2001
DOI: 10.1016/s0300-483x(01)00415-2
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Astroglial reaction during the early phase of acute lead toxicity in the adult rat brain

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Cited by 69 publications
(28 citation statements)
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“…Lead alters the permeability of the mature blood-brain barrier, 31 accumulates in astroglia, 32 which are essential to maintenance of the neuronal environment, especially regarding the excitotoxic neurotransmitter glutamate, and affects glutamate homeostasis. 32,33 Adult lead exposure can produce apoptotic cell death in retinal and hippocampal cells and may interfere with long-term potentiation. 34,35 Lead may alter energy metabolism in mitochondria and synaptosomes, 36 and can interfere with several calcium- vs no ε4 allele).…”
Section: Discussionmentioning
confidence: 99%
“…Lead alters the permeability of the mature blood-brain barrier, 31 accumulates in astroglia, 32 which are essential to maintenance of the neuronal environment, especially regarding the excitotoxic neurotransmitter glutamate, and affects glutamate homeostasis. 32,33 Adult lead exposure can produce apoptotic cell death in retinal and hippocampal cells and may interfere with long-term potentiation. 34,35 Lead may alter energy metabolism in mitochondria and synaptosomes, 36 and can interfere with several calcium- vs no ε4 allele).…”
Section: Discussionmentioning
confidence: 99%
“…Importantly, astrocytes stimulated by proinflammatory cytokines are a major source of chemokines, as well as other bioactive molecules, that can affect bloodbrain barrier integrity, macrophage migration into the brain, and neuronal function (Epstein, 1998;Ge and Pachter, 2004). Astrogliosis is a prominent feature of early HIV-1 infection in the brain (Masliah et al, 1996), and likely serves in the capacity of maintaining neuroprotective functions during disease (Struzynska et al, 2001). Taken together, astrocyte dysfunction may seriously affect neuronal function and viability.…”
Section: Discussionmentioning
confidence: 99%
“…Eight genes coding for proteins with antiapoptotic function (GO:0006916) were prominent in the CR, including peroxiredoxin-2, peroxiredoxin-3, and ornithine decarboxylase antizyme. Regional enrichment of these genes may explain the overall resistance of the CR to damage that is initiated by neurotoxic insult (Struzynska et al, 2001). Moreover, in patients with Creutzfeldt-Jakob disease peroxiredoxin-2 decreases in the PF, a region that suffers severe neuropathology, whereas peroxiredoxin-2 expression remains unchanged in the CR and presumably provides cytoprotection (Krapfenbauer et al, 2002).…”
Section: Region-enriched Genesmentioning
confidence: 99%