Cadmium-induced apoptosis in lymphoblastoid cell line: involvement of caspase-dependent and -independent pathways

Coutant, Alexandre; Lebeau, J.; Bidon-Wagner, N.; Levalois, Céline; Lectard, Bruno; Chevillard, Sylvie

doi:10.1016/j.biochi.2006.09.018

Cited by 38 publications

(23 citation statements)

References 36 publications

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“…After being washed with ice-cold acetone, the protein was incubated for 90 min at 30°C in 10 mM AMS (4-acetamido-4Ј-maleimidylstilbene-2,2Ј-disulfonic acid), denatured in Laemmli buffer without DTT, electrophoresed on a 15% sodium dodecyl sulfatepolyacrylamide gel, and revealed using the Imperial Protein staining reagent (Pierce). on May 9, 2018 by guest http://mcb.asm.org/ (10). At different times during the treatment and after removal of the Cd solution, cell extracts were analyzed for their 8-oxoG DNA glycosylase activity.…”

Section: Western Blot Analysismentioning

confidence: 99%

Redox Regulation of Human OGG1 Activity in Response to Cellular Oxidative Stress

Bravard

Vacher

Gouget

et al. 2006

Molecular and Cellular Biology

141

108

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8-Oxoguanine (8-oxoG), a common and mutagenic form of oxidized guanine in DNA, is eliminated mainly through base excision repair. In human cells its repair is initiated by human OGG1 (hOGG1), an 8-oxoG DNA glycosylase. We investigated the effects of an acute cadmium exposure of human lymphoblastoid cells on the activity of hOGG1. We show that coinciding with alteration of the redox cellular status, the 8-oxoG DNA glycosylase activity of hOGG1 was nearly completely inhibited. However, the hOGG1 activity returned to normal levels once the redox cellular status was normalized. In vitro, the activity of purified hOGG1 was abolished by cadmium and could not be recovered by EDTA. In cells, however, the reversible inactivation of OGG1 activity by cadmium was strictly associated with reversible oxidation of the protein. Moreover, the 8-oxoG DNA glycosylase activity of purified OGG1 and that from crude extracts were modulated by cysteine-modifying agents. Oxidation of OGG1 by the thiol oxidant diamide led to inhibition of the activity and a protein migration pattern similar to that seen in cadmiumtreated cells. These results suggest that cadmium inhibits hOGG1 activity mainly by indirect oxidation of critical cysteine residues and that excretion of the metal from the cells leads to normalization of the redox cell status and restoration of an active hOGG1. The results presented here unveil a novel redox-dependent mechanism for the regulation of OGG1 activity.

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Section: Western Blot Analysismentioning

confidence: 99%

Redox Regulation of Human OGG1 Activity in Response to Cellular Oxidative Stress

Bravard

Vacher

Gouget

et al. 2006

Molecular and Cellular Biology

141

108

View full text Add to dashboard Cite

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“…Studies have shown that cadmium may trigger cell death by caspase-dependent and/or independent apoptotic mechanisms, depending on cell types (Coutant et al, 2006;Mao et al, 2007). Resveratrol was able to potentially improve the cell viability and markedly down-regulate cadmium induced robust up-regulation of caspase-3.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Lin¹,

Peng²,

Yang³

et al. 2015

Bangladesh J Pharmacol

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Cadmium, a toxic environmental contaminant, induces oxidative stress leading to various neurodegenerative disorders, where it interferes with homeos-tasis of intracellular free calcium ([Ca2+]i), leading to cellular damage and apoptosis. We investigated whether resveratrol, a plant-derived antioxidant could offer protection against cadmium-induced neuroapoptosis. Primary cortical neurons were exposed to cadmium (10 or 20 µM) with/without prior exposure to resveratrol (5, 10 or 20 µM) for 12 hours and unexposed cells served as control. Resveratrol caused marked reduction in cadmium-induced neuronal apoptosis and down-regulated caspase-3 expressions. Cadmium-induced marked elevations in reactive oxygen species, and ([Ca2+]i) levels were potentially reduced by resveratrol. Resveratrol effectively regulated the alterations observed in the activation levels of mitogen-activated protein kinases (MAPKs) and proteins of mammalian target of rapamycin (mTOR) pathways. Thus, resveratrol effectively protected the cortical neurons exposed to cadmium by modulating the ([Ca2+]i) levels and regulating the MAPK/mTOR pathways.

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“…Several studies have shown that Cd causes various forms of damage to mammalian organs (such as the lungs, liver, kidneys, testes, and cardiovascular system) [1][2][3]. A previous study found that Cd can also damage the body's immune system [4]. It has been reported that Cd can change the function of many kinds of immune cells by affecting protein expression and normal immune cell function.…”

Section: Introductionmentioning

confidence: 98%

Effects of Agaricus blazei Murill Polysaccharide on Cadmium Poisoning on the MDA5 Signaling Pathway and Antioxidant Function of Chicken Peripheral Blood Lymphocytes

et al. 2017

Biol Trace Elem Res

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This experimental study investigated the effect of Agaricus blazei Murill polysaccharide (ABP) on cadmium (Cd) poisoning on the melanoma differentiation-associated gene 5 (MDA5) signaling pathway and antioxidant function of peripheral blood lymphocytes (PBLs) in chickens. The experiments were divided into four groups: 7-day-old chickens with normal saline (0.2 mL single/day), Cd (140 mg/kg), ABP (30 mg/mL, 0.2 mL single/day), and Cd + ABP(140 mg/kg/day + 0.2 mL ABP). Peripheral blood was collected on the 20th, 40th, and 60th days for each group, and PBLs were separated. We attempted to detect the expression of MDA5, downstream signaling molecules, and convergence protein (interferon promoter-stimulating factor 1); transcription factors (IRF3 and NF-κB); the content of cytokines (IL-1β, IL-6, TNF-α, and IFN-β) in PBLs; and the antioxidant index of superoxide dismutase (SOD), malondialdhyde (MDA), and glutathione peroxidase (GSH-Px). The results showed that ABP can reduce the accumulation of Cd in the peripheral blood of chickens; reduce the expression of MDA5 and downstream signaling molecules; and reduce the content of IL-1β, IL-6, TNF-α, and IFN-β in PBLs of chickens. The activity of antioxidant enzymes (SOD and GSH-Px) significantly increased, and the content of MDA decreased. These results showed that they have a certain protective effect of ABP on Cd poisoning in chicken PBLs caused by injury.

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Cadmium-induced apoptosis in lymphoblastoid cell line: involvement of caspase-dependent and -independent pathways

Cited by 38 publications

References 36 publications

Redox Regulation of Human OGG1 Activity in Response to Cellular Oxidative Stress

Redox Regulation of Human OGG1 Activity in Response to Cellular Oxidative Stress

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Effects of Agaricus blazei Murill Polysaccharide on Cadmium Poisoning on the MDA5 Signaling Pathway and Antioxidant Function of Chicken Peripheral Blood Lymphocytes

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