PMID- 30003842
OWN - NLM
STAT- MEDLINE
DCOM- 20181227
LR  - 20200204
IS  - 1477-0393 (Electronic)
IS  - 0748-2337 (Linking)
VI  - 34
IP  - 10
DP  - 2018 Oct
TI  - Effect of developmental lead exposure on neurogenesis and cortical neuronal 
      morphology in Wistar rats.
PG  - 665-678
LID - 10.1177/0748233718781283 [doi]
AB  - Lead (Pb) is a neurotoxic heavy metal that largely affects the developing nervous 
      system. The present study examined the temporal effect of perinatal Pb exposure 
      on neurogenesis and cortical neuronal morphology. Wistar pregnant rats were 
      exposed to 0.5% lead acetate throughout pregnancy and to postnatal day (PD) 28. 
      Offspring were grouped as gestational day (GD) 18 and 21 and PD 7, 14, 21, and 28 
      in both control and experimental groups. Brain sections were processed for 
      immunohistological staining with anti-proliferating cell nuclear antigen (PCNA) 
      or glial fibrillary acidic protein (GFAP). Brains from 14, 21, and 28 PDs pups 
      were processed for Golgi-Cox stain. Pb exposure significantly increased 
      PCNA-positive nuclei in the ventricular and subventricular zones of the lateral 
      ventricle at 18 and 21 GDs. Postnatally, the Pb-treated groups showed a 
      significant decrease in PCNA-positivity and neuron density compared to control. 
      This reduction was associated with an increase in damaged or apoptotic cell 
      profiles in the experimental groups. At PD 21, there was a significant increase 
      in GFAP immunoreactivity in Pb-exposed groups compared with control. Furthermore, 
      the total apical and basal dendritic length of pyramidal neurons in layer 2-3 of 
      the Golgi-Cox stained sensorimotor cortex was comparable in both control and 
      Pb-exposed groups. Spine density per 10 microm was significantly increased at PD 14 
      and 21 on the apical dendrites but not basal dendrites of Pb-treated groups. In 
      conclusion, developmental Pb exposure in rats induces a toxic effect on 
      neurogenesis and on cortical neurons, which may be related to cognitive 
      disabilities observed in children exposed to lead.
FAU - Mousa, Alyaa M A
AU  - Mousa AMA
AD  - 1 Department of Anatomy, Faculty of Medicine, Kuwait University, Safat, Kuwait.
FAU - Elshahat, Mona A
AU  - Elshahat MA
AD  - 2 Anatomy Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
FAU - Renno, Waleed M
AU  - Renno WM
AUID- ORCID: 0000-0001-9024-9712
AD  - 1 Department of Anatomy, Faculty of Medicine, Kuwait University, Safat, Kuwait.
LA  - eng
PT  - Journal Article
DEP - 20180713
PL  - England
TA  - Toxicol Ind Health
JT  - Toxicology and industrial health
JID - 8602702
RN  - 0 (GFAP protein, rat)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Proliferating Cell Nuclear Antigen)
RN  - 2P299V784P (Lead)
SB  - IM
MH  - Animals
MH  - Cerebral Cortex/*drug effects/pathology
MH  - Female
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Lead/*toxicity
MH  - Neurogenesis/*drug effects
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*pathology
MH  - Proliferating Cell Nuclear Antigen/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Sensorimotor Cortex/drug effects/pathology
OTO - NOTNLM
OT  - Lead exposure
OT  - cerebellum
OT  - glial fibrillary acidic protein
OT  - neurogenesis
OT  - proliferating cell nuclear antigen
EDAT- 2018/07/14 06:00
MHDA- 2018/12/28 06:00
CRDT- 2018/07/14 06:00
PHST- 2018/07/14 06:00 [pubmed]
PHST- 2018/12/28 06:00 [medline]
PHST- 2018/07/14 06:00 [entrez]
AID - 10.1177/0748233718781283 [doi]
PST - ppublish
SO  - Toxicol Ind Health. 2018 Oct;34(10):665-678. doi: 10.1177/0748233718781283. Epub 
      2018 Jul 13.