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Due to a lack of information on the assessment of uranium's (U) toxicity, our work aimed to compare the effects of U on the crayfish Procambarus clarkii with those of the well documented metal: cadmium (Cd). Accumulation and impacts at different levels of biological organization were assessed after acute (40 µM Cd or U; 4-10 days) and chronic (0.1 µM Cd or U; 30-60 days) exposures. The survival rates demonstrated the high tolerance of this species toward both metals and showed that Cd had a greater effect on the sustainability of crayfish. The concentration levels of Cd and U accumulated in gills and hepatopancreas were compared between both conditions. Distinctions in the adsorption capacities and the mobility of the contaminants were suspected. Differences in the detoxification mechanisms of both metals using transmission electron microscopy equiped with an energy dispersive X-ray were also pointed out. In contrast, comparison between the histological structures of contaminated hepatopancreas showed similar symptoms. Principal component analyses revealed different impacts of each metal on the oxidative balance and mitochondria using enzymatic activities and gene expression levels as endpoints. The observation that U seemed to generate more oxidative stress than Cd in our conditions of exposure is discussed., (© 2014 Wiley Periodicals, Inc.)

The main objectives of this study were to evaluate uranium (U) toxicity in the crayfish Procambarus clarkii at a low dose of exposure and to discriminate between the chemotoxicity and radiotoxicity of U. We conducted two sets of experiments using either 30 μg L(-1) of depleted uranium (DU) or (233)U, which differ from each other only in their specific activity (DU=1.7×10(4)Bqg(-1), (233)U=3.57×10(8)Bqg(-1)). The endpoints were oxidative stress responses and mitochondrial functioning in the gills and hepatopancreas, which were measured in terms of enzyme activities and gene expression levels. U accumulation levels were measured in different organs (gills, hepatopancreas, stomach, intestine, green gland, muscles, and carapace), and internal dose rates in the hepatopancreas were compared after DU and (233)U exposures. Significant U accumulation occurred in the organs of P. clarkii, and mitochondrial damage and antioxidant responses were detected. Despite the huge difference (21,000×) in the specific activities of DU and (233)U, few significant differences in biological responses were detected in P. clarkii exposed to these two pollutants. This finding indicates that the radiotoxicity was low compared to the chemotoxicity under our exposure conditions. Finally, genes expression levels were more sensitive markers of U toxicity than enzyme activities., (Copyright © 2012 Elsevier Inc. All rights reserved.)

We examined the impacts of Uranium (U) on mitochondria and on the response of antioxidants in the gills and the hepatopancreas of crayfish Procambarus clarkii after long-term exposure (30 and 60 days) to an environmentally relevant concentration (30 μg U/L). The expression of mitochondrial genes (12s, atp6, and cox1), as well as the genes involved in oxidative stress responses (sod(Mn) and mt) were evaluated. The activities of antioxidant enzymes (SOD, CAT, GPX and GST) were also studied. U accumulation in organs induced changes in genes' expression. The evolution of these transcriptional responses and differences between gene expression levels at high and low doses of exposure were also discussed. This study demonstrated that, after long-term exposure, U caused a decrease in antioxidant activities and induced oxidative stress. A possible ROS-mediated U cytotoxic mechanism is proposed. Expression levels of the investigated genes can possibly be used as a tool to evaluate U toxicity and seem to be more sensitive than the enzymatic activities. However a multiple biomarker approach is recommended as the perturbed pathways and the mode of action of this pollutant are not completely understood., (Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.)

This work aims to investigate the accumulation levels and effects (transcriptional responses, histopathology and survival rate) associated with a wide range of dissolved uranium (U) concentrations (0, 0.03, 0.6, 4 and 8 mg/L of U) on adult male crayfish Procambarus clarkii during 4 (T4) and 10 (T10) days of exposure. The follow-up of the crayfish mortality showed that P. clarkii was highly resistant to U. Increasing waterborne U concentrations led to increasing bioaccumulation in key crayfish organs and increasing histological damages. U distribution in tissues was also evaluated using transmission electron microscopy and showed the presence of a detoxified form of U in the gill's epithelium in the shape of flakes. Expression levels of mitochondrial genes (cox1, atp6 and 12S gene) and genes involved in oxidative stress (sod(Mn) and mt) were examined together with the housekeeping gene 18S. atp6 and mt genes of P. clarkii were cloned and sequenced before analysis. Significant correlations were observed between U bioaccumulation and the down-regulation of both cox1 and sod(Mn) genes. This work provides a first U toxicogenomic and histopathological pattern of P. clarkii, identify U biomarkers and associate gene expression endpoints to accumulation levels. It also provides new insights into the mechanisms involved in U stress., (Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.)

ABSTRACT Due to a lack of information on the assessment of uranium's (U) toxicity, our work aimed to compare the effects of U on the crayfish Procambarus clarkii with those of the well documented metal: cadmium (Cd). Accumulation and impacts at different levels of biological organization were assessed after acute (40 µM Cd or U; 4-10 days) and chronic (0.1 µM Cd or U; 30-60 days) exposures. The survival rates demonstrated the high tolerance of this species toward both metals and showed that Cd had a greater effect on the sustainability of crayfish. The concentration levels of Cd and U accumulated in gills and hepatopancreas were compared between both conditions. Distinctions in the adsorption capacities and the mobility of the contaminants were suspected. Differences in the detoxification mechanisms of both metals using transmission electron microscopy equiped with an energy dispersive X-ray were also pointed out. In contrast, comparison between the histological structures of contaminated hepatopancreas showed similar symptoms. Principal component analyses revealed different impacts of each metal on the oxidative balance and mitochondria using enzymatic activities and gene expression levels as endpoints. The observation that U seemed to generate more oxidative stress than Cd in our conditions of exposure is discussed. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 211-223, 2016. [ABSTRACT FROM AUTHOR]