Hygienic and microbiological examinations of watercourses are usually not carried out during heavy rainfall and runoff events. After rainfall or snowmelt, there are often massive increases in turbidity in flooding creeks in mountain ranges, which are frequently interpreted as an indication of microbial contamination. The aim of this study was to quantify the microbial loads of watercourses during such runoff events and to compare these loads with loads occurring during regular conditions. In a 14-month monitoring period we investigated the microbial loads of three tributaries of different drinking water reservoirs. A total of 99 water samples were taken under different runoff conditions and analyzed to determine physical, chemical, bacterial, and parasitic parameters. Thirty-two water samples were considered event samples during nine measuring series. The criteria for events, based on duration and intensity of precipitation, water depth gauge measurements, and dynamics, had been fixed before the investigation for each creek individually. Of the physical and chemical parameters examined, only the turbidity, pH, and nitrate values differed clearly from the values obtained for regular samples. Most of the bacteriological parameters investigated (colony, Escherichia coli, coliform, fecal streptococcal, and Clostridium perfringens counts) increased considerably during extreme runoff events. If relevant sources of parasitic contamination occurred in catchment areas, the concentrations of Giardia and Cryptosporidium rose significantly during events. The results show that substantial shares of the total microbial loads in watercourses and in drinking water reservoirs result from rainfall and extreme runoff events. Consequently, regular samples are considered inadequate for representing the microbial contamination of watercourse systems. The procedures for raw water surveillance in the context of multiple-barrier protection and risk assessment ought to include sampling during extreme runoff situations.In some regions of Germany surface reservoirs are the main source of drinking water. In the state of North Rhine-Westphalia, 60% of the drinking water production in 1999 was based on surface water resources (2). Surface water bodies are presumed to be more vulnerable to fecal contamination than groundwater reservoirs due to the absence of natural soil protection and filtration and the possibly short distances between the occurrence of contamination and water extraction. It is argued that especially in the case of heavy rainfall the microbial loads of running waters may suddenly increase substantially and reach reservoir bodies very quickly (18,19). For this reason monitoring microbiological raw water quality is an essential component of the protection strategy in catchment areas of surface drinking water reservoirs (8). In Germany, catchment areas of surface water supplies are usually protected by buffer zones, and the intensity of protection increases with proximity to the water body. Protection of entire catchment areas i...

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Objective-Oxidized lipids and proteins, as well as decreased antioxidant levels, have been detected in human atherosclerotic lesions, with oxidation catalyzed by iron and copper postulated to contribute to lesion development. Zinc has been postulated to displace iron from critical sites and thereby protect against damage. In this study, metal ion and protein oxidation levels were quantified in human carotid and abdominal artery specimens containing early-to-advanced lesions, to determine whether zinc concentrations correlate inversely with iron levels and protein oxidation. Methods and Results-Metal ions were quantified by EPR and inductively coupled plasma mass spectroscopy. Native and oxidized protein side-chains were quantified by high-performance liquid chromatography. A therosclerosis is a multifactorial disease to which many factors contribute; defining the role of each of these has proved to be problematic. Oxidation, and in particular that of low-density lipoproteins (LDL), has been linked to disease development, 1 although the significance of this process has not been fully established (reviewed 2 ). Previous studies have variously implicated lipoxygenase, peroxynitrite, myeloperoxidase, oxygen radicals, and metal-ions in lesion oxidation (reviewed 2 ). In the case of metal ions, a correlation between iron accumulation and the extent of protein (but not lipid) oxidation has been reported for human lesions. 3 Cholesterol ester and cholesterol accumulation also correlate positively with iron, suggesting that these processes are interlinked. 3,4 These data are consistent with some, but not all, epidemiological studies on the potential links between iron and cardiovascular disease. [5][6][7][8] Zinc ions have been reported to modulate oxidant damage via the displacement of iron and copper from oxidationsensitive sites on erythrocyte membranes, 9 LDL, 10 or liposomes. 11 Epidemiological data indicate that elevated serum zinc levels may be protective against disease. 12 Serum or plasma measurements of zinc in people with established atherosclerosis indicate that low zinc levels are associated with increased disease 13,14 and a postmortem study has reported lower tissue levels of zinc in the abdominal aorta of patients who died of heart disease compared to other causes. 15 In contrast, zinc supplementation of the human diet does not affect the susceptibility of LDL to oxidation ex vivo 16,17 or the concentrations of LDL-cholesterol, total cholesterol, or triglycerides, but has an adverse effect on high-density lipoprotein levels, suggesting that high serum zinc levels may promote disease. 17 Elevated zinc may stimulate the formation of oxidants and inhibit protective enzymes in some cells. 18 Atherosclerotic lesions of cholesterol-fed rabbits contain elevated levels of iron and reduced levels of zinc. 19 -21 Zinc supplementation, via dietary feeding, reduced lesion area despite insignificant changes in lesion zinc concentrations; these changes were ascribed to a displacement of iron by zinc. 20 Zinc supplement...

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A mutant in the plasma membrane H'-ATPase gene of the yeast Saccharomyces cerevisiae with a reduced H+-ATPase activity, when examined at the singlechannel level with the patch-clamp technique, was found to exhibit K+ channels activated by intracellular application of ATP. In the parent strain, the same channel, identified by its conductance and selectivity, is not activated by ATP. This activity in the mutant is blocked by the ATPase inhibitor NN'-dicyclohexylcarbodiimide. ADP and the ATP analog adenosine 5'-[y [35S]thio]triphosphate do not activate the channel.These findings suggest a tight physical coupling between the plasma membrane ATPase and the K+ channel.The plasma membrane ATPase of yeast is a 100-kDa essential protein that functions as an electrogenic proton pump (1, 2), playing a major role in the regulation of intracellular pH and membrane potential. DNA sequence analysis (3) ofthe PMAJ gene that encodes this H+-ATPase has shown its homology to various H+/K+, Na+/K+, and Ca2+-ATPases. Several lines of evidence (1, 2) suggest that the proton pump is indirectly coupled to a K+-transport system. The transport system responsible for potassium uptake in yeast is known to have multiple affinities (4), and we seek to determine the role played in this process by the recently observed voltage-gated potassium channels (5). We report here patch-clamp experiments (6) on mutant yeast that reveal an unexpected interaction between a voltage-gated K+ channel and the protonpumping ATPase.Recently McCusker et al. (7) isolated a large number of mutations in PMAI, the plasma membrane ATPase gene in the yeast Saccharomyces cerevisiae. The mutations were isolated by their resistance to hygromycin B. The ATPase activity of the pmal mutants is reduced by as much as 75%. These mutants are highly pleiotropic, exhibiting pH, osmotic, and cold sensitivity. Three severely affected mutants, including the pmal -105 mutant discussed here, were unable to grow at pH 3.5 or with NH4'. These severe phenotypes are suppressed by adding 50 mM KCl, but not by NaCl, to the medium. Further analysis has shown that pmal mutant cells have reduced membrane potentials (8). The PMAI-encoded protein probably functions as a dimer or higher-order structure because the 53 pmal mutants display a complex pattern of intragenic complementation. Some combinations of pmal alleles complement for hygromycin B resistance (7), whereas others exhibit negative complementation, such that a diploid heterozygous for two mutant proteins is unable to grow (H. Cooper and J.E.H., unpublished work). RESULTSThe pmal-105 mutation exhibits a 65% reduction in ATPase activity (7). Biochemical analysis shows that the mutant protein is present in the plasma membrane at wild-type levels but exhibits an altered pH optimum, insensitivity to vanadate inhibition, and altered Km for ATP (D. S. Perlin, J.H.McC. and J.E.H., unpublished work). The mutant results from a base substitution of Ser-368 to phenylalanine (S. Harris and J.E.H., unpublished results).K+ channels in the pm...