2 resultados para C-60 ADDUCTS

em Digital Commons at Florida International University


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We performed two litter decomposition experiments using nearly-senesced red mangrove (Rhizophora mangle L.) leaves collected from an Everglades dwarf mangrove wetland to understand the short-term (3 weeks) and long-term (1 year) changes in mass, as well as C-, N-, and P-content of decomposing leaf litter. We expected that leaves decomposing in this oligotrophic environment would be short-term sources of C, N, and P, but potential long-term sinks for N and P. In May 1998, we conducted a 3-week leaching experiment, incubating fresh, individual leaves in seawater for up to 21 days. From May 1997 to May 1998, leaf litter in mesh bags decomposed on the forest floor at two dwarf mangrove sites. Leaching accounted for about 33% loss of dry mass from R. mangle leaves after 3 weeks. Leaching losses were rapid, peaking by day 2, and large, with leachate concentrations of total organic carbon (TOC) and total phosphorus (TP) increasing by more than an order of magnitude after 3 weeks. Mean leaf C:N increased from 105 to 115 and N:P increased from a mean of 74 to 95 after 21 days, reflecting the relatively large leaching losses of N and P. Loss of mass in the litterbags leveled off after 4 months, with roughly 60%dry mass remaining (DMR) after nearly 1 year of decomposition. The mass of carbon in each litterbag declined significantly after 361 days, but the mass of nitrogen and phosphorus doubled, indicating long-term accumulation of these constituents into the detritus. Subsequently, the leaf C:N ratio dropped significantly from 90 to 34 after 361 days. Following an initial 44-day increase, leaf N:P decreased from 222 to 144, reflecting high accumulation of P relative to N. A review of several estuarine macrophyte decomposition studies reveals a trend in nitrogen accumulation through time regardless of site, but suggests no clear pattern for C and P. We believe that the increase in litter P observed in this study was indicative of the P-limited status of the greater Everglades ecosystem and that decomposing mangrove litter may represent a substantial phosphorus pool in the system.

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C-reactive protein (CRP), a normally occurring human plasma protein may become elevated as much as 1,000 fold during disease states involving acute inflammation or tissue damage. Through its binding to phosphorylcholine in the presence of calcium, CRP has been shown to potentiate the activation of complement, stimulate phagocytosis and opsonize certain microorganisms. Utilizing a flow cytometric functional ligand binding assay I have demonstrated that a monocyte population in human peripheral blood and specific human-derived myelomonocytic cell lines reproducibly bind an evolutionarily conserved conformational pentraxin epitope on human CRP through a mechanism that does not involve its ligand, phosphorylcholine. ^ A variety of cell lines at different stages of differentiation were examined. The monocytic cell line, THP-1, bound the most CRP followed by U937 and KG-1a cells. The HL-60 cell line was induced towards either the granulocyte or monocyte pathway with DMSO or PMA, respectively. Untreated HL-60 cells or DMSO-treated cells did not bind CRP while cells treated with PMA showed increased binding of CRP, similar to U-937 cells. T cell and B-cell derived lines were negative. ^ Inhibition studies with Limulin and human SAP demonstrated that the binding site is a conserved pentraxin epitope. The calcium requirement necessary for binding to occur indicated that the cells recognize a conformational form of CRP. Phosphorylcholine did not inhibit the reaction therefore the possibility that CRP had bound to damaged membranes with exposed PC sites was discounted. ^ A study of 81 normal donors using flow cytometry demonstrated that a majority of peripheral blood monocytes (67.9 ± 1.3, mean ± sem) bound CRP. The percentage of binding was normally distributed and not affected by gender, age or ethnicity. Whole blood obtained from donors representing a variety of disease states showed a significant reduction in the level of CRP bound by monocytes in those donors classified with infection, inflammation or cancer. This reduction in monocyte populations binding CRP did not correlate with the concentration of plasma CRP. ^ The ability of monocytes to specifically bind CRP combined with the binding reactivity of the protein itself to a variety of phosphorylcholine containing substances may represent an important bridge between innate and adaptive immunity. ^