Abstract

There are some genes associated to the risk of chronic diseases that present potential nutrigenetic response, such as the human manganese-dependent superoxide dismutase gene (Val16Ala-SOD2, rs4880) for which homozygous genotypes (VV and AA) are associated with higher basal superoxide (S) and hydrogen peroxide (HP) levels, respectively. It is possible that the VV- and AA-imbalance could be attenuated by selenium(Se)-rich foods such as Brazil nut (BN). To test this hypothesis, we conducted an in vitro protocol triggering a chemical S-HP imbalance by exposure of dermal fibroblast cells (HFF-1) to paraquat, which generates high S levels (VV-like treatment) and porphyrin (MnTBAP), which generates high HP levels (AA-like treatment). Modulation of cell growth and pro-oxidative and antioxidant markers were evaluated. BN aqueous extract (BNAE) most effective concentration which increased cell growth and decreased oxidative metabolism indicators of imbalanced cells was 75 ng Se/mL. However, this effect was not directly affected by the S-HP imbalance: in AA-SOD2-like cells, thioredoxin reductase (TrxR-1) gene was upregulated and in VV-SOD2-like cells an upregulation of glutathione peroxidase (GPx-1) gene expression was observed, however, this regulation occured in a homeostatic manner. These results suggest that BNAE was able to minimize negative effects in both directions of the S-HP imbalance, by modulation of different oxidative-metabolic pathways.

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