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ElsevierIgual Ramo, M.; García Martínez, EM.; Martín-Esparza, M.; Martínez Navarrete, N. (2012 Apricots can be considered as a good source of phenolic compounds, which are 9 beneficial for human health. Microwaves may be an alternative to the conventional sun 10 or hot air drying techniques used to obtain dried apricot. Nevertheless, their impact on 11 the functional compounds must be taken into account if they are to be recommended 12 as an attractive drying option. This work compared the drying kinetics and the change 13 in the organic acids, phenolic compounds and antioxidant activity of dried apricot when 14 using hot air drying and microwave energy. Empirical (linear and Page) equations can 15 be used to model the drying kinetics in air, combined air-microwave and microwave 16 processes. From the obtained results, it can be concluded that the industrial processing 17 of dried apricots may be improved by using microwave energy, as the drying time is 18 considerably reduced, and the obtained fruit had a higher phenolic content, particularly 19 of chlorogenic acid, catequin and epicatequin. Nevertheless, as the contribution of 20 these phenols to antioxidant capacity was not significant, microwave dried samples 21 maintained the same antioxidant capacity as the air-dried ones. When sulphite is 22 added previous to the drying processes, care should be taken with the total phenols 23 and the antioxidant capacity quantified as it may interfere with the results depending on 24 the methodology used. 25 26 27

This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Garcia-Martinez EM et al., 2 AbstractMinocycline, an antibiotic of the tetracycline family, has attracted considerable interest for its theoretical therapeutic applications in neurodegenerative diseases. However, the mechanism of action underlying its effect remains elusive. Here we have studied the effect of minocycline under excitotoxic conditions. Fluorescence and bioluminescence imaging studies in rat cerebellar granular neuron cultures using fura-2/AM and mitochondria-targeted aequorin revealed that minocycline, at concentrations higher than those shown to block inflammation and inflammation-induced neuronal death, inhibited NMDA-induced cytosolic and mitochondrial rises in Ca 2+ concentrations in a reversible manner. Moreover, minocycline added in the course of NMDA stimulation decreased Ca 2+ intracellular levels, but not when induced by depolarization with a high K + medium. We also found that minocycline, at the same concentrations, partially depolarized mitochondria by about 5-30 mV, prevented mitochondrial Ca 2+ uptake under conditions of environmental stress, and abrogated NMDAinduced reactive oxygen species (ROS) formation. Consistently, minocycline also abrogates the rise in ROS induced by 75 M Ca 2+ in isolated brain mitochondria. In search for the mechanism of mitochondrial depolarization, we found that minocycline markedly inhibited state 3 respiration of rat brain mitochondria, although distinctly increased oxygen uptake in state 4. Minocycline inhibited NADH-cytochrome c reductase and cytochrome c oxidase activities, whereas the activity of succinate-cytochrome c reductase was not modified, suggesting selective inhibition of complex I and IV. Finally, minocycline affected activity of voltage-dependent anion channel (VDAC) as determined in the reconstituted system. Taken together, our results indicate that mitochondria are a critical factor in minocycline-mediated neuroprotection.

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