PMID- 26774051
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20161230
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 318
DP  - 2016 Mar 24
TI  - Prenatal maternal lipopolysaccharide administration leads to age- and 
      region-specific oxidative stress in the early developmental stage in offspring.
PG  - 84-93
LID - S0306-4522(16)00021-X [pii]
LID - 10.1016/j.neuroscience.2016.01.002 [doi]
AB  - Prenatal exposure to lipopolysaccharide (LPS) has been exploited to simulate 
      brain disorder in animal model. Prenatal LPS-exposure has shown elevated levels 
      of pro-inflammatory cytokines in the early stages of the postnatal period. This 
      study determines the effect of prenatal LPS-exposure on oxidative stress (OS) in 
      the distinct brain regions in the early postnatal stages. LPS (50 mug/kg, i.p.) 
      and water for injection (100 mul, i.p.) were given to the experimental (n=5) and 
      control (n=5) group of pregnant Swiss albino mice respectively on gestational day 
      (GD)-16 and 17. Animals were decapitated on postnatal day (PnD) - 1, 7, 14 and 21 
      to assay levels of oxidative markers from 6 distinct brain regions. When compared 
      with the control, prenatal LPS-exposure alters levels of OS markers: (i) on 
      PnD-1, glutathione (GSH) level is raised and superoxide dismutase (SOD) activity 
      is dropped, (ii) on PnD-7, advanced oxidation of protein product (AOPP) level is 
      elevated, (iii) on PnD-14, lipid peroxidation (MDA) and activity of catalase 
      (CAT) are enhanced, (iv) on PnD-21, increased MDA continued. The hippocampus (HC) 
      and cerebellum (CB) were mostly susceptible to OS in the early postnatal 
      development. Levels of MDA and activity of CAT enzyme were increased on PnD-14 in 
      the cortex, HC and CB. Except MDA, all OS markers recovered and returned to the 
      level of control animals on PnD-21. Taken together, these results suggest that 
      prenatal LPS-exposure induces age- and region-specific OS in the early postnatal 
      stage.
CI  - Copyright (c) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Al-Amin, M M
AU  - Al-Amin MM
AD  - Department of Pharmaceutical Sciences, North South University, Bashundhara, 
      Dhaka, Bangladesh; The Queensland Brain Institute, The University of Queensland, 
      QBI Building 79, St Lucia, QLD 4072, Australia. Electronic address: 
      mamun.al-amin@northsouth.edu.
FAU - Alam, T
AU  - Alam T
AD  - Department of Pharmaceutical Sciences, North South University, Bashundhara, 
      Dhaka, Bangladesh.
FAU - Hasan, S M N
AU  - Hasan SM
AD  - Department of Pharmaceutical Sciences, North South University, Bashundhara, 
      Dhaka, Bangladesh.
FAU - Hasan, A T
AU  - Hasan AT
AD  - Department of Pharmaceutical Sciences, North South University, Bashundhara, 
      Dhaka, Bangladesh.
FAU - Quddus, A H M R
AU  - Quddus AH
AD  - National University, Gazipur, Bangladesh.
LA  - eng
PT  - Journal Article
DEP - 20160108
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Aging
MH  - Animals
MH  - Brain/*drug effects/metabolism
MH  - Disease Models, Animal
MH  - Female
MH  - Lipid Peroxidation/*drug effects
MH  - Lipopolysaccharides/*pharmacology
MH  - Male
MH  - Mice
MH  - Oxidative Stress/*drug effects
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*metabolism
OTO - NOTNLM
OT  - LPS
OT  - cerebellum
OT  - hippocampus
OT  - oxidative stress
OT  - superoxide dismutase
EDAT- 2016/01/17 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/01/17 06:00
PHST- 2015/08/05 00:00 [received]
PHST- 2016/01/03 00:00 [revised]
PHST- 2016/01/04 00:00 [accepted]
PHST- 2016/01/17 06:00 [entrez]
PHST- 2016/01/17 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
AID - S0306-4522(16)00021-X [pii]
AID - 10.1016/j.neuroscience.2016.01.002 [doi]
PST - ppublish
SO  - Neuroscience. 2016 Mar 24;318:84-93. doi: 10.1016/j.neuroscience.2016.01.002. 
      Epub 2016 Jan 8.