Cargando…

pCramoll and rCramoll as New Preventive Agents against the Oxidative Dysfunction Induced by Hydrogen Peroxide

Oxidative stress plays an important role in the induction of cell death and is associated with various pathologic disorders; therefore, the search for natural products that attenuate the effects produced by oxidant agents is greatly increased. Here, the protective effects of native lectin from Craty...

Descripción completa

Detalles Bibliográficos
Autores principales: Nascimento da Silva, Luís Cláudio, Alves, Neyla Maria Pereira, de Castro, Maria Carolina Accioly Brelaz, Higino, Taciana Mirely Maciel, da Cunha, Cássia Regina Albuquerque, Pereira, Valéria Rêgo Alves, da Paz, Nathalia Varejão Nogueira, Coelho, Luana Cassandra Breitenbach Barroso, Correia, Maria Tereza dos Santos, de Figueiredo, Regina Celia Bressan Queiroz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632182/
https://www.ncbi.nlm.nih.gov/pubmed/26576224
http://dx.doi.org/10.1155/2015/520872
Descripción
Sumario:Oxidative stress plays an important role in the induction of cell death and is associated with various pathologic disorders; therefore, the search for natural products that attenuate the effects produced by oxidant agents is greatly increased. Here, the protective effects of native lectin from Cratylia mollis seeds (pCramoll) and recombinant Cramoll 1 (rCramoll) against H(2)O(2)-induced oxidative stress in Vero cells were evaluated. Both lectins significantly attenuated the H(2)O(2)-induced cytotoxicity in a concentration-dependent way. The maximum protective effects were 96.85 ± 15.59% (rCramoll) and 59.48 ± 23.44% (pCramoll). The Live/Dead analysis showed a reduction in the percentage of dead cells from 65.04 ± 3.29% (H(2)O(2)) to 39.77 ± 2.93% (pCramoll) and 13.90 ± 9.01% (rCramoll). The deleterious effects of H(2)O(2) on cell proliferation were reduced to 10.83% (pCramoll) and 24.17% (rCramoll). Lectins treatment attenuated the excessive superoxide production, the collapse of the mitochondrial membrane potential, and the lysosomal and DNA damage in H(2)O(2)-treated cells. In conclusion, our results suggest that pCramoll and rCramoll blocked H(2)O(2)-induced cytotoxicity through decreasing reactive oxygen species, restoring the mitochondrial potential, preventing the lysosomal damage and DNA fragmentation, and thus promoting cell survival and proliferation.