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[P1.10]: A new evolutionary explanation for the huge human brain
Author(s) -
Diaconeasa A.G.,
Spiru L.,
Turcu I.
Publication year - 2010
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2010.07.051
Subject(s) - library science , citation , political science , computer science
the redox status and the expression of Mrp1 in proliferating and differentiating NPC. NPC were obtained from E15 mouse brains, growing as neurospheres in the presence of EGF and bFGF. Differentiation was firstly induced by plating NPC onto poly-d-lysine-coated plates in the presence of low concentrations of bFGF. Cells were cultured in the absence of bFGF for 4, 8 and 18 DIV. Cell viability was determined by trypan blue, total glutathione (GSt) by an enzymatic assay, protein oxidation and lipid peroxidation by slot-blot analysis and Mrp1 by western blot, in NPC and differentiating cells. NPC differentiated in astrocytes and neurons, with the first representing 55% at 4 DIV and 64% at 18 DIV. Loss of cell viability increased ∼6-fold (p < 0.01) from proliferating NPC to 4, 8 and 18 DIV differentiating cells. Curiously, NPC showed a high level of intracellular GSt (∼3-fold, p < 0.05), as well as protein oxidation (∼1.6-fold, p < 0.01) and lipid peroxidation (∼2.5-fold, p < 0.01), as compared to the lower level obtained in differentiating cells. Moreover, our data evidenced that Mrp1 is highly expressed in NPC. Immature cells (4 DIV) presented the lowest levels of Mrp1 and during nerve cell maturation this protein slightly increased, although never reaching the expression levels of NPC (∼0.7-fold for 4 and 8 DIV, p < 0,05; 0.9-fold for 18 DIV; versus NPC). In conclusion, NPC proliferation is associated with increased levels of protein and lipid oxidation. Therefore, the higher concentrations of GSt and Mrp1 expression observed in NPC seem to constitute self-defense mechanisms against oxidative injury. Funded by FCT-PTDC/SAU-NEU/64385/2006 to D.B.