Effect of N,N-diethyldithiocarbamate on ionomycin-induced increase in oxidation of cellular 2′,7′-dichlorofluorescin in dissociated cerebellar neurons

Oyama, Yasuo; Furukawa, Koichi; Chikahisa, Lumi; Hatakeyama, Yoshiko

doi:10.1016/0006-8993(94)90850-8

Cited by 18 publications

(10 citation statements)

References 12 publications

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“…Because DDC is an inhibitor for SOD, the reduction in DCF fluorescence suggests a block in the efficient dismutation of O 2 Ϫ . This observation is in accord with earlier findings [28,29], which demonstrated that SOD inhibition by DDC in isolated rat neutrophils and cerebellar neurons augmented O 2 Ϫ generation and inhibited H 2 O 2 production. This finding strengthens the notion that PCBs, which can bind to proteins [30], have a definite role in inhibiting the activity of SOD, leading to inefficient dismutation of O 2 Ϫ .…”

Section: Discussionsupporting

confidence: 82%

Impairment of human neutrophil oxidative burst by polychlorinated biphenyls: inhibition of superoxide dismutase activity

Narayanan

Carter

Ganey

et al. 1998

Journal of Leukocyte Biology

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We report evidence of a novel mechanism by which polychlorinated biphenyls might act as potent inducers of inflammation. Aroclor 1242 (A1242), a polychlorinated biphenyl mixture, and 2,2',4,4'-tetrachlorobiphenyl (PCB47), a constituent of A1242 that produces the same patterns of effects, impaired the oxidative burst of human neutrophils by inhibiting the antioxidant enzyme superoxide dismutase, which converts O 2 ؊ to H 2 O 2 . Pre-incubation of neutrophils with A1242 or PCB47 before stimulation with phorbol 12-myristate 13-acetate heightened the respiratory burst, producing a significant increase in intracellular O 2 ؊ production along with a significant decrease in H 2 O 2 production compared with unexposed agoniststimulated neutrophils. This was also evident in a physiologically relevant situation in which neutrophils pre-incubated with A1242 were subsequently stimulated with a combination of N-formyl-Lmethionyl-L-leucyl-L-phenylalanine and tumor necrosis factor-␣. Incubation of bovine copper-zinc superoxide dismutase (EC 1.15.1.1) with A1242 or PCB47 in a cell-free system reversed the enzymemediated inhibition of 6-hydroxydopamine autoxidation, indicating that polychlorinated biphenyls inhibited superoxide dismutase activity. Low superoxide dismutase activity in neutrophils leads to imbalances between production of free radicals and antioxidant defense mechanisms, which can in turn induce tissue damage and hasten the onset of neutrophil apoptosis.

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Section: Discussionsupporting

confidence: 82%

Impairment of human neutrophil oxidative burst by polychlorinated biphenyls: inhibition of superoxide dismutase activity

Narayanan

Carter

Ganey

et al. 1998

Journal of Leukocyte Biology

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“…We analysed the net intracellular generation of ROS by flow cytometry using the oxidation-sensitive probes 2#-7#-dichlorodihydrofluorescein diacetate (H 2 DCFDA) and dihydroethidine (DHE). These fluorochromes have been used elsewhere to determine oxidative stress associated with toxic effects (Casado et al, 1993;Oyama et al, 1994;Rothe and Valet, 1990;Yuan et al, 1993). In the present study we observed increased ROS formation in CGCs treated with MPP C , coincident with glutathione depletion (Fig.…”

Section: Discussionsupporting

confidence: 59%

“…These fluorochromes have been used elsewhere to determine oxidative stress associated with toxic effects (Casado et al, 1993;Oyama et al, 1994;Rothe and Valet, 1990;Yuan et al, 1993). In the present study we observed increased ROS formation in CGCs treated with MPP C , coincident with glutathione depletion (Fig.…”

Section: Discussionmentioning

confidence: 60%

Protection against MPP⁺ neurotoxicity in cerebellar granule cells by antioxidants

González‐Polo

Soler

Rodrı́guez-Martı́n

et al. 2004

Cell Biology International

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The neuropathology associated with Parkinson's disease (PD) is thought to involve excessive production of free radicals, dopamine autoxidation, defects in glutathione peroxidase expression, attenuated levels of reduced glutathione, altered calcium homeostasis, excitotoxicity and genetic defects in mitochondrial complex I activity. While the neurotoxic mechanisms are vastly different for excitotoxins and 1-methyl-4-phenylpyridinium ion (MPP(+)), both are thought to involve free radical production, compromised mitochondrial activity and excessive lipid peroxidation. We show here that the levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) increased significantly after treatment of cultured cerebellar granule cells (CGCs) with 50 microM MPP(+). Co-treatment with antioxidants such as ascorbate (ASC), catalase, alpha-tocopherol (alpha-TOH), coenzyme Q(10) (CoQ(10)) or superoxide dismutase (SOD) rescued the cells from MPP(+)-induced death. MPP(+)-induced cell death was also abolished by co-treatment with nitric oxide synthase (NOS) inhibitors such as 7-nitroindazole (7-NI), 2-ethyl-2-thiopseudourea hydrobromide (EPTU) or S-methylisothiourea sulphate (MPTU). We also tested the protective effects of an iron chelator (deferoxamine mesylate, DFx) and a peroxynitrite scavenger (FeTTPS) and the results lend further support to the view that the free radical cytotoxicity plays an essential role in MPP(+)-induced death in primary cultures of CGC.

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“…Ionomycin also augmented the intensity of DCF fluorescence significantly as shown previously (1,13). However, the potency of ionomycin in augmenting DCF fluorescence (the potency of oxidative effect of ionomycin) was unknown.…”

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confidence: 79%

Oxidative Stress-Induced Increase in Intracellular Ca2+ and Ca2+-Induced Increase in Oxidative Stress: An Experimental Model Using Dissociated Rat Brain Neurons

Oyama

Okazaki

Chikahisa

et al. 1996

Japanese Journal of Pharmacology

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Effect of N,N-diethyldithiocarbamate on ionomycin-induced increase in oxidation of cellular 2′,7′-dichlorofluorescin in dissociated cerebellar neurons

Cited by 18 publications

References 12 publications

Impairment of human neutrophil oxidative burst by polychlorinated biphenyls: inhibition of superoxide dismutase activity

Impairment of human neutrophil oxidative burst by polychlorinated biphenyls: inhibition of superoxide dismutase activity

Protection against MPP⁺ neurotoxicity in cerebellar granule cells by antioxidants

Oxidative Stress-Induced Increase in Intracellular Ca2+ and Ca2+-Induced Increase in Oxidative Stress: An Experimental Model Using Dissociated Rat Brain Neurons

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Effect of N,N-diethyldithiocarbamate on ionomycin-induced increase in oxidation of cellular 2′,7′-dichlorofluorescin in dissociated cerebellar neurons

Cited by 18 publications

References 12 publications

Impairment of human neutrophil oxidative burst by polychlorinated biphenyls: inhibition of superoxide dismutase activity

Impairment of human neutrophil oxidative burst by polychlorinated biphenyls: inhibition of superoxide dismutase activity

Protection against MPP+ neurotoxicity in cerebellar granule cells by antioxidants

Oxidative Stress-Induced Increase in Intracellular Ca2+ and Ca2+-Induced Increase in Oxidative Stress: An Experimental Model Using Dissociated Rat Brain Neurons

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Protection against MPP⁺ neurotoxicity in cerebellar granule cells by antioxidants