Sodium thiosulfate protects against acrylonitrile-induced elevation of glial fibrillary acidic protein levels by replenishing glutathione

Enongene, Evaristus; Sun, Pei N; Mehta, Chander S.

doi:10.1016/s1382-6689(00)00036-3

Cited by 26 publications

(14 citation statements)

References 46 publications

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“…Since astrocytes are essential for maintaining neuronal activity, disruption of their function may contribute to neuronal injury in manganism (Gonzalez et al, 2008). Of particular importance, astrocytic activation has been associated with oxidative stress (Andersen, 2004) and decreased GSH levels (Enongene et al, 2000;Costa et al, 2012), consistent with our results.…”

Section: Discussionsupporting

confidence: 89%

Developmental exposure to manganese induces lasting motor and cognitive impairment in rats

et al. 2015

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Section: Discussionsupporting

confidence: 89%

Developmental exposure to manganese induces lasting motor and cognitive impairment in rats

et al. 2015

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“…Comparisons between primary rat and human astrocytes viability after ACN exposure is complex due to species differential responses to ACN. ACN has been shown to increase GFAP, a marker of astrogliosis, in rats, and also to increase number of transformed colonies in Syrian hamster embryo model of cell transformation by chemical carcinogens (Enongene et al, 2000; Zhang et al, 2000). While our primary astrocyte cultures showed no significant cell death, proliferation was not investigated (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The effects of ACN on astrocytes have been well established in vitro . Treatment of ACN in primary and transformed astrocytes leads to gliosis, increased reactive oxygen species (ROS), glutathione (GSH) and ATP depletion, increased oxidative DNA damage, and inhibition of gap junction intercellular communication (Enongene et al, 2000; Esmat et al, 2007; Jacob and Ahmed, 2003; Kamendulis et al, 1999a,b; Whysner et al, 1998). From these studies it is clear that oxidative stress plays a critical role in ACN-mediated neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Differential response to acrylonitrile toxicity in rat primary astrocytes and microglia

Caito

Aschner

2013

NeuroToxicology

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Acrylonitrile (ACN) is a widely used chemical in the production of plastics, resins, nitriles, acrylic fibers, synthetic rubber and acrylamide. While acute high level exposures to ACN are known to be lethal, chronic low dose exposures causes glial cell tumors in rats. Recently, these glial tumors have been characterized as microglial in origin. While effects of ACN on astrocytes, the more numerous glial cell, have been investigated, the effects on microglia are unknown. This study was conducted to compare the responses of astrocytes and microglia to ACN treatment in vitro to address differential sensitivities and adaptive responses to this toxic chemical. Cell viability, ACN uptake, lipid peroxidation byproducts (F2-isoprostanes), glutathione (GSH) levels and expression of NF-E2-related factor 2 (Nrf2) were evaluated in primary rat microglia and astrocytes following ACN treatment. Results indicate that microglia are more sensitive to ACN than astrocytes, accumulating less ACN while demonstrating higher F2-isoprostane levels. GSH levels were up-regulated in both cell types, as a protective mechanism against ACN-induced oxidative stress, while Nrf2 levels were only induced in microglia. Our data suggest that microglia and astrocytes exhibit different sensitivities and responses to ACN, which are linked to the intracellular thiol status inherent to each of these cell types.

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“…Although the nervous system response to acute AN exposure exhibits characteristics analogous to acute cyanide poisoning, the exact mechanism(s) of AN-induced neurotoxicity has yet to be fully defined (Enongene et al, 2000;Ghanayem et al, 1991). Oxidative stress may be involved in AN-induced neurotoxicity secondary to depletion of antioxidants and/or increased production of reactive oxygen species (ROS).…”

Section: Introductionmentioning

confidence: 99%

Differential protection of pre- versus post-treatment with curcumin, Trolox, and N -acetylcysteine against acrylonitrile-induced cytotoxicity in primary rat astrocytes

et al. 2015

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Sodium thiosulfate protects against acrylonitrile-induced elevation of glial fibrillary acidic protein levels by replenishing glutathione

Cited by 26 publications

References 46 publications

Developmental exposure to manganese induces lasting motor and cognitive impairment in rats

Developmental exposure to manganese induces lasting motor and cognitive impairment in rats

Differential response to acrylonitrile toxicity in rat primary astrocytes and microglia

Differential protection of pre- versus post-treatment with curcumin, Trolox, and N -acetylcysteine against acrylonitrile-induced cytotoxicity in primary rat astrocytes

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