Literature DB >> 10814846

Developmental lead exposure disturbs expression of synaptic neural cell adhesion molecules in herring gull brains.

P M Dey1, J Burger, M Gochfeld, K R Reuhl.   

Abstract

Neurobehavioral testing of herring gull chicks (Larus argentatus) in both laboratory and field studies indicates that lead exposure during critical periods of development causes neurological deficits that may compromise survival in the wild. Accumulating evidence suggests that lead impairs neurodevelopment, in part, by altering the expression of cell adhesion molecules (CAMs) responsible for the proper formation and maintenance of neural structure and synaptic function. We examined the adhesion molecules NCAM, L1, and N-cadherin in gull brains to determine whether these CAMs are altered by lead exposure and might serve as markers of developmental neurotoxicity. One-day-old chicks were collected from nesting colonies and were laboratory housed. On post-hatching day (PHD) 2, chicks were given 100 mg/kg lead acetate or saline (intraperitoneally). Birds were killed on PHD 34, 44, or 55 (blood-lead levels averaged 27.4, 20.8, and 19.5 microg/dl, respectively). Brains were removed and stored at -70 degrees C until analysis. Expression of CAMs was determined in synaptosomal preparations by Western blotting and the activity of NCAM-associated sialyltransferase (ST) was determined in purified whole brain golgi apparatus. Elevation in synaptosomal polysialylated NCAM expression and a significant increase in golgi ST activity was observed in lead-treated animals at PHD 34. Reductions in synaptosomal N-cadherin were observed at PHD 34 and 44, while L1 expression appeared unaffected by lead at any time-point. By 55 days post-hatching, no differences in N-cadherin expression, polysialylated NCAM expression or NCAM-associated ST activity were seen in lead-treated animals as compared with age-matched control animals. Lead-induced disruption of CAM expression during early neurodevelopment may contribute to behavioral deficits observed in herring gulls in both the laboratory and the field, and may serve as a marker for heavy metal exposure during postnatal development.

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Year:  2000        PMID: 10814846     DOI: 10.1016/s0300-483x(00)00171-2

Source DB:  PubMed          Journal:  Toxicology        ISSN: 0300-483X            Impact factor:   4.221


  5 in total

Review 1.  Defining potential roles of Pb(2+) in neurotoxicity from a calciomics approach.

Authors:  Rakshya Gorkhali; Kenneth Huang; Michael Kirberger; Jenny J Yang
Journal:  Metallomics       Date:  2016-06-01       Impact factor: 4.526

2.  Lead poisoning and the deceptive recovery of the critically endangered California condor.

Authors:  Myra E Finkelstein; Daniel F Doak; Daniel George; Joe Burnett; Joseph Brandt; Molly Church; Jesse Grantham; Donald R Smith
Journal:  Proc Natl Acad Sci U S A       Date:  2012-06-25       Impact factor: 11.205

3.  Glioprotective effects of Ashwagandha leaf extract against lead induced toxicity.

Authors:  Praveen Kumar; Raghavendra Singh; Arshed Nazmi; Dinesh Lakhanpal; Hardeep Kataria; Gurcharan Kaur
Journal:  Biomed Res Int       Date:  2014-05-28       Impact factor: 3.411

4.  Selenium against lead-induced apoptosis in chicken nervous tissues via mitochondrial pathway.

Authors:  Yihao Zhu; Xiaoyan Jiao; Yang An; Shu Li; Xiaohua Teng
Journal:  Oncotarget       Date:  2017-11-20

5.  The Effect of Ascorbic Acid and Garlic Administration on Lead-Induced Neural Damage in Rat Offspring's Hippocampus.

Authors:  Akram Sadeghi; Alireza Ebrahimzadeh Bideskan; Fatemeh Alipour; Alireza Fazel; Hossein Haghir
Journal:  Iran J Basic Med Sci       Date:  2013-02       Impact factor: 2.699

  5 in total

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