Lead stimulates ERK1/2 and p38MAPK phosphorylation in the hippocampus of immature rats

Córdova, Fabiano Mendes de; Rodrigues, Ana Lúcia S.; Giacomelli, Maria Bertı́lia Oss; Oliveira, Claudio; Posser, Thaís; Dunkley, Peter R.; Leal, Rodrigo Bainy

doi:10.1016/j.brainres.2003.11.012

Cited by 84 publications

(55 citation statements)

References 57 publications

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“…As expected, high level lead exposure might significantly result high BLLs of rats. Our findings show that the measurement of BLLs is an excellent indication of Pb exposure as reported by others [38,39]. Pb in circulation can enter the central nervous system (CNS) and induce negative effects.…”

Section: Discussionsupporting

confidence: 57%

Lead Affects Apoptosis and Related Gene XIAP and Smac Expression in the Hippocampus of Developing Rats

Liu

Han

et al. 2009

Neurochem Res

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Lead (Pb) exposure poses devastating effects on central nervous system development of children. To replicate aspects of this neurotoxicity, we examined the effect of lead on the expression of apoptosis and of apoptosis-related genes, XIAP (X chromosome-linked inhibitor of apoptosis protein) and Smac (second mitochondrial activator of caspase), in the hippocampus of developing rats. A total of 48 rats (30-day old) were randomly divided into four groups for intragastrical perfusion of lead acetate [Pb(Ac)2]: untreated, low (2 mg/kg/d), medium (20 mg/kg/d), and high (200 mg/kg/d) dose groups. Pb content was determined in blood, and the apoptosis indexes and XIAP and Smac gene expression were analyzed in the hippocampus. There was a significant difference in apoptosis indexes (AI) between the exposed and control groups (p < 0.01). AI was highest in the high exposure group. XIAP gene expression was reduced in the exposed groups and the expression was negatively correlated with blood lead levels (BLLs) (p < 0.05). But the four groups did not differ in the expression of Smac (p > 0.05). Our data indicate that exposure to Pb(Ac)2 caused a dose-dependent and significant increase of apoptosis in the hippocampus of developing rats through depressing the expression of the XIAP but not the Smac genes.

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Section: Discussionsupporting

confidence: 57%

Lead Affects Apoptosis and Related Gene XIAP and Smac Expression in the Hippocampus of Developing Rats

Liu

Han

et al. 2009

Neurochem Res

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“…For example, Pb2+ has been shown to interfere with MAPK signaling as it increases the phosphorylation of both ERK1/2 and p38(MAPK) (Cordova et al, 2004). However, the findings regarding calcium/calmodulin kinase II (CamKII) activity are not clear .…”

Section: Empirical Support For Linkagementioning

confidence: 99%

Adverse Outcome Pathway on chronic binding of antagonist to N-methyl-D-aspartate receptors (NMDARs) during brain development induces impairment of learning and memory abilities

Sachana

Munn

Bal‐Price

2016

OECD Series on Adverse Outcome Pathways

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“…The components of the transcription pathway, p38 MAPK and ERK1/2 were phosphorylated more when incubated with Pb 2+ and Cd 2+ . As discussed earlier, P38 MAPK is involved in the induction of LTD whereas ERK1/2 is involved in induction of LTP-3 [79,80,229].…”

Section: Summary Of Long-term Effectsmentioning

confidence: 99%

“…Also, in vivo developmental exposure to 2 mg/kg of Pb 2+ increased both ERK1 and ERK2 phosphorylation in rat hippocampal neurons [80].…”

Section: Disruption Of Long-term Potentiation By Exposure Tomentioning

confidence: 99%

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Metal toxicity at the synapse: presynaptic, postsynaptic and long-term effects

Ghazala

Sadiq

Chowdhury

et al. 2010

Qatar Foundation Annual Research Forum Proceedings

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Metal neurotoxicity is a global health concern. This paper summarizes the evidence for metal interactions with synaptic transmission and synaptic plasticity. Presynaptically metal ions modulate neurotransmitter release through their interaction with synaptic vesicles, ion channels, and the metabolism of neurotransmitters (NT). Many metals (e.g., Pb 2+ , Cd 2+ , and Hg + ) also interact with intracellular signaling pathways. Postsynaptically, processes associated with the binding of NT to their receptors, activation of channels, and degradation of NT are altered by metals. Zn 2+ , Pb 2+ , Cu 2+ , Cd 2+ , Ni 2+ , Co 2+ , Li 3+ , Hg + , and methylmercury modulate NMDA, AMPA/kainate, and/or GABA receptors activity. Al 3+ , Pb 2+ , Cd 2+ , and As 2 O 3 also impair synaptic plasticity by targeting molecules such as CaM, PKC, and NOS as well as the transcription machinery involved in the maintenance of synaptic plasticity. The multiple effects of metals might occur simultaneously and are based on the specific metal species, metal concentrations, and the types of neurons involved.

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Lead stimulates ERK1/2 and p38MAPK phosphorylation in the hippocampus of immature rats

Cited by 84 publications

References 57 publications

Lead Affects Apoptosis and Related Gene XIAP and Smac Expression in the Hippocampus of Developing Rats

Lead Affects Apoptosis and Related Gene XIAP and Smac Expression in the Hippocampus of Developing Rats

Adverse Outcome Pathway on chronic binding of antagonist to N-methyl-D-aspartate receptors (NMDARs) during brain development induces impairment of learning and memory abilities

Metal toxicity at the synapse: presynaptic, postsynaptic and long-term effects

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