Determination of gold accumulation in human tissues caused by gold therapy using x-ray fluorescence analysis

Bacsó, J.; Uzonyi, I.; Dezső, Balázs

doi:10.1016/0883-2889(88)90023-8

Cited by 7 publications

(6 citation statements)

References 5 publications

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“…The radioactive progeny addressed in calculation of dose coefficients for radioisotopes of lead are isotopes of gold, mercury, thallium, lead, bismuth, and polonium. The biokinetic models applied to these elements as progeny of systemic lead are described below. (b) Gold (476) The biokinetic of gold have been investigated extensively in human subjects and laboratory animals in studies related to its medical applications, particularly the use of stable gold for treating rheumatoid arthritis and short-lived radioactive gold as an imaging agent (Block et al., 1942, 1944; Freyberg et al., 1942; Jeffrey et al., 1958; Lawrence, 1961; Rubin et al., 1967; McQueen and Dykes, 1969; Mascarenhas et al., 1972; Sugawa-Katayama et al., 1975; Gottlieb, 1983; Jellum et al., 1980; Massarella and Pearlman, 1987; Andersson et al., 1988; Bacso et al., 1988; Brihaye and Guillaume, 1990). Also, several studies have addressed the biological behaviour of gold as a radioactive contaminant in the workplace or environment (Durbin, 1960; Fleshman et al., 1966; Chertok and Lake, 1971a,b,c; Silva et al., 1973).…”

Section: Lead (Z = 82)mentioning

confidence: 99%

ICRP Publication 137: Occupational Intakes of Radionuclides: Part 3

Paquet¹,

Bailey²,

Leggett³

et al. 2017

Ann ICRP

234

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The 2007 Recommendations of the International Commission on Radiological Protection (ICRP, 2007) introduced changes that affect the calculation of effective dose, and implied a revision of the dose coefficients for internal exposure, published previously in the Publication 30 series (ICRP, 1979, 1980, 1981, 1988) and Publication 68 (ICRP, 1994). In addition, new data are now available that support an update of the radionuclide-specific information given in Publications 54 and 78 (ICRP, 1988a, 1997b) for the design of monitoring programmes and retrospective assessment of occupational internal doses. Provision of new biokinetic models, dose coefficients, monitoring methods, and bioassay data was performed by Committee 2, Task Group 21 on Internal Dosimetry, and Task Group 4 on Dose Calculations. A new series, the Occupational Intakes of Radionuclides (OIR) series, will replace the Publication 30 series and Publications 54, 68, and 78. OIR Part 1 has been issued (ICRP, 2015), and describes the assessment of internal occupational exposure to radionuclides, biokinetic and dosimetric models, methods of individual and workplace monitoring, and general aspects of retrospective dose assessment. OIR Part 2 (ICRP, 2016), this current publication and upcoming publications in the OIR series (Parts 4 and 5) provide data on individual elements and their radioisotopes, including information on chemical forms encountered in the workplace; a list of principal radioisotopes and their physical half-lives and decay modes; the parameter values of the reference biokinetic model; and data on monitoring techniques for the radioisotopes encountered most commonly in workplaces. Reviews of data on inhalation, ingestion, and systemic biokinetics are also provided for most of the elements. Dosimetric data provided in the printed publications of the OIR series include tables of committed effective dose per intake (Sv Bq−1 intake) for inhalation and ingestion, tables of committed effective dose per content (Sv Bq−1 measurement) for inhalation, and graphs of retention and excretion data per Bq intake for inhalation. These data are provided for all absorption types and for the most common isotope(s) of each element. The electronic annex that accompanies the OIR series of publications contains a comprehensive set of committed effective and equivalent dose coefficients, committed effective dose per content functions, and reference bioassay functions. Data are provided for inhalation, ingestion, and direct input to blood. This third publication in the series provides the above data for the following elements: ruthenium (Ru), antimony (Sb), tellurium (Te), iodine (I), caesium (Cs), barium (Ba), iridium (Ir), lead (Pb), bismuth (Bi), polonium (Po), radon (Rn), radium (Ra), thorium (Th), and uranium (U).

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Section: Lead (Z = 82)mentioning

confidence: 99%

ICRP Publication 137: Occupational Intakes of Radionuclides: Part 3

Paquet¹,

Bailey²,

Leggett³

et al. 2017

Ann ICRP

234

View full text Add to dashboard Cite

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“…For example, mercury concentrations in brain tissue in individuals chronically exposed to low levels of mercury vapor have been shown to reach 2.1 M. 35 For gold, concentrations of Au(III) in spleen have been observed as high as 700 M in patients undergoing chrysotherapy for rheumatoid arthritis. 36 Nickel concentrations in animal studies have been shown to reach over 400 M in tissues adjacent to nickel wire. 37 Palladium concentrations are less well studied, however.…”

Section: Discussionmentioning

confidence: 99%

Au(III), Pd(II), Ni(II), and Hg(II) alter NFκB signaling in THP1 monocytic cells

Lewis¹,

Wataha²,

McCloud³

et al. 2005

J Biomedical Materials Res

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The transcription factor NFkappaB plays a key role in the tissue inflammatory response. Metal ions released into tissues from biomaterials (e.g., Au, Pd, Ni, Hg) are known to alter the binding of NFkappaB proteins to DNA, thereby modulating the effect of NFkappaB on gene activation and, ultimately, the tissue response to biomaterials. Little is known about the effect of these metals on key signaling steps prior to NFkappaB-DNA binding such as transcription factor activation or nuclear translocation, yet these steps are equally important to modulation of the pathway. Oxidative stress is known to alter NFkappaB proteins and is suspected to play a role in metal-induced NFkappaB signaling modulation. Our aim in the current study was to assess the effects of sublethal levels of Ni, Hg, Pd, and Au ions on NFkappaB activation and nuclear translocation in the monocyte, which is acknowledged as an important orchestrator of the biological response to materials and the pathogenesis of chronic disease. Sublethal concentrations of Au(III), Ni(II), Hg(II), and Pd(II) were added to cultures of human THP1 monocytic cells for 72 h. In parallel cultures, lipopolysaccharide (LPS) was added for the last 30 min to activate the monocytic cells. Then cellular cytoplasmic and nuclear proteins were isolated, separated by electrophoresis, and probed for IkappaBalpha degradation (activation) and NFkappaB p65 translocation. Protein levels were digitally quantified and statistically compared. The levels of reactive oxygen species (ROS) in the monocytic cells were measured as a possible mechanism of metal-induced NFkappaB modulation. Only Au(III) activated IkappaBalpha degradation by itself. Au(III) and Pd(II) enhanced LPS-induced IkappaBalpha degradation, but Hg(II) and Ni(II) suppressed it. Au(III), Ni(II), and Pd(II) activated p65 nuclear translocation without LPS, and all but Ni(II) enhanced LPS-induced translocation. Collectively, the results suggest that these metal ions alter activation and translocation of NFkappaB, each in a unique way at unique concentrations. Furthermore, even when these metals had no overt effects on signaling by themselves, all altered activation of signaling by LPS, suggesting that the biological effects of these metals on monocytic function may only be manifest upon activation. None of the metal ions elevated levels of ROS at 72 h, indicating that ROS were probably not direct modulators of the NFkappaB activation or translocation at this late time point.

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“…Systemic distribution, retention, and excretion of gold 35.2.3.1. Biokinetic data (648) The biokinetics of gold has been investigated in human subjects and laboratory animals in studies related to its medical applications, particularly the use of stable gold for treating rheumatoid arthritis, and short-lived radioactive gold as an imaging agent (Block et al, 1942(Block et al, , 1944Freyberg et al, 1942;Jeffrey et al, 1958;Lawrence, 1961;Rubin et al, 1967;McQueen and Dykes, 1969;Mascarenhas et al, 1972;Sugawa-Katayama et al, 1975;Jellum et al, 1980;Gottlieb, 1983;Massarella and Pearlman, 1987;Andersson et al, 1988;Bacso et al, 1988;Brihaye and Guillaume, 1990). Other studies have addressed the biological behaviour of gold as a radioactive contaminant in the workplace or environment (Durbin, 1959;Fleshman et al, 1966;Chertok and Lake, 1971a,b,c;Silva et al, 1973).…”

Section: Ingestionmentioning

confidence: 99%