Activation of extracellular signal-regulated kinases (ERK 44/42) by chlorpyrifos oxon in Chinese hamster ovary cells

Bomser, Joshua A.; Casida, John E.

doi:10.1002/1099-0461(2000)14:6<346::aid-jbt7>3.0.co;2-h

Cited by 19 publications

(9 citation statements)

References 39 publications

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“…Extracellular signal-regulated protein kinases (ERK) also contribute to M2 receptor regulation in some cell types (Rousell et al, 1997). Moreover, CPO activated ERK 44/42 in CHO cells expressing M2 receptors (Bomser & Casida, 2000). Activation or inhibition of other kinases by CPO might lead to differential effects on M2 receptor trafficking in different cell types.…”

Section: Discussionmentioning

confidence: 99%

Effects of Chlorpyrifos Oxon on M2 Muscarinic Receptor Internalization in Different Cell Types

Zamora

Liu

Pope

2008

Journal of Toxicology and Environmental Health, Part A

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The muscarinic M2 receptor is a member of the G protein-coupled receptor (GPCR) superfamily. Agonist activation of GPCR leads to their phosphorylation, desensitization, internalization, and subsequent endocytic recycling or lysosomal degradation. Agonist-induced phosphorylation of M2 receptors is mediated by G-protein receptor kinase 2 (GRK2). The active metabolite of the organophosphorus insecticide chlorpyrifos, i.e., chlorpyrifos oxon (CPO), inhibited agonist-induced phosphorylation of human recombinant M2 receptors by GRK2 in vitro in a concentration-dependent manner. In both intact HEL 299 cells (human embryonic lung fibroblasts expressing M2 receptors) and CHO-M2 cells (stably expressing M2 receptors), the muscarinic agonist carbachol (100 microM) led to receptor internalization as determined by reduced specific binding to the membrane-impermeable radioligand [(3)H]-N-methylscopolamine (NMS). CPO alone (100 microM) exerted no significant effect on NMS binding in either HEL 299 or CHO-M2 cells. In HEL 299 cells, CPO did not influence carbachol-induced internalization, whereas in CHO-M2 cells CPO blocked internalization. In primary striatal neurons, M2 receptors appeared widely and diffusely distributed. Exposure to either carbachol or CPO led to apparent receptor internalization with an increased percent of cells exhibiting punctate domains of immunostaining, while combined exposure to both carbachol and CPO led to a significantly higher percent of cells exhibiting this appearance. The data suggest that CPO may differentially influence agonist-stimulated M2 receptor internalization in a cell-dependent manner.

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Section: Discussionmentioning

confidence: 99%

Effects of Chlorpyrifos Oxon on M2 Muscarinic Receptor Internalization in Different Cell Types

Zamora

Liu

Pope

2008

Journal of Toxicology and Environmental Health, Part A

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“…3). Some of these differential responses, which are not linked to the generic OP structure, are related to cell growth and differentiation, central nervous system cell damage, and disruption of brain development [32][33][34][35]. Ornithine decarboxylase activity was significantly diminished (40%) because of exposure to 4 mg/L chlorpyrifos.…”

Section: Discussionmentioning

confidence: 99%

“…Chlorpyrifos probably triggers specific mechanisms because of its particular chemical structure. Some of these differential responses, which are not linked to the generic OP structure, are related to cell growth and differentiation, central nervous system cell damage, and disruption of brain development [32][33][34][35]. A decrease of polyamine levels may result in the inhibition of cell proliferation and differentiation and cell death [36].…”

Section: Discussionmentioning

confidence: 99%

Developmental and polyamine metabolism alterations in Rhinella arenarum embryos exposed to the organophosphate chlorpyrifos

Sotomayor

Lascano

D’Angelo

et al. 2012

Enviro Toxic and Chemistry

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Organophosphorus pesticides (OPs) are widely applied in the Alto Valle of Río Negro and Neuquén, Argentina, due to intensive fruit growing. Amphibians are particularly sensitive to environmental pollution, and OPs may transiently accumulate in ponds and channels of the region during their reproductive season. Organophosphorus pesticide exposure may alter amphibian embryonic development and the reproductive success of autochthonous species. In the present study, embryos of the common toad Rhinella arenarum were employed to assess developmental alterations and to study polyamine metabolism, which is essential to normal growth, as a possible target underlying the effects of the OP chlorpyrifos. As the duration of chlorpyrifos exposure increased and embryonic development progressed, the median lethal concentration (LC50) values decreased, and the percentage of malformed embryos increased. Developmental arrest was also observed and several morphological alterations were recorded, such as incomplete and abnormal closure of the neural tube, dorsal curvature of the caudal fin, reduction of body size and caudal fin length, atrophy, and edema. An early decrease in ornithine decarboxylase (ODC) activity and polyamine levels was also observed in embryos exposed to chlorpyrifos. The decrease in polyamine contents in tail bud embryos might be a consequence of the reduction in ODC activity. The alteration of polyamine metabolism occurred before embryonic growth was interrupted and embryonic malformations were observed and may be useful as a biomarker in environmental studies.

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“…However, the p38-MAPK inhibitor (SB202190) significantly increased cell death. The results showed that activation of the p38-MAPK signaling pathway had a protective effect against CPF-induced cytotoxicity, and the p38-MAPK inhibitor might influence the isoform of p38-MAPK and might contribute to the activation of the survival signaling pathways [57]. CPF and CPF-oxone activated ERK44/42 signaling in both wild-type (CHOK1) and human muscarinic receptor-expressing ovarian cells of the Chinese hamster (CHO-M2).…”

Section: Organophosphorus Compound-induced Reproductive Toxicity Is Mmentioning

confidence: 99%

Organophosphorus Compounds and MAPK Signaling Pathways

Farkhondeh

Buhrmann

Pourbagher‐Shahri

et al. 2020

IJMS

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The molecular signaling pathways that lead to cell survival/death after exposure to organophosphate compounds (OPCs) are not yet fully understood. Mitogen-activated protein kinases (MAPKs) including the extracellular signal-regulated protein kinase (ERK), the c-Jun NH2-terminal kinase (JNK), and the p38-MAPK play the leading roles in the transmission of extracellular signals into the cell nucleus, leading to cell differentiation, cell growth, and apoptosis. Moreover, exposure to OPCs induces ERK, JNK, and p38-MAPK activation, which leads to oxidative stress and apoptosis in various tissues. However, the activation of MAPK signaling pathways may differ depending on the type of OPCs and the type of cell exposed. Finally, different cell responses can be induced by different types of MAPK signaling pathways after exposure to OPCs.

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Activation of extracellular signal-regulated kinases (ERK 44/42) by chlorpyrifos oxon in Chinese hamster ovary cells

Cited by 19 publications

References 39 publications

Effects of Chlorpyrifos Oxon on M2 Muscarinic Receptor Internalization in Different Cell Types

Effects of Chlorpyrifos Oxon on M2 Muscarinic Receptor Internalization in Different Cell Types

Developmental and polyamine metabolism alterations in Rhinella arenarum embryos exposed to the organophosphate chlorpyrifos

Organophosphorus Compounds and MAPK Signaling Pathways

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