Literature DB >> 7991218

Homogeneity of regional brain lead concentrations.

D V Widzowski1, D A Cory-Slechta.   

Abstract

It has been proposed that the neurobiological basis of many of the behavioral manifestations arising in response to Pb exposure may be due to selective vulnerability of particular brain regions, such as hippocampus, a region in which preferential accumulation has been reported in some studies. However, these findings have not been invariant and, in fact, have been found to vary with dosing parameters. This study examined potential regional accumulation of Pb in brain following postnatal exposure of rats to Pb via nursing dams consuming Pb acetate solutions of 0, 100, 350, 1000, or 2000 ppm. Offspring were sacrificed at 7, 14, 21, 40 or 60 days of age and brains dissected into 12 regions, including striatum, nucleus accumbens, hypothalamus, thalamus, ventral (tegmentum) and dorsal (tectum) midbrain, hippocampus, frontal, parietal/temporal, and occipital cortices, cerebellum and brain stem for regional Pb analyses. All brain regions generally accumulated Pb in a similar pattern. Regional elimination half-lives, determined for the 350, 1000 and 2000 ppm exposure groups, averaged about 20 days and did not vary between regions. Regional brain Pb levels were not different whether brains were perfused or not prior to brain Pb determinations. However, regional differences in brain Pb levels could be introduced by using dry, rather than wet weights in the calculation of Pb concentrations, and by procedures including soaking in formaldehyde prior to drying, probably as a result of the differential fluid volume of different brain regions. Taken together, these data do not support previous findings of selective regional accumulation of Pb in any brain region, including the hippocampus, at least under conditions of postnatal Pb exposure and wet weight measures. While there may indeed be differences among brain regions in sensitivity to Pb, any differences in response among brain regions should probably be ascribed to differences in the interactions of Pb with biochemical or cellular targets unique or enriched in that region rather than to differences in accumulation of Pb.

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Year:  1994        PMID: 7991218

Source DB:  PubMed          Journal:  Neurotoxicology        ISSN: 0161-813X            Impact factor:   4.294


  14 in total

1.  Developmental lead exposure and two-way active avoidance training alter the distribution of protein kinase C activity in the rat hippocampus.

Authors:  H H Chen; T Ma; I A Paul; J L Spencer; I K Ho
Journal:  Neurochem Res       Date:  1997-09       Impact factor: 3.996

2.  Mechanisms of lead and manganese neurotoxicity.

Authors:  April P Neal; Tomas R Guilarte
Journal:  Toxicol Res (Camb)       Date:  2013-03-01       Impact factor: 3.524

3.  Cumulative exposure to lead and cognition in persons with Parkinson's disease.

Authors:  Jennifer Weuve; Daniel Z Press; Francine Grodstein; Robert O Wright; Howard Hu; Marc G Weisskopf
Journal:  Mov Disord       Date:  2012-11-09       Impact factor: 10.338

4.  Protein kinase C in rat brain is altered by developmental lead exposure.

Authors:  H H Chen; T Ma; I K Ho
Journal:  Neurochem Res       Date:  1999-03       Impact factor: 3.996

Review 5.  Molecular targets of lead in brain neurotoxicity.

Authors:  Carla Marchetti
Journal:  Neurotox Res       Date:  2003       Impact factor: 3.911

6.  CNS effects of developmental Pb exposure are enhanced by combined maternal and offspring stress.

Authors:  M B Virgolini; A Rossi-George; R Lisek; D D Weston; M Thiruchelvam; D A Cory-Slechta
Journal:  Neurotoxicology       Date:  2008-03-16       Impact factor: 4.294

7.  Chronic low-level lead exposure affects the monoaminergic system in the mouse superior olivary complex.

Authors:  Tyler Fortune; Diana I Lurie
Journal:  J Comp Neurol       Date:  2009-04-10       Impact factor: 3.215

8.  Sex-dependent impacts of low-level lead exposure and prenatal stress on impulsive choice behavior and associated biochemical and neurochemical manifestations.

Authors:  Hiromi I Weston; Douglas D Weston; Joshua L Allen; Deborah A Cory-Slechta
Journal:  Neurotoxicology       Date:  2014-07-07       Impact factor: 4.294

9.  Alterations in glucocorticoid negative feedback following maternal Pb, prenatal stress and the combination: a potential biological unifying mechanism for their corresponding disease profiles.

Authors:  A Rossi-George; M B Virgolini; D Weston; D A Cory-Slechta
Journal:  Toxicol Appl Pharmacol       Date:  2008-10-15       Impact factor: 4.219

10.  Enhanced stimulus sequence-dependent repeated learning in male offspring after prenatal stress alone or in conjunction with lead exposure.

Authors:  D A Cory-Slechta; M B Virgolini; S Liu; D Weston
Journal:  Neurotoxicology       Date:  2012-07-13       Impact factor: 4.294

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