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Biomedical subjects

J G Pounds

Publications and source records attributed to J G Pounds.

At least 37 records · Page 2Linked to original sources
PubMed1988

X-ray fluorescence with synchrotron radiation.

The use of synchrotron radiation for X-ray fluorescence has several advantages over the use of other conventional X-ray sources. The principles of synchrotron radiation and methods for applying synchrotron radiation to the X-ray fluorescence measurements of trace elements are discussed. The Brookhaven National Laboratory X-ray microprobe, facilities dedicated to X-ray fluorescence, and related analytical techniques are discussed. Some examples of trace element analyses in biological materials with synchrotron radiation are presented.

Electron Probe Microanalysis↗
PubMed1986

Cellular metabolism of lead: a kinetic analysis in cultured osteoclastic bone cells.

Detailed characterization of the modulation of lead metabolism in bone is necessary to understand the role of skeletal lead in the expression of clinical and biochemical effects of lead intoxication. The metabolism of lead in osseous tissue is also clinically important because it is the major site of chelation by therapeutic agents, such as CaNa2-EDTA and D-penicillamine. Experiments were conducted to characterize the steady-state kinetic distribution and behavior of 210Pb in osteoclastic bone cells and to identify the biological structures or functions associated with the kinetic pools. Bone cells, derived from mouse calvaria, were enriched for osteoclasts by a sequential collagenase digestion and maintained in primary culture for 1 week. Cultures were labeled with 210Pb as 5 microM lead acetate for 20 hr and the kinetic parameters were obtained by analysis of 210Pb washout curves. Cellular metabolism was defined by three kinetic pools of intracellular lead containing approximately 10% (S1). Approximately 12% (S2), and approximately 78% (S3) of total cellular lead (1.2 nmol/mg cell protein). The halftimes for isotopic exchange were 1, 27, and 480 min, respectively. These data indicate that lead is readily exchangeable from osteoclastic bone cells and, as in soft tissues (hepatocytes), the bulk of cellular lead is associated with mitochondria.

Animals↗
PubMed1984

Potentiation of dimethylnitrosamine genotoxicity in rat hepatocytes isolated following ethanol treatment in vivo.

Unscheduled DNA synthesis (UDS), following exposure to dimethylnitrosamine (DMN), was potentiated in cultured hepatocytes isolated following treatment of rats for 14 or 28 days with 20% ethanol/5% sucrose solution. Ethanol treatment was associated with increased UDS, a concomitant increase in hepatic microsomal protein concentration and DMN N-demethylase activity. Increased aniline hydroxylase activity of hepatic microsomes from ethanol-treated rats preceded the measured increase in microsomal protein content or DMN metabolism. The increase in metabolism of DMN in vitro and potentiation of DMN-induced UDS associated with ethanol treatment may contribute to a synergistic effect of ethanol on DMN hepatotoxicity and carcinogenicity. In contrast, ethanol pretreatment did not increase the cytotoxicity of DMN as characterized by enzyme release.

Aminopyrine↗
PubMed1984

Subcellular distribution of lead in cultured rat hepatocytes.

A clear understanding of the sequence and molecular mechanism of the events involved in lead toxicity is hampered by a lack of information about lead compartmentation within the cell. As part of a continuing effort to identify the mechanism by which lead affects cellular functions, we examined the subcellular distribution of 210Pb in cultured hepatocytes. The cells were isolated, labeled, homogenized in sucrose-N-[(2-hydroxyethyl)piperazine]-N'-2-ethanesulfonic acid buffer, and fractionated into mitochondrial, microsomal, and cytosolic components by differential centrifugation. Complete fractionation of the cells revealed that 71% of the cellular 210Pb was associated with the mitochondria, 5% with the microsomes, and 24% with the cytosol. A modified, rapid fractionation procedure indicated that 45% of the cellular lead was associated with both the mitochondria and the cytosol and 10% with the microsomes. When the cells were separated into total particulates and cytosol with a single centrifugation, 22% of the 210Pb was associated with the soluble fraction. The process of homogenization and fractionation of the isolated hepatocytes altered the intracellular distribution of 210Pb. This experimental approach to studying the localization of lead may be compromised by the redistribution of 210Pb during the extensive centrifugations and resuspensions required for subcellular fractionation and suggests that the subcellular distribution patterns of 210Pb obtained by the fractionation of cells reflects the distribution of lead in the homogenate rather than the distribution of 210Pb in the intact cell.

Animals↗
PubMed1984

Effect of lead intoxication on calcium homeostasis and calcium-mediated cell function: a review.

The interaction between lead and essential metals is a complex, well recognized, but poorly understood phenomenon. Dietary deficiencies or excesses of certain essential metals may alter the absorption, elimination, or dose response of lead. Lead, in turn, may alter the homeostasis and function of essential metals. This review will be limited to the effect of lead on calcium, an essential metal with elaborate systemic and cellular homeostatic mechanisms and innumerable second messenger and coupling-factor functions. Lead may ultimately perturb calcium-regulated or calcium-mediated functions (a) directly by interfering with calcium transport or storage processes, e.g., Ca2+ transport proteins, calcium gates, etc.; (b) indirectly by altering cell functions required for calcium homeostasis, e.g., energy production, plasma membrane permeability, etc.; (c) by substitution of Pb2+ for Ca2+ at functionally important calcium binding sites, e.g., calmodulin. While any individual study may not provide adequate experimental verification of the causal role of perturbations of calcium metabolism and function as the primary toxic lesion of lead intoxication, the collective observations of many studies do strongly support lead-calcium interactions as an important functional lesion in lead intoxicated organelles, cells, tissues, and organ systems.

Animals↗
PubMed1983

Mobilization of cellular calcium-45 and lead-210: effect of physiological stimuli.

Isolated rat hepatocytes in primary culture were used as a model system to evaluate the effects of selected hormones and culture conditions on the efflux of calcium-45 and lead-210 from cells labeled with these isotopes. Alpha-adrenergic stimuli, angiotensin, vasopressin, dibutyryl adenosine 3',5'-monophosphate, and reduced phosphate concentrations in the medium increased the efflux of calcium-45 and lead-210. Glucagon and insulin had no effect, but increased phosphate concentrations decreased the efflux of both isotopes. Experiments with hepatocytes cultured in a medium free of calcium and lead demonstrated that the increased efflux of calcium-45 and lead-210 induced by hormones was the result of mobilization of the ions from intracellular stores. The data indicate that the physiological stimuli that mobilized calcium ions also mobilized lead ions, and that the mobilized lead would be available to interact with calcium-mediated cell functions.

Angiotensin II↗
PubMed1983

A method for rapid, sensitive quantitation of short-patch DNA repair in cultured rat hepatocytes.

The sensitivity of DNA-repair detection after incubation of cultured rat hepatocytes with dimethylnitrosamine (DMN) and [Me-1',2'-3H]thymidine ([3H]TdR) was enhanced by the preparation of isolated nuclei. Nuclear isolation-liquid scintillation counting (NI-LSC) provided a rapid method for the determination of unscheduled DNA synthesis (UDS). DMN-induced UDS detected by autoradiography and NI-LSC correlated well and provided similar dose-response curves, indicating the utility of the NI-LSC method for the quantitation of short-patch DNA repair.

Animals↗
PubMed1981

The potential laboratory health hazard of 210Pb and a simple procedure for separation of 210Pb from the daughters 210Bi and 210Po.

Lead 210 (Radium D) is a naturally occurring radionuclide which is frequently used in toxicological studies due to its long half-life. The use of 210Pb in tracer studies poses two problems. First, 210Pb, along with its daughters 210Bi and 210Po, presents a significant health hazard to laboratory personnel. Second, the presence of the daughter products may interfere with the detection of 210Pb, particularly by techniques which discriminate poorly between different radioactive emissions, e.g., autoradiography. The potential laboratory health hazards of 210Pb and its daughters are briefly reviewed and a simple dithiozone extraction procedure which allows quantitative separation of 210Pb frm the daughters 210Po and 210Bi is described. The purified 210Pb may then be utilized to reduce the health hazard from the daughter products and to construct calibration curves for the quantitation of 210Pb in the presence of 210Bi and 210Po by liquid scintillation counting.

Bismuth↗
PubMed1978

Metabolism of lead-210 in juvenile and adult rhesus monkeys (Macaca mulatta).

Experiments were conducted measuring the gastrointestinal absorption and elimination of a single dose of lead-210 acetate in infant and adult rhesus monkeys. Urinary and fecal excretion of absorbed lead was followed for 23 days. Infant monkeys eliminated less and absorbed more orally administered lead. Adult animals excreted more absorbed lead in feces, while urinary excretion between adults and infants was similar. Increased absorption of administered lead and reduced fecal excretion of absorbed lead resulted in significantly greater body burden of lead-210 in infant animals. Blood lead values were increased in the infant animals, and were inversely correlated with body burden and percent absorption of ingested lead.

Aging↗
PubMed1978

Dehydroretronecine-induced skin tumors in mice.

Female Swiss mice susceptible to skin tumors received 6 sc injections and/or topical applications of dehydroretronecine, a metabolite of the pyrrolizidine alkaloid monocrotaline, and were observed for 15 months for tumor development. Of 92 animals examined, 63 had tumors at the site of application or injection; 47 of these had skin tumors, mainly basal cell and squamous cell carcinomas. These data indicate that dehydroretronecine is a proximate carcinogen capable of causing a high incidence of skin tumours in mice at the site of sc injection or topical application.

Administration, Topical↗