Proposed biokinetic model for phosphorus.

This paper reviews data related to the biokinetics of phosphorus in the human body and proposes a biokinetic model for systemic phosphorus for use in updated International Commission on Radiological Protection (ICRP) guidance on occupational intake of radionuclides. Compared with the ICRP's current occupational model for systemic phosphorus (Publication 68, 1994), the proposed model provides a more realistic description of the paths of movement of phosphorus in the body and greater consistency with experimental, medical, and environmental data regarding its time-dependent distribution. For acute uptake of (32)P to blood, the proposed model yields roughly a 50% decrease in dose estimates for bone surface and red marrow and a six-fold increase in estimates for liver and kidney compared with the model of Publication 68. For acute uptake of (33)P to blood, the proposed model yields roughly a 50% increase in dose estimates for bone surface and red marrow and a seven-fold increase in estimates for liver and kidney compared with the model of Publication 68.

Actin polymerization, calcium-transients, and phospholipid metabolism in human neutrophils after stimulation with interleukin-8 and N-formyl peptide.

Signal transduction of interleukin-8 (IL-8) was analyzed in neutrophils, and compared with the well known neutrophil activator N-formyl peptide. Stimulation of human neutrophils with IL-8 induced a rapid polymerization of actin as detected by 7-nitrobenz-2-oxa-1,3-diazol-(NBD)-phallacidin staining of f-actin and reduction of monitored right-angle light scatter. Actin polymerization peaked within 10 seconds after the addition of IL-8 and was short-lived as compared to N-formyl peptide-induced stimulation. Analysis of phospholipids by thin-layer chromatography and analysis of deacylation products of lipid extracts by high-pressure liquid chromatography (HPLC) showed that IL-8 triggered a rapid rise of [32P]phosphatidyl-inositol(3,4,5)trisphosphate (PtdInsP3) followed by a slower increase of [32P]phosphatidylinositol(3,4)bisphosphate (PtdIns-3,4-P2) along with a rapid decrease of [32P]phosphatidylinositol(4,5)bisphosphate (PtdIns-4,5-P2). Changes in polyphosphoinositide metabolism were more moderate and transient than those obtained by N-formyl peptide. Moreover, [32P]phosphatidic acid (PA) production stimulated by IL-8 was minimal and transient as compared to the response activated by N-formyl peptide. Both IL-8 and N-formyl peptide induced Ca++ mobilization from intracellular stores, but IL-8 in contrast to N-formyl peptide failed to trigger the secondary influx of Ca++ from the extracellular medium. In summary, IL-8 and N-formyl peptide stimulated similar and distinct patterns of intracellular activation steps. This study indicates that IL-8 is a potent activator of intracellular events presumably required for chemotaxis, but a relatively weak activator for events associated with superoxide anion generation and proinflammatory activity.

Whole-body distribution of radioactivity after intraperitoneal administration of 32P colloids.

The whole-body distribution of radioactivity after intraperitoneal instillation of 32P-labelled chromic hydroxide particles has been studied in patients operated for early-stage ovarian cancer. Gamma-camera imaging of the abdominal 32P-distribution revealed that the administration procedure was critical for obtaining a homogeneous plating of the radiocolloids on the serosal surface. Dose calculations based on a uniform distribution of 32P in a capillary layer covering the intraperitoneal surface gave an estimated tissue surface dose of about 30 Gy per 370 MBq of 32P administered. The amount of 32P in peripheral blood increased for seven days after instillation followed by a continuous decrease. Bone marrow concentration was from two to five times as high as that in blood, but the total amounts were too small to give significant radiation doses. Gel chromatography showed that 33% of the activity in blood consisted of high molecular weight material, probably colloids. The remainder of the activity (67%) was attached to material of very low molecular weight, appearing as a consequence of physiological degradation of the colloids.

Validation and verification of the ICRP biokinetic model of 32P: the criticality accident at Tokai-Mura, Japan.

Regrettably, a criticality accident occurred at a uranium conversion facility in Tokai-mura, Ibaraki, Japan, on 30 September 1999. Radioactivities of 32P in urine, blood and bone samples of the victims, who were severely exposed to neutrons, were measured. 32P was induced in their whole bodies at the moment of the first nuclear release by the reaction 31P (n, gamma) 32P and 32S (n, p) 32P. A realistic biokinetic model was assumed, as the exchange of 32P between the extracellular fluid compartment and the soft tissue compartment occurs only through the intracellular compartment, and the model was used for preliminary calculations. Some acute excretion of 32P, caused by decomposition or elution of tissues which occurred at the time of the accident, may have happened in the victims' bodies in the first few days. The working hypotheses in the present work should initiate renewed discussion of 32P biokinetics.

[The kinetics of radionuclide distribution between the plasma and formed elements of the blood in dogs]. / Kinetika raspredeleniia nekotorykh radionuklidov mezhdu plazmoi i formennymi élementami krovi sobak.

The investigation of microkinetics of 90Sr, 137Cs and 32P penetration into erythrocytes of dog's blood was made. It was shown that processes of penetration of 90Sr and 32P are monomolecular. The slow stage is monomolecular destruction of complexes of 90Sr and 32P with plasma components. The process of 137Cs penetration is bimolecular. The slowest stage of 137Cs penetration is adsorption on the surface of erythrocytes.

Radioactivity in blood and urine following intraperitoneal instillation of chromic phosphate in patients with and without ascites.

Systemic distribution of radioactive colloidal chromic phosphate P 32 after intraperitoneal instillation was studied in 10 patients with ovarian or endometrial malignancies. Seven patients without ascites received chromic phosphate P 32 for positive peritoneal washings, rupture of the capsule of the cyst during operation, or minimal Stage III disease. Three patients received chromic phosphate P 32 for recurrent ascites after multiple abdominal paracenteses. Blood and urine radioactivity measurements were performed at selected intervals. There was a clear statistically significant difference (p less than 0.01) between chromic phosphate P 32 activity levels in whole blood, red blood cells, and plasma in patients with and without ascites.