NDLI: Calmodulin–CaMKII mediated alteration of oxidative stress: interplay of the cAMP/PKA–ERK 1/2-NF-κB–NO axis on arsenic-induced head kidney macrophage apoptosis

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Calmodulin–CaMKII mediated alteration of oxidative stress: interplay of the cAMP/PKA–ERK 1/2-NF-κB–NO axis on arsenic-induced head kidney macrophage apoptosis

Biocompatibility evaluation of aniline oligomers with different end-functional groups

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Toxicology Research Vol - 2 Issue - 5

Toxicology Research Vol - 2 Issue - 4

Toxicology Research Vol - 2 Issue - 3

Toxicology Research Vol - 2 Issue - 2

Toxicology Research Vol - 2 Issue - 1

Toxicology Research Vol -1

Calmodulin–CaMKII mediated alteration of oxidative stress: interplay of the cAMP/PKA–ERK 1/2-NF-κB–NO axis on arsenic-induced head kidney macrophage apoptosis

Content Provider	Royal Society of Chemistry (RSC)
Author	Raman, Rajagopal Singh, Ambika Mazumder, Shibnath Banerjee, Chaitali
Copyright Year	2013
Abstract	Using the head kidney macrophages (HKM) from catfish (Clarias batrachus) we earlier demonstrated the role of calcium (Ca2+) and its dependent neutral protease calpain in arsenic-induced apoptosis. Here, we report the role of the CaM–CaMKII axis as an initiator of the process. With the help of specific assay kits and inhibitors we document the pro-apoptotic role of CaM and CaMKII in arsenic-induced HKM apoptosis. CaM-induced CaMKII activity influenced superoxide ion production in exposed cells with a consequent increase in intracellular cAMP levels. Using H-89, the specific inhibitor for PKA, we show for the first time the pro-apoptotic role of the cAMP/PKA pathway in arsenic-induced HKM apoptosis. We report the cAMP/PKA pathway to be critical for initiating downstream activation of MAPKs, namely ERK 1/2. The superoxide ions generated due to arsenic-stress also induce NF-κB activation in HKM. Inducible NOS activity and consequent NO production were evident in the exposed HKM and our study implicates the involvement of ERK 1/2 and NF-κB in the process. Arsenic exposure alters mitochondrial membrane potential, releases cytochrome C and activates caspase-9 leading to caspase-3 mediated apoptosis of HKM. Our findings, thus, provide insight into the underlying mechanism of arsenic toxicity and indicate that HKM could serve as an important in vitro model for immunotoxicity assays.
Starting Page	413
Ending Page	426
Page Count	14
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	2
Issue Number	6
Journal	Toxicology Research
DOI	10.1039/c3tx50026h
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Protein kinase A Arsenic poisoning CAMK Enzyme inhibitor Mitogen-activated protein kinase Caspase Calpain Ion Superoxide Kidney Cytochrome c NF-κB Catfish Protease Clarias Nitric oxide synthase Calcium in biology Membrane potential Macrophage Apoptosis Cyclic adenosine monophosphate
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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