mg/kg MeHg-treated group. Epithelial atrophy was observed in the 3.0 mg/kg MeHg-treated group. In conclusion, the MeHg affects prostatic homoeostasis resulting in histopathological changes that may be relevant in the pathogenesis of prostatic disease.