All treatments increased the bioaccessibility of the antioxidant activity (IC(50)), minerals (dialysis and solubility) and starch (resistant and digestible) compared to the untreated sample. Bioaccessibility of calcium, iron and zinc in the treated sample for 500 MPA at 10 min, expressed as percentage solubility, was several-fold higher (three, three and

five times, respectively) than in the untreated sample. Similar effect was observed in IC(50) value, algarrobo seed untreated sample exhibited the lowest antioxidant activity (0.11 +/- 0.005 mg/ml), and followed by all treated samples (500 MPa at 2, 4, Sand 10 min) which showed the strongest activity.

In summary, the antioxidant capacity, mineral and starch content of the seed may be underestimated in the 4EGI-1 ic50 literature because the extraction solvents usually used do not allow a complete release of antioxidant compounds and, additionally, non-extractable polyphenols with a high antioxidant capacity are ignored. This correspondingly applies to the starch and mineral content. On the other hand, the analysis of in vitro digestive enzymatic extracts suggests that the antioxidant activity, minerals and starch of seed in the human gut may be higher than what might be expected from literature data based on measurements of aqueous-organic

extracts. (C) 2011 Elsevier Ltd. All rights reserved.”
“Brassinosteroids (BRs) have been shown to induce hydrogen peroxide (H2O2) accumulation, and BR-induced H2O2 up-regulates antioxidant defence systems in plants. However, the mechanisms find more by which BR-induced H2O2 regulates antioxidant defence systems in plants remain to be determined. In the present study, the role of ZmMPK5, a mitogen-activated

protein kinase, in BR-induced anitioxidant defence and the relationship between the activation of ZmMPK5 and H2O2 production in BR signalling PFTα cost were investigated in leaves of maize (Zea mays) plants. BR treatment activated ZmMPK5, induced apoplastic and chloroplastic H2O2 accumulation, and enhanced the total activities of antioxidant enzymes. Such enhancements were blocked by pre-treatment with mitogen-activated protein kinase kinase (MAPKK) inhibitors and H2O2 inhibitors or scavengers. Pre-treatment with MAPKK inhibitors substantially arrested the BR-induced apoplastic H2O2 production after 6 h of BR treatment, but did not affect the levels of apoplastic H2O2 within 1 h of BR treatment. BR-induced gene expression of NADPH oxidase was also blocked by pre-treatment with MAPKK inhibitors and an apoplastic H2O2 inhibitor or scavenger after 120 min of BR treatment, but was not affected within 30 min of BR treatment. These results suggest that the BR-induced initial apoplastic H2O2 production activates ZmMPK5, which is involved in self-propagation of apoplastic H2O2 via regulation of NADPH oxidase gene expression in BR-induced antioxidant defence systems.