Lead and Hyperactivity

David, Oliver; Clark, Julian; Voeller, Kytja K. S.

doi:10.1016/s0140-6736(72)92534-2

Cited by 311 publications

(82 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The increased susceptibility of young animals is due in part to their increased capacity to absorb lead from the gastrointestinal tract (3,4,(27)(28)(29). Such observations have been extended to include young children (1,5,10,30,31). In addition to increased lead retention, age-related differences in tissue distribution also contribute to the enhanced sensitivity of the young to lead poisoning.…”

Section: Discussionmentioning

confidence: 99%

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

Rader¹,

Peeler²,

Mahaffey³

1981

Environ Health Perspect

View full text Add to dashboard Cite

The relative toxicity of low doses of lead acetate provided steadily in drinking water or by mouth once per week was studied in weanling and adult rats. Free erythrocyte protoporphyrin and urinary 8-aminolevulinic acid levels were measured, as well as lead levels in blood and kidney. The accumulation of lead in brain tissue and in bone (femur) was measured to determine the effect of age and schedule of administration on tissue distribution and retention of lead. Total intakes of lead during the 60-week experimental period were: weanling and adult rats exposed to drinking water supplemented with 200 ,g of lead acetate/ml: 127 + 10 mg and 160 ± 16 mg, respectively; weanling and adult rats dosed with lead acetate orally once per week: 132 mg and 161 mg, respectively. Increased toxic effects of lead in the weanling animals were apparent in most of the parameters measured (urinary 8-aminolevulinic acid and blood, brain, femur and kidney lead levels). This pattern was observed in weanling rats exposed to lead steadily through drinking water or dosed orally with an equivalent quantity of lead once per week. Lead levels in blood were highly correlated with the accumulation of lead in brain, femur, and kidney tissue in both groups of weanling rats. In adult rats, significant correlations between blood lead and kidney lead and between blood lead and femur lead were found only in the rats receiving lead steadily in drinking water.

show abstract

Section: Discussionmentioning

confidence: 99%

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

Rader¹,

Peeler²,

Mahaffey³

1981

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…Chronic exposure of children to lead was found to be associated with behavioral disorders, learning disabilities and mental retarda tion (38)(39)(40). Animal studies also demonstrated that chronic perinatal low level of lead exposure produced alterations of both learned and spontaneous behavioral patterns (10,11,(41)(42)(43)(44).…”

Section: Discussionmentioning

confidence: 99%

Impact of Lead Toxicity on Brain Metabolisms of Nucleic Acid and Catecholamine in Protein Malnourished Rats.

Ghosh

Chatterjee

Gupta

1992

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

View full text Add to dashboard Cite

SummaryThe brain biochemistry in terms of certain key substances of brain were studied in 18% protein and 6% protein-fed rats following lead ingestion at a level of 1% in the diet. Lead ingestion diminished the protein and increased the RNA content of brain, and, consequently reduced the protein/RNA ratio. The RNA/DNA ratio in brain was elevated in lead toxicity, while the protein/DNA ratio remained unaltered. The RNase and DNase activities of brain were decreased. Lead treatment diminished the glutathione (GSH) level of blood but the GSH level of brain was not altered significantly by the lead treatment. The plasma protein level was also diminished after lead treatment. The effects of lead on some of these parameters were found to be more pronounced in rats receiving the 6% protein diet. The serotonin (5-HT) level of brain was reduced, while the norepinephrine (NE) and dopamine (DA) levels of brain were elevated following lead treatment. The monoamine oxidase (MAO) and tryptophan hydroxylase (TPH) activities and 5-hydroxy indole acetic acid (5-HIAA) content of brain were elevated in lead ingested rats. The effects of lead on these parameters were found to be potentiated when the rats were fed on a 6% protein diet. These studies suggest that lead at the present dose affects brain biochemistry in terms of both nucleic acids and amine metabolism, and protein deficiency potenti ates some of these lead-induced changes.

show abstract

“…Impulsivity, hyperactivity, perceptual disorders, and learning disabilities are frequent symptoms in children who in early infancy and childhood have been exposed to lead (63)(64)(65)(66)(67)(68)(69)(70)(71). In severe cases oflead poisoning, mental retardation and other hard neurological symptoms may also be present (63,65,72).…”

mentioning

confidence: 99%

Morphological and behavioral markers of environmentally induced retardation of brain development: an animal model.

Altman

1987

Environ Health Perspect

View full text Add to dashboard Cite

In most neurotoxicological studies morphological assessment focuses on pathological effects, like degenerative changes in neuronal perikarya, axonopathy, demyelination, and glial and endothelial cell reactions. Similarly, the assessment of physiological and behavioral effects center on evident neurological symptoms, like EEG and EMG abnormalities, resting and intention tremor, abnormal gait, and abnormal reflexes. This paper reviews briefly another central nervous system target of harmful environmental agents, which results in behavioral abnormalities without any qualitatively evident neuropathology. This is called microneuronal hypoplasia, a retardation of brain development characterized by a quantitative reduction in the normal population of late-generated, short-axoned neurons in specific brain regions.Correlated descriptive and experimental neurogenetic studies in the rat have established that all the cerebellar granule cells and a very high proportion of hippocampal granule cells are produced postnatally, and that focal, low-dose X-irradiation either of the cerebellum or of the hippocampus after birth selectively interferes with the acquisition of the full complement of granule cells (microneuronal hypoplasia). Subsequent behavioral investigations showed that cerebellar microneuronal hypoplasia results in profound hyperactivity without motor abnormalities, while hippocampal microneuronal hypoplasia results in hyperactivity, as well as attentional and learning deficits.There is much indirect clinical evidence that various harmful environmental agents affecting the pregnant mother and/or the infant lead to such childhood disorders as hyperactivity and attentional and learning disorders. As the developing human brain is more mature at birth than the rat brain, the risk for microneuronal hypoplasia and consequent behavioral disorders may be highest at late stages of fetal development, in prematurely born and small-for-weight infants, and during the early stages of infant development. Recent technological advances in brain imaging techniques make it possible to test this hypothesis and to assess the possible relationship between the degree of retarded brain development and ensuing behavioral disorders.

show abstract

Lead and Hyperactivity

Cited by 311 publications

References 8 publications

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

Impact of Lead Toxicity on Brain Metabolisms of Nucleic Acid and Catecholamine in Protein Malnourished Rats.

Morphological and behavioral markers of environmentally induced retardation of brain development: an animal model.

Contact Info

Product

Resources

About