| pubmed-article:10894127 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0007804 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0023175 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0038727 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0017431 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0332157 | lld:lifeskim |
| pubmed-article:10894127 | lifeskim:mentions | umls-concept:C0699900 | lld:lifeskim |
| pubmed-article:10894127 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:10894127 | pubmed:dateCreated | 2000-11-7 | lld:pubmed |
| pubmed-article:10894127 | pubmed:abstractText | Lead exposure causes cognitive and behavioral deficits in some affected children. We propose that a contributing mechanism for the neurological damage is that lead induces critically low levels of arylsulfatase A (ASA) at sensitive stages of nervous system development. It is hypothesized that the combined effects of a single nucleotide polymorphism (SNP) in human ASA which results in reduced levels of the enzyme, and lead concentrations which decrease ASA activity culminate in cellular enzymic activity that is below a critical threshold required for the maintenance of normal nervous system function. Human fibroblasts grown in the presence of 20 microM lead acetate exhibit a more than 60% decrease of cellular ASA enzyme protein. Lead treatment of cells from individuals with the SNP(s) of pseudodeficient ASA, but not those from subjects with the normal gene, results in a significant decrease in ability of the cells to desulfate sulfatide, the substrate of ASA. The decrease in the degree of sulfatide catabolism is consistent with possible enhanced lead-induced neurobehavioral effects in individuals homozygous for the pseudodeficiency polymorphism(s) of ASA. | lld:pubmed |
| pubmed-article:10894127 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10894127 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10894127 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10894127 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10894127 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10894127 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10894127 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10894127 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10894127 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10894127 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:10894127 | pubmed:issn | 0161-813X | lld:pubmed |
| pubmed-article:10894127 | pubmed:author | pubmed-author:DemlMM | lld:pubmed |
| pubmed-article:10894127 | pubmed:author | pubmed-author:YanoII | lld:pubmed |
| pubmed-article:10894127 | pubmed:author | pubmed-author:ManowitzPP | lld:pubmed |
| pubmed-article:10894127 | pubmed:author | pubmed-author:PoretzR DRD | lld:pubmed |
| pubmed-article:10894127 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10894127 | pubmed:volume | 21 | lld:pubmed |
| pubmed-article:10894127 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10894127 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10894127 | pubmed:pagination | 379-87 | lld:pubmed |
| pubmed-article:10894127 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:10894127 | pubmed:meshHeading | pubmed-meshheading:10894127... | lld:pubmed |
| pubmed-article:10894127 | pubmed:meshHeading | pubmed-meshheading:10894127... | lld:pubmed |
| pubmed-article:10894127 | pubmed:meshHeading | pubmed-meshheading:10894127... | lld:pubmed |
| pubmed-article:10894127 | pubmed:meshHeading | pubmed-meshheading:10894127... | lld:pubmed |
| pubmed-article:10894127 | pubmed:meshHeading | pubmed-meshheading:10894127... | lld:pubmed |
| pubmed-article:10894127 | pubmed:meshHeading | pubmed-meshheading:10894127... | lld:pubmed |
| pubmed-article:10894127 | pubmed:meshHeading | pubmed-meshheading:10894127... | lld:pubmed |
| pubmed-article:10894127 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10894127 | pubmed:articleTitle | The interaction of lead exposure and arylsulfatase A genotype affects sulfatide catabolism in human fibroblasts. | lld:pubmed |
| pubmed-article:10894127 | pubmed:affiliation | Department of Biochemistry and Microbiology, Rutgers University, New Brunswick, NJ 08901-8525, USA. poretz@rci.rutgers.edu | lld:pubmed |
| pubmed-article:10894127 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10894127 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10894127 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10894127 | lld:pubmed |
