Literature DB >> 4366850

The Mongolian gerbil as a model for lead toxicity. I. Studies of acute poisoning.

C D Port, D W Baxter, W R Richter.   

Abstract

Mongolian gerbils fed diets containing lead acetate maintained body weight comparable to gerbils fed the same diet without added lead. Intranuclear lead inclusion bodies in epithelial cells of the proximal convoluted tubules of the kidney were first observed at 4 weeks, and increased in number to about 50 per high power field at 12 weeks. At this time, a corticomedullary area of empty-appearing tubules was prominent. Transmission electron microscopy confirmed the increase in number and size of nuclear lead inclusion over the 12-week period. Cytoplasmic changes observed in proximal tubule cells containing lead inclusions were considered indicative of acute lethal injury. Distinct cytoplasmic fibrillar structures, first apparent at 8 weeks, were present in some proximal tubular lining cells and strongly resembled newly formed intranuclear lead inclusions. After 12 weeks, the total amount of lead present in the gerbil kidney was four to six times greater than that in rat kidney as determined by atomic absorption spectrophotometry. A hypothesis has been formulated that relates the more efficient nephron of the gerbil kidney to the rapid and extensive development of intranuclear inclusion bodies and the greater accumulation of total lead.

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Year:  1974        PMID: 4366850      PMCID: PMC1910738     

Source DB:  PubMed          Journal:  Am J Pathol        ISSN: 0002-9440            Impact factor:   4.307


  20 in total

1.  RENAL LESIONS IN EXPERIMENTAL PLUMBISM AND THEIR CLINICAL IMPLICATIONS.

Authors:  J D TANGE; N J HAYWARD; D A BREMNER
Journal:  Australas Ann Med       Date:  1965-02

2.  Studies on the chemical forms of urinary lead.

Authors:  G T DINISCHIOTU; B NESTORESCU; I C RADULESCU; C IONESCU; N PREDA; G ILUTZA
Journal:  Br J Ind Med       Date:  1960-04

3.  The renal tubule in lead poisoning. II. In vitro studies of mitochondrial structure and function.

Authors:  R A Goyer; A Krall; J P Kimball
Journal:  Lab Invest       Date:  1968-07       Impact factor: 5.662

4.  The renal tubule in lead poisoning. I. mMitochondrial swelling and aminoacidura.

Authors:  R A Goyer
Journal:  Lab Invest       Date:  1968-07       Impact factor: 5.662

5.  Another look at lead inclusion bodies.

Authors:  G W Richter; Y Kress; C C Cornwall
Journal:  Am J Pathol       Date:  1968-08       Impact factor: 4.307

6.  Lead and protein content of isolated intranuclear inclusion bodies from kidneys of lead-poisoned rats.

Authors:  R A Goyer; P May; M M Cates; M R Krigman
Journal:  Lab Invest       Date:  1970-03       Impact factor: 5.662

7.  Intracellular distribution of lead in the liver and kidney of the rat.

Authors:  N Castellino; S Aloj
Journal:  Br J Ind Med       Date:  1969-04

8.  The role of chelation in iron metabolism.

Authors:  P Saltman
Journal:  J Chem Educ       Date:  1965-12       Impact factor: 2.979

9.  The renal tubule in experimental lead intoxication.

Authors:  C N Sun; M Mellies; M W Yin; R A Goyer
Journal:  Arch Pathol       Date:  1966-08

10.  Biliary excretion of lead in the rat.

Authors:  N Castellino; P Lamanna; B Grieco
Journal:  Br J Ind Med       Date:  1966-07
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  2 in total

1.  Animal model of human disease: acute and chronic lead nephropathy.

Authors:  C D Port
Journal:  Am J Pathol       Date:  1976-11       Impact factor: 4.307

2.  Localization of lead in the kidney and liver of rats treated in vivo with lead acetate: ultrastructural studies on unstained sections.

Authors:  M A Russo; S C Kapoor; G D van Rossum
Journal:  Br J Exp Pathol       Date:  1988-04
  2 in total

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