Effets des pesticides sur la microflore fongique du sol (biodégradation des herbicides par les souches isolées)

GRENOBLE1-BU Médecine pharm. (385162101) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF

Les maladies à prions (risque pour la santé publique et mesures de prévention)

Les maladies à prions ou encéphalopathies spongiformes subaiguës transmissibles sont des maladies anciennes qui connaissent un regain de notoriété depuis 1996, avec la crise de la vache folle. Ce sont des maladies qui sont dues à un nouveau type d'agent pathogène, le prion, qui fait partie des Agents Transmissibles Non Conventionnels (ATNC). Le prion présente des propriétés biologiques et physico-chimiques particulières qui font de lui un agent redoutable. Les encéphalopathies spongiformes subaiguës transmissibles touchent aussi bien l'homme que l'animal, avec une issue irrémédiablement fatale. Depuis la crise de la vache folle et l'apparition du nouveau variant de la Maladie de Creutzfeldt-Jakob, on s'est aperçu que les risques auxquels l'homme est soumis sont nombreux et pas toujours évidents, le matériel bovin rentrant dans la composition de très nombreux produits de consommation : alimentation, cosmétique, pharmaceutique, et produits médicaux. Il est donc essentiel de chercher à savoir ce qu'est le prion, comment il agit et quelles sont les mesures que l'on peut prendre pour diminuer au maximum le risque de transmission à l'homme.GRENOBLE1-BU Médecine pharm. (385162101) / SudocSudocFranceF

Characterization of the cell death induced by cadmium in HaCaT and C6 cell lines

International audienceCell death resulting from cadmium (Cd) intoxication has been confirmed to induce both necrosis and apoptosis. The ratio between both types of cell death is dose- and cell-type-dependent. This study used the human keratinocytes HaCaT expressing a mutated p53 and the rat glial cells C6 expressing a wild p53 as models to characterize Cd-induced apoptosis, using sub-lethal and lethal doses. At these concentrations, features of apoptosis were observed 24 h after C6 cell treatment: apoptotic DNA fragmentation and caspase-9 activation, whereas Cd did not induce caspase-3. In HaCaT, Cd did not induce apoptotic DNA fragmentation or caspase-9 and -3 activation. The results also showed that the inhibition of p53 led to a resistance of the C6 cells to 20 µm Cd, decreased the apoptosis and increased the metallothioneins in these cells. p53 restoration increased the sensitivity of HaCaT cells to Cd but did not affect the MT expression. The results suggest that Cd induced apoptosis in C6 cells but a non-apoptotic cellular death in HaCaT cells

Oxidative Stress Induced by Cadmium in the C6 Cell Line: Role of Copper and Zinc

International audienceIn this report, we have investigated the role of copper (Cu) and zinc (Zn) in oxidative stress induced by cadmium (Cd) in C6 cells. Cells were exposed to 20 μM Cd, 500 μM Cu, and 450 μM Zn for 24 h. Then, toxic effects, cellular metals levels, oxidative stress parameters, cell death, as well as DNA damage were evaluated. Cd induced an increase in cellular Cd, Cu, and Zn levels. This results not only in the inhibition of GSH-Px, GRase, CAT, and SOD activities but also in ROS overproduction, oxidative damage, and apoptotic cell death not related to Cu and Zn mechanisms. The thiol groups and GSH levels decreased, whereas the lipid peroxidation and DNA damage increased. The toxicity of Zn results from the imbalance between the inhibition of antioxidant activities and the induction of MT synthesis. The increase in Cu and Zn levels could be explained by the disruption of specific transporter activities, Cd interference with signaling pathways, and metal displacement. Our results suggest that the alteration of Cu and Zn homeostasis is involved in the oxidative stress induced by Cd

Metallothionein expression in HaCaT and C6 cell lines exposed to cadmium

International audienceMetallothioneins (MT) are low-molecular weight, cysteine-rich metal-binding proteins. MT play a role in the homeostasis of essential metals such as zinc (Zn) and copper (Cu), detoxification of toxic metals such as cadmium (Cd) and protection against oxidative stress. In this study, we examined the expression of MT in HaCaT and C6 cells as a strategy to enhance protection against Cd-mediated toxicity. At basal level, HaCaT cells showed higher MT level than C6 cells which could explain the resistance of HaCaT cells. Western blot showed that C6 cells treated with 20 μmol/L Cd for 24 h did not express any MT. MT were initially expressed in the cytoplasmic or periplasmic compartment and were then translocated in the nucleus after 24 h treatment by Cd both in HaCaT and C6 cells. In addition, the cell treatment with Cd was followed by an increase in the cellular zinc level but the electrophoretic mobility shift assay (EMSA) experiment did not show any translocation of metal-responsive transcription factor-1 (MTF-1) to the nucleus of HaCaT cells. These absence of translocation could be due to the presence of MT in these cells at the basal state. The translocation study in HaCaT cells suggested that the MT translocation in the nucleus was greater than observed in C6 cells. The latter observation could explain HaCaT cells resistance to Cd concentrations up to 50 μmol/L. Our results suggested that the C6 cell sensitivity was correlated with the decrease in MT level at 20 μmol/L Cd occurring after the transcription of MT gene