We sampled macroinvertebrates at 75 locations in the Mondego river catchment, Central Portugal, and developed a predictive
model for water quality assessment of this basin, based on the Reference Condition Approach. Sampling was done from June to
September 2001. Fifty-five sites were identified as “Reference sites” and 20 sites were used as “Test sites” to test the model.
At each site we also measured 40 habitat variables to characterize water physics and chemistry, habitat type, land use, stream
hydrology and geographic location. Macroinvertebrates were generally identified to species or genus level; a total of 207
taxa were found. By Unweighted Pair Group Method with Arithmetic mean (UPGMA) clustering and analysis of species contribution
to similarities percentage (SIMPER), two groups of reference sites were established. Using Discriminant Analysis (stepwise
forward), four variables correctly predicted 78% of the reference sites to the appropriate group: stream order, pool quality,
substrate quality and current velocity. Test sites’ environmental quality was established from their relative distance to
reference sites, in MDS ordination space, using a series of bands (BEAST methodology). The model performed well at upstream
sites, but at downstream sites it was compromised by the lack of reference sites. As with the English RIVPACS predictive model,
the Mondego model should be continually improved with the addition of new reference sites. The adaptation of the Mondego model
methodology to the Water Framework Directive is possible and would consist mainly of the integration of the WFD typology and
increasing the number of ellipses that define quality bands.
Handling editor: K. Martens 相似文献
In this review, we address the regulatory and toxic role of ·NO along several pathways, from the gut to the brain. Initially, we address the role on ·NO in the regulation of mitochondrial respiration with emphasis on the possible contribution to Parkinson’s disease via mechanisms that involve its interaction with a major dopamine metabolite, DOPAC. In parallel with initial discoveries of the inhibition of mitochondrial respiration by ·NO, it became clear the potential for toxic ·NO-mediated mechanisms involving the production of more reactive species and the post-translational modification of mitochondrial proteins. Accordingly, we have proposed a novel mechanism potentially leading to dopaminergic cell death, providing evidence that NO synergistically interact with DOPAC in promoting cell death via mechanisms that involve GSH depletion. The modulatory role of NO will be then briefly discussed as a master regulator on brain energy metabolism. The energy metabolism in the brain is central to the understanding of brain function and disease. The core role of ·NO in the regulation of brain metabolism and vascular responses is further substantiated by discussing its role as a mediator of neurovascular coupling, the increase in local microvessels blood flow in response to spatially restricted increase of neuronal activity. The many facets of NO as intracellular and intercellular messenger, conveying information associated with its spatial and temporal concentration dynamics, involve not only the discussion of its reactions and potential targets on a defined biological environment but also the regulation of its synthesis by the family of nitric oxide synthases. More recently, a novel pathway, out of control of NOS, has been the subject of a great deal of controversy, the nitrate:nitrite:NO pathway, adding new perspectives to ·NO biology. Thus, finally, this novel pathway will be addressed in connection with nitrate consumption in the diet and the beneficial effects of protein nitration by reactive nitrogen species.
