The copper content of grape and wine from 16 wine-farms in Italy was studied during the harvest of 2003. The influence of the number of copper applications, the period between the last application and harvest, and the total amount of copper applied was examined. Of the total number of samples analysed, 13% of grape samples and 18% of wine samples exceeded the maximum residue level (MRL). The total amount of copper applied and the number of days between the last application and harvest explained 44% of the concentration of copper in grape. This low correlation may be due to other influencing factors, such as meteorology and the application method. In 2003, conditions were unusually dry and the recommended safety interval for copper application (20 days) was not sufficient to guarantee a residue level in grape below the MRL (20 mg kg(-1)). In order to reduce the probability of copper residues being close to the MRL, a period of 40-50 days between the last application and harvest is suggested. Furthermore, the copper content of grape and wine was not dependent on the pest management strategy of the farm (conventional, integrated or organic). A more important factor influencing copper residue levels may be that copper applications are made in response to the prediction of a disease outbreak rather than being dependent on the pest management strategy in place. No difference in copper content was observed between red and white grape or wine.
Ochratoxin A (OTA) is a mycotoxin produced by different Aspergillus and Penicillium species, and it is considered a common contaminant in food and animal feed worldwide. On the other hand, human embryonic stem cells (hESCs) have been suggested as a valuable model for evaluating drug embryotoxicity. In this study, we have evaluated potentially toxic effects of OTA in hESCs. By using in vitro culture techniques, specific cellular markers, and molecular biology procedures, we found that OTA produces mild cytotoxic effects in hESCs by inhibiting cell attachment, survival, and proliferation in a dose-dependent manner. Thus, we suggest that hESCs provide a valuable human and cellular model for toxicological studies regarding preimplantation stage of human fetal development.
Ochratoxin A (OTA), a mycotoxin that was discovered as a secondary metabolite of the fungal species Aspergillus and Penicillium, is a common contaminant in food and animal feed. This mycotoxin has been described as teratogenic, carcinogenic, genotoxic, immunotoxic and has been proven a potent neurotoxin. Other authors have previously reported the effects of OTA in different structures of the central nervous system as well as in some neurogenic regions. However, the impact of OTA exposure in the subventricular zone (SVZ) has not been assessed yet. To elucidate whether OTA affects neural precursors of the mouse SVZ we investigated, in vitro and in vivo, the effects of OTA exposure on the SVZ and on the neural precursors obtained from this neurogenic niche. In this work, we prove the cumulative effect of OTA exposure on proliferation, differentiation and depletion of neural stem cells cultured from the SVZ. In addition, we corroborated these results in vivo by immunohistochemistry and electron microscopy. As a result, we found a significant alteration in the proliferation process, which was evidenced by a decrease in the number of 5-bromo-2-deoxyuridine-positive cells and glial cells, as well as, a significant decrease in the number of neuroblasts in the SVZ. To summarize, in this study we demonstrate how OTA could be a threat to the developing and the adult SVZ through its impact in cell viability, proliferation and differentiation in a dose-dependent manner.
We have previously observed that in vivo lipoic acid (LA) treatment induced a protective effect onto primary cortical neurons after brain injury. In an effort to better understand LA action mechanism in the brain, in the present study, we stressed brain cells in vitro and ex vivo and then analyzed by inmmunocytochemistry and biochemical assays, the changes induced by LA on cell survival and on the concentration of oxidative stress markers, such as glutathione (GSH), oxidized glutathione (GSSG), and malondialdehyde (MDA). The stressors used were lipopolysaccharide (LPS), dopamine, and l-buthionine-S,R-sulfoximine (BSO). Our results showed that LA decreased cell death and increased GSH/GSSG ratio in cells stressed by LPS + dopamine, suggesting that the mechanism underlying LA action is regeneration of GSSG to GSH. When cells were stressed by BSO, LA diminished cell death and decreased GSH/GSSG ratio. In this case, it could be concluded that, due to the low GSH basal levels, GSSG reduction is not possible and therefore it might be thought that cell death prevention might be mediated through other mechanisms. Finally, we induced chemical oxidative damage in brain homogenate. After LA treatment, GSH and GSH/GSSG ratio increased and MDA concentration decreased, demonstrating again that LA was not able to increase de novo GSH synthesis but is able to increase GSSG conversion to GSH.
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