344 research outputs found
Joint toxicity of cadmium and ionizing radiation on zooplankton carbon incorporation, growth and mobility
The risk of exposure to radioactive elements is seldom assessed considering mixture toxicity, potentially over- or underestimating biological and ecological effects on ecosystems. This study investigated how three end points, carbon transfer between phytoplankton and Daphnia magna, D. magna mobility and growth, responded to exposure to γ-radiation in combination with the heavy metal cadmium (Cd), using the MIXTOX approach. Observed effects were compared with mixture effects predicted by concentration addition (CA) and independent action (IA) models and with deviations for synergistic/antagonistic (S/A), dose-level (DL), and dose-ratio (DR) dependency interactions. Several patterns of response were observed depending on the end point tested. DL-dependent deviation from the IA model was observed for carbon incorporation with antagonism switching to synergism at higher doses, while the CA model indicated synergism, mainly driven by effects at high doses of γ-radiation. CA detected antagonism regarding acute immobilization, while IA predicted DR-dependency. Both CA and IA also identified antagonism for daphnid growth. In general, effects of combinations of γ-radiation and Cd seem to be antagonistic at lower doses, but synergistic at the higher range of the doses tested. Our results highlight the importance of investigating the effects of exposure to γ-radiation in a multistressor context
Including albedo in time-dependent LCA of bioenergy
Albedo change during feedstock production can substantially alter the life cycle climate impact of bioenergy. Life cycle assessment (LCA) studies have compared the effects of albedo and greenhouse gases (GHGs) based on global warming potential (GWP). However, using GWP leads to unequal weighting of climate forcers that act on different timescales. In this study, albedo was included in the time-dependent LCA, which accounts for the timing of emissions and their impacts. We employed field-measured albedo and life cycle emissions data along with time-dependent models of radiative transfer, biogenic carbon fluxes and nitrous oxide emissions from soil. Climate impacts were expressed as global mean surface temperature change over time ( increment T) and as GWP. The bioenergy system analysed was heat and power production from short-rotation willow grown on former fallow land in Sweden. We found a net cooling effect in terms of increment T per hectare (-3.8 x 10(-11) K in year 100) and GWP(100) per MJ fuel (-12.2 g CO(2)e), as a result of soil carbon sequestration via high inputs of carbon from willow roots and litter. Albedo was higher under willow than fallow, contributing to the cooling effect and accounting for 34% of GWP(100), 36% of increment T in year 50 and 6% of increment T in year 100. Albedo dominated the short-term temperature response (10-20 years) but became, in relative terms, less important over time, owing to accumulation of soil carbon under sustained production and the longer perturbation lifetime of GHGs. The timing of impacts was explicit with increment T, which improves the relevance of LCA results to climate targets. Our method can be used to quantify the first-order radiative effect of albedo change on the global climate and relate it to the climate impact of GHG emissions in LCA of bioenergy, alternative energy sources or land uses
Oxaliplatin neurotoxicity – no general ion channel surface-charge effect
<p>Abstract</p> <p>Background</p> <p>Oxaliplatin is a platinum-based chemotherapeutic drug. Neurotoxicity is the dose-limiting side effect. Previous investigations have reported that acute neurotoxicity could be mediated via voltage-gated ion channels. A possible mechanism for some of the effects is a modification of surface charges around the ion channel, either because of chelation of extracellular Ca<sup>2+</sup>, or because of binding of a charged biotransformation product of oxaliplatin to the channel. To elucidate the molecular mechanism, we investigated the effects of oxaliplatin and its chloride complex [Pt(dach)oxCl]<sup>- </sup>on the voltage-gated Shaker K channel expressed in <it>Xenopus </it>oocytes. The recordings were made with the two-electrode and the cut-open oocyte voltage clamp techniques.</p> <p>Conclusion</p> <p>To our surprise, we did not see any effects on the current amplitudes, on the current time courses, or on the voltage dependence of the Shaker wild-type channel. Oxaliplatin is expected to bind to cysteines. Therefore, we explored if there could be a specific effect on single (E418C) and double-cysteine (R362C/F416C) mutated Shaker channels previously shown to be sensitive to cysteine-specific reagents. Neither of these channels were affected by oxaliplatin. The clear lack of effect on the Shaker K channel suggests that oxaliplatin or its monochloro complex has no general surface-charge effect on the channels, as has been suggested before, but rather a specific effect to the channels previously shown to be affected.</p
Renal Morphology, Clinical Findings, and Progression Rate in Mesoamerican Nephropathy
BackgroundMesoamerican nephropathy (MeN) is a chronic kidney disease affecting rural inhabitants in Central America. We have previously described the renal morphology in 8 patients from El Salvador. To confirm the renal pathology, we have studied kidney biopsies from patients with MeN in Nicaragua. Follow-up urine and blood samples from both biopsy studies were collected to investigate the natural history
Cadmium-induced oxidative cellular damage in human fetal lung fibroblasts (MRC-5 cells).
Epidemiological evidence suggests that cadmium (Cd) exposure causes pulmonary damage such as emphysema and lung cancer. However, relatively little is known about the mechanisms involved in Cd pulmonary toxicity. In the present study, the effects of Cd exposure on human fetal lung fibroblasts (MRC-5 cells) were evaluated by determination of lipid peroxidation, intra-cellular production of reactive oxygen species (ROS), and changes of mitochondrial membrane potential. A time- and dose-dependent increase of both lactate dehydrogenase leakage and malondialdehyde formation was observed in Cd-treated cells. A close correlation between these two events suggests that lipid peroxidation may be one of the main pathways causing its cytotoxicity. It was also noted that Cd-induced cell injury and lipid peroxidation were inhibited by catalase and superoxide dismutase, two antioxidant enzymes. By using the fluorescent probe 2',7'-dichlorofluorescin diacetate, a significant increase of ROS production in Cd-treated MRC-5 cells was detected. The inhibition of dichlorofluorescein fluorescence by catalase, not superoxide dismutase, suggests that hydrogen peroxide is the main ROS involved. Moreover, the significant dose-dependent changes of mitochondrial membrane potential in Cd-treated MRC-5 cells, demonstrated by increased fluorescence of rhodamine 123 examined using a laser-scanning confocal microscope, also indicate the involvement of mitochondrial damage in Cd cytotoxicity. These findings provide in vitro evidence that Cd causes oxidative cellular damage in human fetal lung fibroblasts, which may be closely associated with the pulmonary toxicity of Cd
Cadmium Exposure and Hypertension in the 1999–2004 National Health and Nutrition Examination Survey (NHANES)
Joint Toxicity of Cadmium and Ionizing Radiation on Zooplankton Carbon Incorporation Growth and Mobility
Promoting a healthy diet and physical activity in adults with intellectual disabilities living in community residences: Design and evaluation of a cluster-randomized intervention
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