PMID- 17333127
OWN - NLM
STAT- MEDLINE
DCOM- 20070921
LR  - 20121115
IS  - 0340-5761 (Print)
IS  - 0340-5761 (Linking)
VI  - 81
IP  - 6
DP  - 2007 Jun
TI  - Exposure of C6 glioma cells to Pb(II) increases the phosphorylation of p38(MAPK) 
      and JNK1/2 but not of ERK1/2.
PG  - 407-14
AB  - Pb(II) is a neurotoxic pollutant that produces permanent cognitive deficits in 
      children. Pb(II) can modulate cell signaling pathways and cell viability in a 
      variety of cell types. However, these actions are not well demonstrated on glial 
      cells, which represent an important target for metals into the central nervous 
      system. The present work was undertaken to determine the ability of Pb(II) in 
      modulating the activity of mitogen activated protein kinases (MAPKs) in cultures 
      of C6 rat glioma cells, a useful functional model for the study of astrocytes. 
      Additionally, cell viability was analyzed by measurement of MTT reduction. Cells 
      were exposed to lead acetate 0.1, 1, 10 microM for 24 and 48 h. MAPKs activation 
      - in particular ERK1/2, p38(MAPK) and JNK1/2 - were analyzed by western blotting. 
      Results showed that 10 microM Pb(II) treatment for 24 h caused a discrete 
      stimulation of p38(MAPK) phosphorylation. However, 1 and 10 microM Pb(II) 
      treatment for 48 h provoked a significant stimulation in the phosphorylation 
      state of p38(MAPK) and JNK1/2. The phosphorylation state of ERK1/2 was not 
      modified by any Pb(II) treatment. Moreover, data indicate that at 48 h treatment 
      even 1 microM Pb(II) can be cytotoxic, causing impairment on cell viability. 
      Therefore, depending on a long incubation period, a significant concomitant 
      activation of p38(MAPK) and JNK1/2 by Pb(II) took place in parallel with the 
      impairment of C6 glioma cells viability.
FAU - Posser, Thais
AU  - Posser T
AD  - Departamento de Bioquimica, Centro de Ciencias Biologicas, Universidade Federal 
      de Santa Catarina, Florianopolis, SC, 88040-900, Brazil.
FAU - de Aguiar, Claudia B N Mendes
AU  - de Aguiar CB
FAU - Garcez, Ricardo C
AU  - Garcez RC
FAU - Rossi, Francesco M
AU  - Rossi FM
FAU - Oliveira, Camila S
AU  - Oliveira CS
FAU - Trentin, Andrea G
AU  - Trentin AG
FAU - Neto, Vivaldo Moura
AU  - Neto VM
FAU - Leal, Rodrigo B
AU  - Leal RB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070228
PL  - Germany
TA  - Arch Toxicol
JT  - Archives of toxicology
JID - 0417615
RN  - 0 (Environmental Pollutants)
RN  - 0 (Organometallic Compounds)
RN  - EC 2.7.1.24 (Mitogen-Activated Protein Kinase 9)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - RX077P88RY (lead acetate)
SB  - IM
MH  - Animals
MH  - Brain Neoplasms/*enzymology/pathology
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Environmental Pollutants/*toxicity
MH  - Glioma/*enzymology/pathology
MH  - MAP Kinase Signaling System/*drug effects
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3/metabolism
MH  - Mitogen-Activated Protein Kinase 8/*metabolism
MH  - Mitogen-Activated Protein Kinase 9/*metabolism
MH  - Organometallic Compounds/*toxicity
MH  - Phosphorylation
MH  - Rats
MH  - Time Factors
MH  - p38 Mitogen-Activated Protein Kinases/*metabolism
EDAT- 2007/03/03 09:00
MHDA- 2007/09/22 09:00
CRDT- 2007/03/03 09:00
PHST- 2006/08/08 00:00 [received]
PHST- 2007/01/09 00:00 [accepted]
PHST- 2007/03/03 09:00 [pubmed]
PHST- 2007/09/22 09:00 [medline]
PHST- 2007/03/03 09:00 [entrez]
AID - 10.1007/s00204-007-0177-6 [doi]
PST - ppublish
SO  - Arch Toxicol. 2007 Jun;81(6):407-14. doi: 10.1007/s00204-007-0177-6. Epub 2007 
      Feb 28.