Effects of D-Aspartate Treatment on D-Aspartate Oxidase, Superoxide Dismutase, and Caspase 3 Activities in Frog (Rana esculenta) Tissues

Autor: Lavinia Burrone, Gabriella Chieffi Baccari, Maria Maddalena Di Fiore, Alessandra Santillo, Marcello Di Giovanni
Přispěvatelé: H. Bruckner, N. Fujii, Burrone, L, DI GIOVANNI, M, DI FIORE, Maria Maddalena, Chieffi, Gabriella, Santillo, Alessandra
Rok vydání: 2010
Předmět:
Zdroj: Chemistry & Biodiversity. 7:1459-1466
ISSN: 1612-1880
1612-1872
Popis: Although D-aspartate (D-Asp) has been recognized to have a physiological role within different organs, high concentrations could elicit detrimental effects on those same organs. In this study, we examined the D-aspartate oxidase (D-AspO) activity and the expression of superoxide dismutase 1 (SOD1) and caspase 3 in different tissues of the frog Rana esculenta after chronic D-Asp treatment. Our in vivo experiments, consisting of intraperitoneal (ip) injections of D-Asp (2.0 μmol/g b.w.) in frogs for ten consecutive days, revealed that all examined tissues can take up and accumulate D-Asp. Further, in D-Asp treated frogs, i) the D-AspO activity significantly increased in all tissues (kidney, heart, testis, liver, and brain), ii) the SOD1 expression (antioxidant enzyme) significantly increased in the kidney, and iii) the caspase 3 level (indicative of apoptosis) increased in both brain and heart. Particularly, after the D-Asp treatment we found in both brain and heart (which showed the lowest SOD1 levels) a significant increase of the caspase 3 expression and, vice versa, in the kidney (which showed the highest SOD1 expression) a significant decrease of the caspase 3 expression. Therefore, we speculate that, in frog tissue, D-AspO plays an essential role in modulating the D-Asp concentration. In addition, exaggerated D-Asp concentrations activated SOD1 as cytoprotective mechanism in the kidney, whereas, in the brain and in the heart, where the antioxidant action of SOD1 is limited, caspase 3 was activated. © 2010 Verlag Helvetica Chimica Acta AG.
Databáze: OpenAIRE