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Toxic Forms (toxic + form)
Selected AbstractsOral toxicity of the cyanobacterial toxin cylindrospermopsin in male Swiss albino mice: Determination of no observed adverse effect level for deriving a drinking water guideline valueENVIRONMENTAL TOXICOLOGY, Issue 2 2003A. R. Humpage Abstract The cyanobacterial toxin cylindrospermopsin (CYN) is a frequent contaminant of freshwaters throughout the world, including those that are sources of drinking water. The first cases of human poisoning attributed to this toxin occurred from a treated drinking water supply in Queensland, Australia, in 1979. The toxin causes extensive damage to the liver, kidneys, spleen, heart, and other organs. It is known to be a potent protein synthesis inhibitor, but there is mounting evidence for genotoxicity and that it metabolizes to even more toxic forms. As part of a risk assessment process leading to a guideline for a safe drinking water level for this toxin, we performed a series of experiments to determine a no-observed-adverse-effect level (NOAEL) for this toxin. In the first trial male mice were exposed to CYN-containing cyanobacterial extract in their drinking water (0,657 ,g CYN kg,1 day,1) for 10 weeks. In the second trial mice received purified CYN by daily gavage (0,240 ,g CYN kg,1 day,1) for 11 weeks. Body and organ weights were recorded; urine, serum, and hematology analyses were performed; and histopathological examination of tissues was carried out. Body weights were significantly increased at low doses (30 and 60 ,g kg,1 day,1) and decreased at high doses (432 and 657 ,g kg,1 day,1). Liver and kidney weights were significantly increased at doses of 240 ,g kg,1 day,1 and 60 ,g kg,1 day,1, respectively. Serum bilirubin levels were significantly increased and bile acids significantly decreased at doses of 216 ,g kg day,1 and greater. Urine total protein was significantly decreased at doses above 60 ,g kg,1 day,1. The kidney appeared to be the more sensitive organ to this toxin. If it is assumed that increased organ weights and changes in functional capacity are responses to an underlying toxic effect, then the NOAEL based on this data is 30 ,g kg,1 day,1, which, with standard calculations and uncertainty factors, provides a proposed guideline safety value of 1 ,g/L in drinking water. © 2003 Wiley Periodicals, Inc. Environ Toxicol 18: 94,103, 2003. [source] Exploiting the genetic and biochemical capacities of bacteria for the remediation of heavy metal pollutionFEMS MICROBIOLOGY REVIEWS, Issue 4 2002Marc Valls Abstract The threat of heavy metal pollution to public health and wildlife has led to an increased interest in developing systems that can remove or neutralise its toxic effects in soil, sediments and wastewater. Unlike organic contaminants, which can be degraded to harmless chemical species, heavy metals cannot be destroyed. Remediating the pollution they cause can therefore only be envisioned as their immobilisation in a non-bioavailable form, or their re-speciation into less toxic forms. While these approaches do not solve the problem altogether, they do help to protect afflicted sites from noxious effects and isolate the contaminants as a contained and sometimes recyclable residue. This review outlines the most important bacterial phenotypes and properties that are (or could be) instrumental in heavy metal bioremediation, along with what is known of their genetic and biochemical background. A variety of instances are discussed in which valuable properties already present in certain strains can be combined or improved through state-of-the-art genetic engineering. In other cases, knowledge of metal-related reactions catalysed by some bacteria allows optimisation of the desired process by altering the physicochemical conditions of the contaminated area. The combination of genetic engineering of the bacterial catalysts with judicious eco-engineering of the polluted sites will be of paramount importance in future bioremediation strategies. [source] The role of monitored natural recovery in sediment remediationINTEGRATED ENVIRONMENTAL ASSESSMENT AND MANAGEMENT, Issue 1 2006Victor S Magar Abstract The long-term goal of monitored natural recovery (MNR) is to achieve ecological recovery of biological endpoints in order to protect human and ecological health. Insofar as ecological recovery is affected by surface-sediment-contaminant concentrations, the primary recovery processes for MNR are natural sediment burial and contaminant transformation and weathering to less toxic forms. This paper discusses the overall approach for effective implementation of MNR for contaminated sediment sites. Several lines of evidence that may be used to demonstrate natural recovery processes are summarized, including documentation of source control; evidence of contaminant burial; measurement of surface sediment mixing depths and the active sediment benthic layer; measurement of sediment stability; contaminant transformation and weathering; modeling sediment transport, contaminant transport, and ecological recovery; measuring ecological recovery and long-term risk reduction; knowledge of future plans for use and development of the site; and watershed and institutional controls. In general, some form of natural recovery is expected and should be included as part of a remedy at virtually all contaminated sediment sites. Further, MNR investigations and an understanding of natural recovery processes provide cost-effective information and support the evaluation of more aggressive remedies such as capping, dredging, and the use of novel amendments. The risk of dredging or capping may be greater than the risk of leaving sediments in place at sites where capping or dredging offer little long-term environmental gain but pose significant short-term risks for workers, local communities, and the environment. [source] Synapse loss in dementiasJOURNAL OF NEUROSCIENCE RESEARCH, Issue 10 2010Ryan Clare Abstract Synaptic transmission is essential for nervous system function, and its dysfunction is a known major contributing factor to Alzheimer's-type dementia. Antigen-specific immunochemical methods are able to characterize synapse loss in dementia through the quantification of various synaptic proteins involved in the synaptic cycle. These immunochemical methods applied to the study of Alzheimer's disease (AD) brain specimens have correlated synaptic loss with particularly toxic forms of amyloid-, protein and have also established synapse loss as the best correlate of dementia severity. A significant but comparatively circumscribed amount of literature describes synaptic decline in other forms of dementia. Ischemic vascular dementia (IVD) is quite heterogeneous, and synapse loss in IVD seems to be variable among IVD subtypes, probably reflecting its variable neuropathologic correlates. Loss of synaptic protein has been identified in vascular dementia of the Binswanger type and Spatz-Lindenberg's disease. Here we demonstrate a significant loss of synaptophysin density within the temporal lobe of frontotemporal dementia (FTD) patients. © 2010 Wiley-Liss, Inc. [source] Overview of on-farm bioremediation systems to reduce the occurrence of point source contaminationPEST MANAGEMENT SCIENCE (FORMERLY: PESTICIDE SCIENCE), Issue 2 2007Tineke De Wilde Abstract Contamination of ground and surface water puts pressure on the use of pesticides. Pesticide contamination of water can often be linked to point sources rather than to diffuse sources. Examples of such point sources are areas on farms where pesticides are handled and filled into sprayers, and where sprayers are cleaned. To reduce contamination from these point sources, different kinds of bioremediation system are being researched in various member states of the EU. Bioremediation is the use of living organisms, primarily microorganisms, to degrade the environmental contaminants into less toxic forms. The systems available for biocleaning of pesticides vary according to their shape and design. Up till now, three systems have been extensively described and reported: the biobed, the Phytobac® and the biofilter. Most of these constructions are excavations or different sizes of container filled with biological material. Typical overall clean-up efficiency exceeds 95%, realising even more than 99% in many cases. This paper provides an overview of the state of the art of these bioremediation systems and discusses their construction, efficiency and drawbacks. Copyright © 2007 Society of Chemical Industry [source] Hyperhydricity in micropropagated carnation shoots: the role of oxidative stressPHYSIOLOGIA PLANTARUM, Issue 1 2004Shady Saher The physiology of hyperhydricity in relation to oxidative stress, mineral nutrients, antioxidant enzymes and ethylene has been studied in three micropropagated carnation cultivars under experimentally induced hyperhydricity. A marked increase in Fe content in comparison with normal tissues was observed in the hyperhydric tissues from the three cultivars. The levels of ethylene, solute leakage and malondialdehyde content were also significantly higher in the hyperhydric tissues. In relation to the time course of H2O2 production measured by fluorescence quenching, a similar trend could be observed for the three cultivars, with a clear increase in the generation of hydrogen peroxide in hyperhydric tissues. The activities of all the antioxidative enzymes studied, except lipoxygenase, were higher in the hyperhydric shoots. Phenylalanine ammonia-lyase (PAL) showed a significant decrease in activity in the hyperhydric tissues in comparison with the controls for the three cultivars. Soluble guaiacol peroxidase had a strong increase in activity in hyperhydric shoots of the three cultivars. These results provide, for the first time, direct evidence of H2O2 generation in hyperhydric tissues, characterize the response of the antioxidant system to an oxidative stress during hyperhydricity in carnation leaves and point to the accumulation of toxic forms of oxygen as the inducer of some of the abnormalities observed. [source] Alzheimer vaccine: amyloid-, on trialBIOESSAYS, Issue 3 2003Stephen R. Robinson A new therapeutic approach is being developed for the treatment of Alzheimer's disease (AD). This approach involves the deliberate induction of an autoimmune response to amyloid-, (A,) peptide, the constituent of neuritic plaques that is thought to cause the neurodegeneration and dementia in AD. If this approach is to be effective, antibodies must be produced that can selectively target the toxic forms of A,, while leaving the functionally-relevant forms of A, and its precursor protein untouched. Furthermore, an approach needs to be found that avoids provoking an acute neuroinflammatory response. The situation is made even more challenging by uncertainty regarding which isoforms of A, contribute to the pathogenesis of AD. BioEssays 25:283,288, 2003. © 2003 Wiley Periodicals, Inc. [source] | ||||||||||