Occupational lead nephropathy

Wedeen, Richard P.; Maesaka, John K.; Weiner, Brian C.; Lipat, Gregorio A.; Lyons, Michael M.; Vitale, Leonard F.; Joselow, Morris M.

doi:10.1016/0002-9343(75)90224-7

Cited by 164 publications

(76 citation statements)

References 31 publications

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“…Exposure to lead in food and the environment in general or in industry in particular can cause anemia [1], renal insufficiency [2,3], and encephalopathy [4], the latter resulting in disturbed behavior [5]. Lead is retained in liver, kidneys, and blood, and especially in bone, teeth, and brain [6].…”

mentioning

confidence: 99%

Lattice parameters and cation distribution of solid solutions of calcium and lead hydroxyapatite

Verbeeck

Lassuyt

Heijligers³

et al. 1981

Calcif Tissue Int

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Summary. Solid solutions of calcium hydroxyapatite (CaOHA) and lead hydroxyapatite (PbOHA) of the formula Ca,0.x Pbx (PO4)6 (OH)2 were prepared by coprecipitation followed by heating at 800~ in a stream of CO2-free water vapor of 1 atm. The samples were apatitic in the range 0 < x < 6 and contained lead phosphates as a second phase at higher Pb/Ca ratios. Lattice parameters and cation distribution of the apatitic samples were determined by X-ray diffraction. The lattice parameters varied linearly with x in the range considered, whereas all Pb 2+ were located in the sixfold position for cations. There was a miscibility gap in the apatite series of solid solutions in the range 1 < x < 4, whereas apatites in the range 6 < x < 10 were not stable under the conditions of preparation. It is concluded that apatites in the range 4 < x < 6 represent a minimum in the free energy of solid solutions between CaOHA and PbOHA.

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mentioning

confidence: 99%

Lattice parameters and cation distribution of solid solutions of calcium and lead hydroxyapatite

Verbeeck

Lassuyt

Heijligers³

et al. 1981

Calcif Tissue Int

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“…The following reviews are some that are useful (1,16,32,96,(152)(153)(154). A few recent references will introduce some aspects of the actions of lead on the tissues: liver (155), kidney (156)(157)(158), and nervous system (126,(159)(160)(161)(162)(163)(164)(165).…”

Section: Other Tissuesmentioning

confidence: 99%

Indices of potential lead hazard.

Posner¹

1977

Environ Health Perspect

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This review is concerned with the concentrations of lead in human whole blood, erythrocytes, plasma, serum, soft tissues, bone, and urine. The extent to which redistribution of some of the bound lead occurs is outlined. The effects of lead on enzyme activities and on the accumulation of metabolic intermediates in the blood and urine are described. A brief section deals with the range ofsigns and symptoms that can occur and differences seen between symptomatic children and adults.

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“…As a result of lead exposure, the mammalian kidney, a primary target organ in the initial accumulation of absorbed lead [1], takes it up through glomerular filtration, tubular reabsorption, and a small fraction through direct absorption [2][3][4][5]. Lead-induced nephrotoxicity in workers and experimental animals is well-documented and characterized as decreased glomerular filtration rate and nephropathy of proximal tubules [6,7]. In terms of lead induced pathological damage to myocardium of humans, few studies are available, but histological examination of individuals who died from lead poisoning revealed degenerative and inflammatory changes in the myocardium [8].…”

Section: Introductionmentioning

confidence: 99%

Protein Markers of Chemical Exposure and Molecular Epidemiology

Witzmann¹

1999

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PubKc reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources gathering and rnaintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect Of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 222024302, and to the Office of Management and Budget, Paperwork Reduction Project (0704-0188), Washington, DC 20503. AGENCY USE ONLY (Leave Blank)2. REPORT DATE July 30,1999 TITLE AND SUBTITLE Protein Markers of Chemical Exposure and Molecular Epidemiology AUTHOR(S)Frank A. Witzmann PERFORMING ORGANIZATION NAME(S) AND ADDRESSES)Molecular Anatomy Laboratory, Dept of Biology Indiana University Purdue University -Columbus 4601 Central Avenue Columbus IN 47203 SPONSORINGyMONITORING AGENCY NAME(S) AND ADDRESS(ES)AFOSR 12b. DISTRIBUTION CODE ABSTRACT (Maximum 200 words)This final technical report describes the results of experiments that 1) explored, at the molecular level, the toxicity of lead in various exposure systems; 2) enabled the development a system of general and tissue-specific protein markers for lead in rabbits and rats that might be indicative of its effect in human toxicologic targets; 3) assessed the cellular expression of GST isoenzymes as protein markers of lead toxicity in rat kidney, and 4) investigated the suitability of tissue-slice in vitro toxicologic approaches by evaluating their patterns of protein expression and comparing them to patterns from whole tissues. High resolution large-scale two-dimensional polyacrylamide gel electrophoresis (2-DE) with computerized image analysis was used to map cell/tissue proteins of various lead targets. In the case of lead experiments, proteomics technology, e.g. mass spectrometric analysis of tryptic digests (peptide-mass fingerprinting) of selected proteins resolved by 2-DE , was used to identify altered proteins. Quantitative and qualitative assessments of toxic effect were made, individual protein data was compiled in annotated databases, and protein markers identified. Protein digestion 9 Matrix-assisted laser desorption mass spectrometric (MALDI) protein identification 9 SUBJECT TERMSResults and Discussion 1" Toxicity of lead in rabbit ventricle and kidney 10 Assessment of regional differences in renal lead toxicity 12 Assessment of glutathione S-transferase (GST) isoenzyme expression 14 AbstractThis final technical report describes the results of experiments that 1) explored, at the molecular level, the toxicity of lead in various exposure systems; 2) enabled the development a system of general and tissuespecific protein markers for lead in rabbits and rats that might be indicative of its effect in human toxicologic targets; 3) assessed the cellular expression of GST isoenzymes as ...

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Occupational lead nephropathy

Cited by 164 publications

References 31 publications

Lattice parameters and cation distribution of solid solutions of calcium and lead hydroxyapatite

Lattice parameters and cation distribution of solid solutions of calcium and lead hydroxyapatite

Indices of potential lead hazard.

Protein Markers of Chemical Exposure and Molecular Epidemiology

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