http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Nivedita Chatterjee,Ji Su Yang,Kwangsik Park,Seung Min Oh,Jeonggue Park,Jinhee Choi 환경독성보건학회 2015 환경독성보건학회지 Vol.30 No.-
Objectives: The widely promising applications of graphene nanomaterials raise considerable concerns regarding their environmental and human health risk assessment. The aim of the current study was to evaluate the toxicity profiling of graphene family nananomaterials (GFNs) in alternative in vitro and in vivo toxicity testing models. Methods: The GFNs used in this study are graphene nanoplatelets ([GNPs]–pristine, carboxylate [COOH] and amide [NH2]) and graphene oxides (single layer [SLGO] and few layers [FLGO]). The human bronchial epithelial cells (Beas2B cells) as in vitro system and the nematode Caenorhabditis elegans as in vivo system were used to profile the toxicity response of GFNs. Cytotoxicity assays, colony formation assay for cellular toxicity and reproduction potentiality in C. elegans were used as end points to evaluate the GFNs’ toxicity. Results: In general, GNPs exhibited higher toxicity than GOs in Beas2B cells, and among the GNPs the order of toxicity was pristine>NH2>COOH. Although the order of toxicity of the GNPs was maintained in C. elegans reproductive toxicity, but GOs were found to be more toxic in the worms than GNPs. In both systems, SLGO exhibited profoundly greater dose dependency than FLGO. The possible reason of their differential toxicity lay in their distinctive physicochemical characteristics and agglomeration behavior in the exposure media. Conclusions: The present study revealed that the toxicity of GFNs is dependent on the graphene nanomaterial’s physical forms, surface functionalizations, number of layers, dose, time of exposure and obviously, on the alternative model systems used for toxicity assessment.
Chatterjee, Nivedita,Jeong, Jaeseong,Yoon, Dahye,Kim, Suhkmann,Choi, Jinhee Elsevier 2018 Chemico-biological interactions Vol.293 No.-
<P><B>Abstract</B></P> <P>The present study aimed to investigate the mechanisms involved in amorphous silica nanoparticles (aSiNPs)-mediated hepatotoxicity through the evaluation of changes in global metabolomics in <I>in vitro</I> and <I>in vivo</I> systems. <SUP>1</SUP>H NMR-based non-targeted global metabolomics and biochemical approaches were conducted in an aSiNPs-treated human hepatoma cell line (HepG2) and in ICR mice liver. The non-targeted NMR-based metabolomic analysis, followed by pathway analysis, revealed the perturbation of glutathione metabolism and the depletion of the glutathione pool after aSiNPs treatment in both <I>in vitro</I> (HepG2 cells) and <I>in vivo</I> systems. The total glutathione level, glutathione-S-transferase enzyme activity, and antioxidant gene expression strongly corroborated the metabolomic analysis results. The <I>in vitro</I> results were further supported by the <I>in vivo</I> data, specifically for metabolites profiling (Pearson Correlation coefficient is 0.462 (p = 0.026)). Furthermore, the depletion of glutathione, the formation of NADPH oxidase-mediated reactive oxygen species, and oxidative stress were evident in aSiNPs-treated HepG2 cells. Overall, the suppression of glutathione metabolism and oxidative stress are among the principal causes of aSiNPs-mediated hepatotoxicity.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Amorphous Silica nanoparticles (aSiNPs) exposure to HepG2 cells and ICR mice liver. </LI> <LI> Global metabolomics (NMR based) and biochemical assays reveal glutathione depletion. </LI> <LI> NADPH oxidase dependent ROS formation in aSiNPs exposed HepG2 cells. </LI> <LI> Alteration in antioxidative gene expression and GST enzyme activity. </LI> <LI> Conserved mechanisms of aSiNPs toxicity between <I>in vitro</I> and <I>in vivo</I> models. </LI> </UL> </P>
Chatterjee, Nivedita,Yang, Ji Su,Park, Kwangsik,Oh, Seung Min,Park, Jeonggue,Choi, Jinhee The Korean Society of Environmental Toxicology 2015 환경독성보건학회지 Vol.30 No.-
Objectives The widely promising applications of graphene nanomaterials raise considerable concerns regarding their environmental and human health risk assessment. The aim of the current study was to evaluate the toxicity profiling of graphene family nanano-materials (GFNs) in alternative in vitro and in vivo toxicity testing models. Methods The GFNs used in this study are graphene nanoplatelets ([GNPs]-pristine, carboxylate [COOH] and amide [$NH_2$]) and graphene oxides (single layer [SLGO] and few layers [FLGO]). The human bronchial epithelial cells (Beas2B cells) as in vitro system and the nematode Caenorhabditis elegans as in vivo system were used to profile the toxicity response of GFNs. Cytotoxicity assays, colony formation assay for cellular toxicity and reproduction potentiality in C. elegans were used as end points to evaluate the GFNs' toxicity. Results In general, GNPs exhibited higher toxicity than GOs in Beas2B cells, and among the GNPs the order of toxicity was pristine > $NH_2$ > COOH. Although the order of toxicity of the GNPs was maintained in C. elegans reproductive toxicity, but GOs were found to be more toxic in the worms than GNPs. In both systems, SLGO exhibited profoundly greater dose dependency than FLGO. The possible reason of their differential toxicity lay in their distinctive physicochemical characteristics and agglomeration behavior in the exposure media. Conclusions The present study revealed that the toxicity of GFNs is dependent on the graphene nanomaterial's physical forms, surface functionalizations, number of layers, dose, time of exposure and obviously, on the alternative model systems used for toxicity assessment.
Chatterjee, Nivedita,Kim, Youngho,Yang, Jisu,Roca, Carlos P.,Joo, Sang-Woo,Choi, Jinhee Informa UK (TaylorFrancis) 2017 Nanotoxicology Vol.11 No.1
<P>The potential hazards of graphene nanomaterials were investigated by exposing the nematode Caenorhabditis elegans to graphene oxide (GO) and reduced graphene oxide (rGO). The underlying mechanisms of the nano-bio interaction were addressed with an integrated systems toxicology approach using global transcriptomics, network-based pathway analysis, and experimental validation of the in-silico-derived hypotheses. Graphene oxide was found to reduce the worms' reproductive health to a greater degree than rGO, but it did not affect survival (24h endpoint). Comparative analysis of GO vs. rGO effects found that the wingless-type MMTV integration site family (Wnt) pathway and the mitogen-activated protein kinase (MAPK) pathway were evoked in GO- but not in rGO-exposed worms. We therefore hypothesized that crosstalk between the Wnt and MAPK pathways is responsible for C. elegans' reproductive sensitivity to GO exposure. By targeting the individual components of the Wnt-MAPK crosstalk pathway (with qPCR gene expression and mutant reproduction analysis), we found a signaling cascade of MOM-2 -> MOM-5 -> MOM-4 -> LIT-1 -> POP-1 -> EGL-5. Specifically, the activation of POP-1 (the TCF protein homolog) and subsequent repression of the Wnt/beta-catenin target gene (EGL-5), analyzed with target-gene-specific RNAi in POP-1 mutant [pop-1(q645)] worms, were the central mechanisms of reduced reproductive potential in the worms exposed to GO. Our results highlight the distinct biological and molecular mechanisms of GO and rGO exposure and the role of Wnt-MAPK pathway crosstalk in regulating GO-induced reproductive failure in in vivo systems, and they will contribute to the development of efficient and innocuous graphene applications as well to improvements in mechanism-based risk assessment.</P>
Yang, Jisu,Chatterjee, Nivedita,Kim, Youngho,Roh, Ji-Yeon,Kwon, Jung-Hwan,Park, Myung-Sook,Choi, Jinhee Elsevier 2018 CHEMOSPHERE - Vol.200 No.-
<P><B>Abstract</B></P> <P>As part of a study to explore the long-term effects of the Hebei Spirit oil spill accident, transgenerational toxicity and associated epigenetic changes were investigated in the nematode <I>Caenorhabditis elegans.</I> Under experimental conditions, worms were exposed to Iranian heavy crude oil (IHC) under three different scenarios: partial early-life exposure (PE), partial late-life exposure (PL), and whole-life exposure (WE). Growth, reproduction, and histone methylation were monitored in the exposed parental worms (P0) and in three consecutive unexposed offspring generations (F<SUB>1-3</SUB>). Reproductive potential in the exposed P0 generation in the WE treatment group was reduced; additionally, it was inhibited in the unexposed offspring generations of the P0 worms. This suggests that there was transgenerational inheritance of defective reproduction. Comparison of developmental periods of exposure showed that IHC-treated worms in the PL group had a greater reduction in reproductive capacity than those in the PE group. Decreased methylation of histone H3 (H3K9) was found in the IHC-exposed parental generation. A heritable reduction in reproductive capacity occurred in wildtype <I>N2</I> but was not found in a H3K9 histone methyltransferase (HMT) mutant, <I>met-2</I>(<I>n4256</I>), suggesting a potential role for HMT in transgenerational toxicity. Our results suggest that the reproductive toxicity after IHC exposure could be heritable and that histone methylation is associated with the transmission of the inherited phenotype.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Transgenerational toxicity of Iranian heavy crude oil (IHC) was investigated in the nematode <I>Caenorhabditis elegans</I> in the four consecutive generations under different exposure scenarios. </LI> <LI> <I>C. elegans</I> reproduction potential was inhibited by the IHC in the unexposed generations and in the exposed parental generation. </LI> <LI> Whole-life exposure condition exhibited transgenerational inheritance of defective reproduction. </LI> <LI> Decreased methylation of histone H3K9 was found in the exposed generation; however, a heritable diminution in reproduction did not occur in the H3K9 histone methyltransferase defective mutant. </LI> <LI> Reproductive toxicity caused by IHC exposure was found to be transmitted to subsequent unexposed generations, and methylation of histone H3K9 seems to be involved in it. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>