Zinc Chelation Mediates the Lysosomal Disruption without Intracellular ROS Generation

Autor(es)

Matias, Andreza Candido ; Manieri, Tania Maria ; Cerchiaro, Giselle

• Tipo de documento: Artigo Científico
• Fonte: OXIDATIVE MEDICINE AND CELLULAR LONGEVITY; v. 2016, p. 13-pg., 2016-01-01.

Resumo

We report the molecular mechanism for zinc depletion caused by TPEN (N,N,N',N'-Tetrakis(2-pyridylmethyl)ethylenediamine) in neuroblastoma cells. The activation of p38 MAP kinase and subsequently caspase 3 is not due to or followed by redox imbalance or ROS generation, though these are commonly observed in literature. We found that TPEN is not responsible for ROS generation and the mechanism involves essentially lysosomal disruption caused by intracellular zinc depletion. We also observed a modest activation of Bax and no changes in the Bcl-2 proteins. As a result, we suggest that TPEN causes intracellular zinc depletion which can influence the breakdown of lysosomes and cell death without ROS generation. (AU)

• Processo FAPESP: 12/01397-9 - Efeitos da expressão da metaloenzima superóxido dismutase na regulação da geração de espécies reativas de oxigênio em células de mamíferos em cultura e em neurônios motores
• Beneficiário: Giselle Cerchiaro
• Modalidade de apoio: Auxílio à Pesquisa - Regular