PBDE-47-induced oxidative stress, DNA damage and apoptosis in primary cultured rat hippocampal neurons

He, Ping; He, Weidong; Wang, Aiguo; Xia, Tao; Xu, Bo; Zhang, Ming; Chen, Xuemin

doi:10.1016/j.neuro.2007.10.002

Cited by 185 publications

(122 citation statements)

References 35 publications

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“…There is supporting evidence for the ability of PBDEs to induce oxidative stress. BDE-47 was reported to cause oxidative stress in different cells, such as human neutrophil granulocytes (Reistad and Mariussen, 2005), human neuroblastoma cells (He et al, 2008b), hippocampal neurons (He et al, 2008a), and human fetal hematopoietic cells (Shao et al, 2008). While BDE-209 was shown to increase oxidative stress in human hepatoma cells Hep G2 (Hu et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity and apoptosis induction on RTG-2 cells of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) and decabrominated diphenyl ether (BDE-209)

Jin

Yang

et al. 2010

Toxicology in Vitro

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Section: Discussionmentioning

confidence: 99%

Cytotoxicity and apoptosis induction on RTG-2 cells of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) and decabrominated diphenyl ether (BDE-209)

Jin

Yang

et al. 2010

Toxicology in Vitro

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“…Further, BDE-47 interferes with the expression of cytochrome c, caspase 12 and procaspase 3, which might indicate that BDE-47 alters the apoptotic machinery in neuronal cell lines (He et al, 2009b). BDE-47 induced oxidative stress in hippocampal neurons in parallel to a reduced expression level of antioxidative proteins and enzymes (GSH, SOD, GSH-Px), which might lead to induction of apoptosis (He et al, 2008a). In addition, alterations in calcium homeostasis were observed in mitochondria prepared from rat brain (Coburn et al, 2008) and SHSY5Y cells (He et al, 2009b).…”

Section: Neurotoxicitymentioning

confidence: 99%

Scientific Opinion on Polybrominated Diphenyl Ethers (PBDEs) in Food

2011

EFS2

195

147

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EFSA was asked by the European Commission to deliver a scientific opinion on polybrominated diphenyl ethers (PBDEs) in food. PBDEs are additive flame retardants which are applied in plastics, textiles, electronic castings and circuitry. PBDEs are ubiquitously present in the environment and likewise in biota and in food and feed. Data from the analysis of 19 PBDE congeners in 3,971 food samples were provided to EFSA by 11 European countries. Eight congeners were considered by the Panel on Contaminants in the Food Chain (CONTAM Panel) to be of primary interest: . The highest dietary exposure is to . Toxicity studies were carried out with technical PBDE mixtures or individual congeners. Main targets were the liver, thyroid hormone homeostasis and the reproductive and nervous system. PBDEs cause DNA damage through the induction of reactive oxygen species. The Panel identified effects on neurodevelopment as the critical endpoint, and derived benchmark doses (BMDs) and their corresponding lower 95 % confidence limit for a benchmark response of 10 %, BMDL 10 s, for a number of PBDE congeners: BDE-47, 309 μg/kg b.w.; BDE-99, 12 μg/kg b.w.; BDE-153, 83 μg/kg b.w.; BDE-209, 1,700 μg/kg b.w. Due to the limitations and uncertainties in the current database, the Panel concluded that it was inappropriate to use these BMDLs to establish health based guidance values, and instead used a margin of exposure (MOE) approach for the health risk assessment. Since elimination characteristics of PBDE congeners in animals and humans differ considerably, the Panel used the body burden as starting point for the MOE approach. The CONTAM Panel concluded that for BDE-47, -153 and -209 current dietary exposure in the EU does not raise a health concern. For BDE-99 there is a potential health concern with respect to current dietary exposure. 4 The term "intra-species" has been replaced by "inter-species" in the Summary and in Chapter 9.1. The chemical stability of the PBDE congeners varies with the individual structure. In general PBDE congeners with up to three bromine substituents and those with nine or ten bromine substituents are more sensitive to abiotic transformations. PBDE congeners with four to eight bromine substituents show the highest stability. PBDE congeners are particularly susceptible to photolysis, reductive debromination and radical reactions whereas they are less susceptible to oxidation and hydrolysis. In general, PBDE congeners are persistent and bioaccumulative with the exception of BDE-209 bioaccumulative properties of which seem to be species dependent. BDE-209 undergoes debromination reactions both in the abiotic environment and in biota, leading to formation of PBDE congeners containing seven to nine bromine atoms. © European Food SafetyBased on the composition of the technical PBDE mixtures, occurrence in the environment and in food, the Panel on Contaminants in the Food Chain (CONTAM Panel) considered the following eight PBDE congeners to be of primary interest: which are relevant for dietary PBDE exposur...

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“…3A) and GSH depletion (Fig. 3B), two markers of oxidative stress-induced cell damage, 20,21) which could explain the mechanism by which 5HI protects cells. GSH depletion by oxidative stress is associated with mitochondrial dysfunction and the induction of apoptosis.…”

Section: -Bhpmentioning

confidence: 92%

“…20,21) We examined whether 5HI repairs the induction of lipid peroxidation and GSH depletion by t-BHP. 5HI alone did not change MDA levels, but did block the increases in MDA and GSH depletion caused by t-BHP (Figs.…”

Section: Hi Attenuates T-bhp-inducedmentioning

confidence: 99%

The Anti-apoptotic Action of 5-Hydroxyindole: Protection of Mitochondrial Integrity

Bae

Lee

et al. 2010

Biological & Pharmaceutical Bulletin

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5-Hydroxyindole (5HI) is a metabolite of tryptophan that is involved in learning and memory as well as in central nervous system regulation, such as in blocking desensitization.1) 5HI also has anti-oxidant activity, 2,3) but its cellular targets are unclear.Oxidative stress can be induced by endogenous processes in which the balance between reductants and oxidants becomes slanted towards the oxidative side. Most oxidants are derived from oxygen and nitrogen based reactive species (RS), including reactive oxygen species (ROS) and lipid peroxidation byproducts.4) ROS cause oxidative modification and play important roles in abnormal pathological processes and biochemical functions. 5,6) ROS also can induce apoptosis in many different cell systems. 7) tert-Butylhydroperoxide (t-BHP) can cause oxidative stress and cell damage. 8) t-BHP is a strong RS inducer of lipid peroxidation, and causes glutathione (GSH) depletion and peroxynitrite (ONOO Ϫ ) generation.9,10) A short-chain analog of lipid hydroperoxides, t-BHP is used often as a model compound to establish the mechanism of cell damage initiated by oxidative stress. 8)Mitochondrial integrity is constantly threatened by the presence of RS produced in the membrane. High RS levels in the mitochondria can compromise mitochondrial membrane potential (Dym), leading to depolarization 11) and apoptotic events, including cytochrome c release and caspase activation.12) Here, we attempted to identify the cellular mechanisms of 5HI by focusing on mitochondria and associated apoptotic processes. Our findings show that 5HI treatment inhibited damage from oxidative stress and apoptosis in t-BHP-induced human fibroblast cell. These findings are supported by the data gained on GSH, lipid peroxidation, RS generation, DNA damage, decreased mitochondrial membrane potential, cytochrome c release, and caspase activity. MATERIALS AND METHODS MaterialsHuman fibroblasts were obtained from the American Type Culture Collection (ATCC, Manassas, VA, U.S.A.). 5HI and Dulbecco's modified Eagle's media (DMEM) were purchased form Sigma-Aldrich Chemical (St. Louis, MO, U.S.A.), as were all reagents unless otherwise stated. Fetal bovine serum (FBS), trypsin-ethylenediamineteraacetic acid, and penicillin-streptomycin were purchased from Gibco BRL (Ground Island, NY, U.S.A.). 3-(4,5-Dimethylthiazol-yl)-diphenyl tetrazolium bromide (MTT) was provided by DUCHEFA Biochemie (Haarlem, Netherlands). Antibodies for human cytochrome c, cleavedcaspase-3, and caspase-9 were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, U.S.A.). Human a-tubulin antibody and 2Ј,7Ј-dichlorodihydrofluorescein diacetate (DCFDA) were obtained from Sigma-Aldrich (St. Louis, MO, U.S.A.) Horseradish peroxidase-conjugated goat antirabbit immunoglobulin G (IgG) and goat anti-mouse IgG was provided by Santa Cruz (Santa Cruz, CA, U.S.A.). 5HI was dissolved in dimethyl sulfoxide (DMSO), and the final concentration of DMSO was Ͻ0.1%.Cell Culture and MTT Assay Human fibroblast cells were cultured in DMEM containing 10% FBS, 2 mM gl...

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PBDE-47-induced oxidative stress, DNA damage and apoptosis in primary cultured rat hippocampal neurons

Cited by 185 publications

References 35 publications

Cytotoxicity and apoptosis induction on RTG-2 cells of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) and decabrominated diphenyl ether (BDE-209)

Cytotoxicity and apoptosis induction on RTG-2 cells of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) and decabrominated diphenyl ether (BDE-209)

Scientific Opinion on Polybrominated Diphenyl Ethers (PBDEs) in Food

The Anti-apoptotic Action of 5-Hydroxyindole: Protection of Mitochondrial Integrity

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