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Toxicological information

Neurotoxicity

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Administrative data

Endpoint:
neurotoxicity: acute oral
Type of information:
experimental study
Adequacy of study:
other information
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Acceptable, well-documented publication which meets basic scientific principles

Data source

Reference
Reference Type:
publication
Title:
The pathogenesis of lead encephalopathy. Effects of lead carbonate feedings on morphology, lead content, and mitochondrial respiration in brains of immature and adult rats.
Author:
Hsu JS, Herman MM, Hsu HJ, Mortell P
Year:
1980
Bibliographic source:
VIRCHOWS ARCH A PATHOL ANAT HISTOL; 387 (2).

Materials and methods

Test guideline
Qualifier:
no guideline followed
Principles of method if other than guideline:
The toxic effects of inorganic lead feedings on the immature brain were studied in the rat pup.
PbCO3 was fed to nursing mothers and then to pups directly after weaning. Results in lead-fed pups were compared to age-matched controls and to lead-fed young adult males (60 days old).
GLP compliance:
not specified
Limit test:
no

Test material

Constituent 1
Chemical structure
Reference substance name:
Lead carbonate
EC Number:
209-943-4
EC Name:
Lead carbonate
Cas Number:
598-63-0
Molecular formula:
CH2O3.Pb
IUPAC Name:
λ²-lead(2+) carbonate

Test animals

Species:
rat
Strain:
Sprague-Dawley
Sex:
male/female

Administration / exposure

Route of administration:
oral: feed
Vehicle:
unchanged (no vehicle)
Analytical verification of doses or concentrations:
not specified
Duration of treatment / exposure:
2 d: 7 animals
1 wk: 3 animals
2 wk: 3 animals
Frequency of treatment:
ad libitum
Doses / concentrations
Remarks:
Doses / Concentrations:
4 %
Basis:
nominal in diet
Control animals:
yes, plain diet

Results and discussion

Applicant's summary and conclusion

Conclusions:
Altered mitochondrial respiration occurs early in regional and age-dependent association with lead encephalopathy in the rat pup.
The development of lead encephalopathy also is associated with increased mitochondrial lead concentrations.

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