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The oxidative stress generation in bacteria by the presence of antibiotics (in this case silver nanoparticles (AgNPs)) is already widely known. Previously, we demonstrated that AgNPs generate oxidative stress in Staphylococcus aureus and Escherichia coli mediated by the increase of reactive oxygen species (ROS). In this work we are demonstrating the consequences of the oxidative stress by the presence of AgNPs; these bacterial strains increased the levels of oxidized proteins and lipids. In addition, it was possible to determine which reactive oxygen species are mainly responsible for the oxidative damage to macromolecules. Also, we found that the bacterial DNA was fragmented and the membrane potential was modified. This increase in the levels of ROS found in both, S. aureus and E. coli, was associated with the oxidation of different types of important macromolecules for the normal functioning of cell, so the oxidative stress would be one of the mechanisms by which the AgNPs would exert their toxicity in both strains, one Gram positive and the other Gram negative of great clinical relevance., (Published by Elsevier Ltd.)

Fusarium verticillioides is a major maize pathogen and there are susceptible and resistant cultivars to this fungal infection. Recent studies suggest that its main mycotoxin fumonisin B1 (FB1) may be involved in phytopathogenicity, but the underlying mechanisms are mostly still unknown. This work was aimed at assessing whether FB1 disseminates inside the plants, as well as identifying possible correlations between the maize resistant/susceptible phenotype and the unbalances of the FB1-structurally-related sphingoid base sphinganine (Sa) and phytosphingosine (Pso) due to toxin accumulation. Resistant (RH) and susceptible hybrid (SH) maize seedlings grown from seeds inoculated with a FB1-producer F. verticillioides and from uninoculated ones irrigated with FB1 (20 ppm), were harvested at 7, 14 and 21 days after planting (dap), and the FB1, Sa and Pso levels were quantified in roots and aerial parts. The toxin was detected in roots and aerial parts for inoculated and FB1-irrigated plants of both hybrids. However, FB1 levels were overall higher in SH seedlings regardless of the treatment (infection or watering). Sa levels increased substantially in RH lines, peaking at 54-fold in infected roots at 14 dap. In contrast, the main change observed in SH seedlings was an increase of Pso in infected roots at 7 dap. Here, it was found that FB1 disseminates inside seedlings in the absence of FB1-producer fungal infections, perhaps indicating this might condition the fungus-plant interaction before the first contact. Furthermore, the results strongly suggest the existence of at least two ceramide synthase isoforms in maize with different substrate specificities, whose differential expression after FB1 exposure could be closely related to the susceptibility/resistance to F. verticillioides., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Aflatoxin B1 (AFB(1)) and fumonisin B1 (FB(1)) are mycotoxins widely found as cereal contaminants. Their immunotoxicities predispose to infectious diseases and may alter the tumor immunosurveillance of human and animals, but the mechanisms underlying have not been fully elucidated, and the induction of oxidative stress has been proposed as a probable mechanism. This work was aimed at evaluating in spleen mononuclear cells (SMC) from Wistar rats the effects of the exposure, in vitro for up to 48 h, to 20 μM AFB(1), 10 μM FB(1) and AFB(1)-FB(1) mixture (MIX), over cellular oxidative status, as well as at elucidating the contribution of different reactive oxygen species (ROS) to biomolecular oxidative damage, the biochemical pathways involved, and the probable interaction of both toxins to induce oxidative stress. All the treatments increased total ROS and oxidation of biomolecules, with MIX having the greatest effects. However, only MIX increased superoxide anion radical. The main ROS involved in oxidation of proteins, lipids and DNA appear to be hydrogen peroxide and hydroxyl radical. The mitochondrial complex I and CYP450 were involved in the ROS generation induced by all treatments. The NADPH oxidase system was induced by FB1 and MIX. The arachidonic acid metabolism contributed to the ROS formation induced by AFB(1) and MIX. These results demonstrate that an interaction between AFB(1) and FB(1) occur in the oxidative stress induction, and show the biochemical pathways involved in ROS generation in SMC. The oxidative stress could mediate the AFB(1) and FB(1) individual and combined immunotoxicities., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

The disruption of lipidic metabolism was considered a good candidate to explain FB1 toxicity mechanism. In the present work we investigated molecular organizational changes induced by FB1-biomembrane interaction possibly involved in mycotoxic effects. FB1 was self-aggregated with a critical micellar concentration of 1.97 mM. FB1 (0-81.4 microM), decreased in a dose-dependent manner, the fluorescence anisotropy of TMA-DPH (from 0.349+/-0.003 to 0.1720+/-0.0035) in dpPC bilayers, whilst no differences were registered with DPH. At 5.6 microM in the subphase, FB1 increased the lateral surface pressure (pi) of a Langmuir film to an extent that depended on the monolayer composition (Deltapi dpPC:DOTAP 3:1>Deltapi dpPC:dpPA3:1>Deltapi dpPC), the molecular packing (Deltapi decreased linearly as a function of the initial pi) and the subphase pH (Deltapi pH 2.6>Deltapi pH 7.4 and maximal pi allowing the drug penetration pi cut-off was 34.3 and 27.7 mN/m at pH 2.63 and 7.4, respectively). FB1 increased the surface potential of dpPC and dpPC:DOTAP monolayers and decreased that of dpPC:dpPA. This suggested that FB1 acquired different orientations and/or foldings depending on the surface electrostatics and the toxin charge state. Moreover, FB1-lipid interactions were transduced into long-range effects at the mesoscopic level affecting the lipidic self-separated lateral domains shape and density.