Managing heavily manured soils for decreased P loss to waters requires improved understanding of the chemical and sorption-desorption characteristics of P in these soils. We used soils from agricultural fi elds receiving ≥8 yr of dairy, poultry, swine manure or spent mushroom compost for the determination of P functional groups in NaOH-EDTA extracts by solution 31 P nuclear magnetic resonance (NMR) spectroscopy, degree of P saturation (DPS), and P sorption-desorption isotherms. The 31 P NMR results show that inorganic orthophosphate was the primary form of P in manure treated (79-93% of total extract P) and untreated soils (33-71%). Pyrophosphate and phosphate monoesters were identifi ed in all soils, whereas phosphate diesters were present in small proportions (<3%) in only a few soils. Polyphosphate, a more condensed form of inorganic P, was present in seven out of nine manured soils (9-47 mg P kg −1 , <2%) but absent in untreated soils. Concentrations of inositol hexakisphosphate (IHP), mostly myo-IHP plus some scyllo-IHP, were similar in manured soils (52-116 mg P kg −1 , 2-8%) and untreated soils (43-137 mg P kg −1 , 6-22%), suggesting a lack of IHP accumulation despite long-term manure applications, including poultry manures that are typically rich in IHP. Most of the treated soils had DPS ≈ 80 to 90% compared with 11 to 33% for the untreated samples. Results from P sorption isotherms showed that potential P release was 3 to 30 times greater from treated than untreated soils. The lack of IHP accumulation in soils receiving long-term manure applications implies that manure-derived IHP may not be biologically and environmentally benign.

We reported recently that the complement (C) system may play a role in the febrile response of guinea pigs to intravenous lipopolysaccharide (LPS) administration because C depletion abolished the LPS-induced rise in core temperature (T(c)). The present study was designed to investigate further the relation between C reduction [induced by cobra venom factor (CVF); 20, 50, 100, and 200 U/animal iv] and the fever of adult, conscious guinea pigs produced by LPS injected intravenously (2 microg/kg) or intraperitoneally (8, 16, 32 microg/kg) 18 h after CVF; control animals received pyrogen-free saline. Serum C levels were measured as total hemolytic C activity before and 18 h after CVF injection and expressed as CH(100) units. In other experiments, serum C levels were determined at various intervals after the intravenous and intraperitoneal injections at different doses of LPS alone. LPS produced fevers generally of similar heights but of different onset latencies and durations, depending on the dose and route of administration. CVF caused dose-related reductions in serum C, from approximately 1,136 U to below detection. These reductions proportionately attenuated the fevers induced by intraperitoneal LPS, but not by intravenous LPS. Intravenous and intraperitoneal LPS per se caused reductions in serum C of 25 and 40%, respectively, indicating activation of the C cascade. These decreases were transient, however, occurring early during the febrile rise approximately 30 min after LPS injection. These data thus support the notion that the C system may be critically involved in the febrile response of guinea pigs to systemic, particularly intraperitoneal, LPS.

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