Cell Biology and Toxicology (CELL BIOL TOXICOL)

Publisher: Springer Verlag

Journal description

Cell Biology and Toxicology is an international journal which provides a rapid publication outlet for papers of high scientific standards in the areas of cell biology genetic molecular and cellular toxicology. The scope of publication includes scientific reports dealing with the basic biology and with the physiological pharmacological and toxic response of cellular systems. Studies of subcellular and cellular systems derived from both prokaryotic and eukaryotic cell types are appropriate. Studies of toxic effects may include but are not limited to cytotoxicity mutagenicity carcinogenicity and teratogenicity. Moreover investigations on the development of cell systems for these purposes are relevant. In particular the journal welcomes approaches to cellular studies or molecular structure activity correlations that provide sound scientific information leading to the reduced use of experimental animals. Cell Biology and Toxicology publishes several types of articles including papers describing original research results and reviews on subjects of contemporary importance to cell biologists and cell toxicologists. Also brief announcements of scientific meetings or courses and of the availability of funding fellowships and scholarships are published.

Current impact factor: 2.68

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.677
2013 Impact Factor 1.971
2012 Impact Factor 2.338
2011 Impact Factor 2.511
2010 Impact Factor 2.056
2009 Impact Factor 1.746
2008 Impact Factor 2.155
2007 Impact Factor 1.758
2006 Impact Factor 1.4
2005 Impact Factor 1.548
2004 Impact Factor 1.338
2003 Impact Factor 1.58
2002 Impact Factor 1.275
2001 Impact Factor 1.177
2000 Impact Factor 1.107
1999 Impact Factor 1.3
1998 Impact Factor 0.511
1997 Impact Factor 0.492
1996 Impact Factor 0.883
1995 Impact Factor 0.711
1994 Impact Factor 0.696
1993 Impact Factor 0.703
1992 Impact Factor 0.981

Impact factor over time

Impact factor

Additional details

5-year impact 2.48
Cited half-life 7.70
Immediacy index 0.35
Eigenfactor 0.00
Article influence 0.61
Website Cell Biology and Toxicology website
Other titles Cell biology and toxicology (Princeton Scientific Publishers: Online)
ISSN 0742-2091
OCLC 41558232
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Springer Verlag

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Author's pre-print on pre-print servers such as arXiv.org
    • Author's post-print on author's personal website immediately
    • Author's post-print on any open access repository after 12 months after publication
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Nano-Mg(OH)2 is efficiently used in pollutant adsorption and removal due to its high adsorption capability, low-cost, and recyclability. A recent research from our group showed that Mg(OH)2 nanoflakes are not evidently internalized by cancer cells and are not cytotoxic. But the biocompatibility and potential toxicity of nano-Mg(OH)2 in a normal biological system are largely unclear. Nanoparticles could affect the function of endothelial cells, and endothelial dysfunction represents an early sign of lesion within the vasculature. Here, we applied the human umbilical vein vascular endothelial cells (HUVECs) as an in vitro model of the endothelium to study the cytotoxicity of nano-Mg(OH)2. Our results showed that nano-Mg(OH)2 at 200 μg/ml impaired proliferation and induced dysfunction of HUVECs, but did not result in cell necrosis and apoptosis. Transmission electron microscopy images and immunofluorescence results showed that the nano-Mg(OH)2 could enter HUVECs through caveolin-1-mediated endocytosis. Nano-Mg(OH)2 at high concentrations decreased the level of caveolin-1 and increased the activity of endothelial nitric oxide synthase (eNOS), thus leading to the production of excess nitric oxide (NO). In this work, we provide the cell damage concentrations of nano-Mg(OH)2 nanoparticles, and we propose a mechanism of injury induced by nano-Mg(OH)2 in HUVECs.
    Cell Biology and Toxicology 01/2015; 31(1). DOI:10.1007/s10565-014-9291-4
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    ABSTRACT: Many contaminated sites are characterized by the presence of different metals, thus increasing the complexity of toxic responses in exposed organisms. Within toxicogenomics, transcriptomics can be approached through the use of microarrays aimed at producing a genetic fingerprint for the response of model organisms to the presence of chemicals. We studied temporal changes in the early gene expression profiles of Escherichia coli cells exposed to three metal doses of a polymetallic solution over three exposure times, through the application of cDNA microarray technology. In the absence of metals, many genes belonging to a variety of cellular functions were up- and down-regulated over time. At the lowest metal dose, an activation of metal-specific transporters (Cus and ZraP proteins) and a mobilization of glutathione transporters involved in metal sequestration and trafficking was observed over time; this metal dose resulted in the generation of ROS capable of stimulating the transcription of Mn-superoxide dismutase, the assembly of Fe-S clusters and the synthesis of cysteine. At the intermediate dose, an overexpression of ROS scavengers (AhpF, KatG, and YaaA) and heat shock proteins (ClpP, HslV, DnaK, and IbpAB) was observed. Finally, at the highest dose, E. coli cells showed a repression of genes related with DNA mutation correctors (MutY glycopeptidases).
    Cell Biology and Toxicology 06/2014; 30(4). DOI:10.1007/s10565-014-9281-6
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    ABSTRACT: Oxidative stress has been involved in various neurological disorders and, in the central nervous system, astrocytes represent the cell type that contributes to neuroprotection via glutathione (GSH) metabolism, GSH-metabolizing enzymes like γ-glutamyltransferase (GGT), and apoE secretion. In this study, using IL-1β, a proinflammatory and prooxidant cytokine that is increased in numerous pathological situations, cells of astrocytoma cell line U373-MG were exposed to an oxidative stress, leading to c-Jun and c-Fos activation. IL-1β decreased both GGT activity and intracellular GSH content and increased apoE secretion, initiating astroglial response to injury. We observed that antioxidants inhibit IL-1β effects on c-Jun and c-Fos proteins, GGT activity and the GSH pool but not on apoE secretion. Our results allow us to conclude that neurological disorders associated with an IL-1β-induced oxidative stress could be, at least experimentally, reversible in the presence of one antioxidant, N-acetylcysteine.
    Cell Biology and Toxicology 04/2012; 16(3):155-163. DOI:10.1023/A:1007654804730
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    ABSTRACT: Exposure of rat alveolar epithelial cells to 10 μmol/L CdCl2 causes time-dependent increases in steady-state mRNA levels of the γ-glutamylcysteine synthetase catalytic (heavy) subunit (γ-GCS) and of glutathione S-transferase isoforms (GST-α and GST-π). The expression of γ-GCS was significantly increased as early as 2 h after addition of cadmium. Maximal induction of γ-GCS mRNA (∼4-fold), at 8 h, was subsequently followed by increases in γ-GCS activity/protein and glutathione (GSH) levels. Maximal elevations in GST-π (∼2-fold) and GST-α (∼10-fold) transcripts, at 8 and 24 h, respectively, were also accompanied by enhanced GST activity. Cadmium-induced oxidative stress, assessed by alterations in GSH homeostasis and an accelerated rate of intracellular oxidant production, could constitute early events in the signal transduction pathway mediating these responses. The dimeric transcription factor, activator protein-1 (AP-1), may also play a regulatory role in this process. This association is suggested by transcriptional activation of the immediate-early response genes, c-fos and c-jun, within 15 min after exposure to cadmium and by the enhancement of AP-1 DNA binding activity, involving a c-Jun protein complex, which is maximally induced (∼4-fold) by 2 h. These molecular changes likely function together to protect alveolar epithelial cells against cadmium toxicity.
    Cell Biology and Toxicology 04/2012; 16(6):347-362. DOI:10.1023/A:1007696610186

  • Cell Biology and Toxicology 01/2012;
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    ABSTRACT: Apoptosis is a highly regulated and programmed cell breakdown process characterized by numerous changes. It was reported as the major mechanism of anticancer drug-induced cells death. Unfortunately, many of these drugs are non-specific and cause severe side effects. The effects of 5-flourouracil (5-FU) on the apoptotic events in normal murine thymus were evaluated using an in vivo model. A single dose of 5-FU (150mg/kg ip) was injected to CF-1 mice. A multiparametric analysis of thymic weight, cellularity, viability, architectural organization, apoptosis, DNA fragmentation, and the expression of several apoptotic proteins was evaluated in 10days time-course study post-5-FU dosing. Total organ weights, thymocyte counts, and cell viabilities diminished drastically from the second day. The thymus architecture assessed through electron scanning microscopy revealed deep alterations and the lost of cell–cell contact between the first and the third days. DNA fragmentation and apoptotic indexes (May Grünwald Giemsa staining, double flourescent dyes, and TdT-mediated dUTP nick-end labeling assay) revealed that cell death was maximal on the second day (three times over control). Furthermore, the pro-apoptotic proteins FAS and Bax were strongly up-regulated during the first 2days. The aforementioned morphological and biochemical changes were also accompanied within the same period by caspase 3 activation. This study revealed that in vivo apoptosis in normal thymus after 5-FU administration is related to FAS, Bax, and Caspase 3 co-expressions under the current experimental conditions, these findings, therefore, contribute to a new insight into the molecular mechanisms involved during 5-FU administration upon the thymus and the possible events committed in the lymphophenia associated with chemotherapy.
    06/2009: pages 131-142;
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    ABSTRACT: Western lifestyle plays an important role in the prevalence of type 2 diabetes by causing insulin resistance and pancreatic β-cell dysfunction, a prerequisite for the development of diabetes. High fat diet and alcohol are major components of the western diet. The aim of the present study was to investigate the effects of ethanol and fatty acids on β-cell survival and metabolism. We treated the rat β-cell line RINm5F with ethanol, a mixture of palmitic and oleic acids, or both. Reactive oxygen species (ROS) were determined by (5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate) (CM-H2DCFDA) fluorescence assay, and mitochondrial activity was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) reduction assay and by determining ATP production. Cell viability was assessed with a cell counter and trypan blue exclusion, and the mode of cell death by Hoechst33342 and propidium iodide staining. With both ethanol and fatty acid treatments, MTT reduction and ATP production decreased, whereas ROS production increased. Ethanol treatment had no effect on cell number, whereas fatty acid treatment reduced the cell number. Cell incubation with ethanol, fatty acids, or both increased the number of Hoechst 33342-positive nuclei. However, the majority of nuclei from fatty acid-treated cells were stained with propidium iodide, indicating a loss of plasma membrane integrity. We conclude that both ethanol and fatty acids generate cellular oxidative stress, and affect mitochondrial function in RINm5F β-cells. However, ethanol causes β-cell death by apoptosis, whereas fatty acids cause cell death predominantly by necrosis. It is not known whether these results are applicable to human β-cells.
    Cell Biology and Toxicology 04/2009; 25(2):141-152. DOI:10.1007/s10565-008-9067-9
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    ABSTRACT: This report summarises practical aspects to measuring cell motility in culture. The methods described here were discussed at a 1-day European Tissue Culture Society (ETCS-UK) workshop organised by John Masters and Gareth E Jones that was held at University College London on 19th April 2007.
    Cell Biology and Toxicology 10/2008; 24(5):381-9. DOI:10.1007/s10565-007-9049-3
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    ABSTRACT: 2-(6-(2-thieanisyl)-3(Z)-hexen-1, 5-diynyl) aniline (THDA), an enediyne compound, was identified in our laboratory as a novel antineoplastic agent against human leukemia K562 cells. THDA-induced apoptosis was associated with the upregulation of Bax, downregulation of X-linked inhibitor of apoptosis (XIAP), as well as the activation of caspase-3 and caspase-9. In addition, the mitogen-activated protein family kinases, including c-Jun N-terminal kinase (JNK) and extracellular signal-regulated protein kinase (ERK) kinases, and the transcription factor c-Jun were all activated by phosphorylation after 6 h exposure to THDA. Phosphorylation (activation) of JNK and ERK kinases by THDA was blocked by an ERK inhibitor, PD98059, or a JNK inhibitor, JNK-1, respectively, suggesting that THDA-induced apoptosis in K562 cells is ERK and JNK dependent. Moreover, the blockade of ERK and JNK also attenuated the modulation of Bax and XIAP, as well as the activation of caspase-3 and caspase-9 induced by THDA. These findings suggest that the activation of JNK and ERK is involved in the THDA-induced apoptosis of K562 cells. Therefore, this investigation, for the first time, uncovered the biological properties of this novel antitumor enediyne.
    Cell Biology and Toxicology 08/2008; 24(4):291-302. DOI:10.1007/s10565-007-9038-6
  • Article: Abstract.

    Cell Biology and Toxicology 08/2008; 24(4):341-80. DOI:10.1007/s10565-008-9082-x
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    ABSTRACT: Medical devices and implanted biomaterials are often assessed for biological reactivity using visual scores of cell-material interactions. In such testing, biomaterials are assigned cytotoxicity ratings based on visual evidence of morphological cellular changes, including cell lysis, rounding, spreading, and proliferation. For example, ISO 10993 cytotoxicity testing of medical devices allows the use of a visual grading scale. The present study compared visual in vitro cytotoxicity ratings to quantitative in vitro cytotoxicity measurements for biomaterials to determine the level of correlation between visual scoring and a quantitative cell viability assay. Biomaterials representing a spectrum of biological reactivity levels were evaluated, including organo-tin polyvinylchloride (PVC; a known cytotoxic material), ultra-high molecular weight polyethylene (a known non-cytotoxic material), and implantable tissue adhesives. Each material was incubated in direct contact with mouse 3T3 fibroblast cell cultures for 24 h. Visual scores were assigned to the materials using a 5-point rating scale; the scorer was blinded to the material identities. Quantitative measurements of cell viability were performed using a 3-(4,5-dimethylthiozol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay; again, the assay operator was blinded to material identities. The investigation revealed a high degree of correlation between visual cytotoxicity ratings and quantitative cell viability measurements; a Pearson's correlation gave a correlation coefficient of 0.90 between the visual cytotoxicity score and the percent viable cells. An equation relating the visual cytotoxicity score and the percent viable cells was derived. The results of this study are significant for the design and interpretation of in vitro cytotoxicity studies of novel biomaterials.
    Cell Biology and Toxicology 08/2008; 24(4):315-9. DOI:10.1007/s10565-007-9040-z
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    ABSTRACT: Dimerumic acid (DMA) is contained in Monascus anka and Monascus pilosus fermented products. The purpose of this study was to evaluate the effect of DMA against salicylic acid (SA)- and tert-butylhydroperoxide (t-BHP)-induced oxidative stress and cytotoxicity in the liver, using rat liver microsomes and isolated rat hepatocytes. DMA was extracted from monascus-garlic-fermented extract using M. pilosus. In rat liver microsomes, 1 microM DMA decreased SA-induced lipid peroxidation but did not affect the production of the oxidative metabolite of SA via CYP. In isolated rat hepatocytes, 1 microM DMA decreased SA-induced lipid peroxidation and chemiluminescence (CL) generation and the intracellular glutathione-reduced form/oxidized form (GSH/GSSG) ratio in the presence of 1 microM DMA was higher than that without DMA; however, 100 microM DMA suppressed the leakage of lactate dehydrogenase (LDH). On the other hand, t-BHP-induced lipid peroxidation, CL generation, and LDH leakage were prevented by 100 microM DMA. Thus, DMA showed an antioxidative effect in hepatocytes and protected against hepatotoxicity by suppressing oxidative stress without affecting CYP enzymes.
    Cell Biology and Toxicology 08/2008; 24(4):283-90. DOI:10.1007/s10565-007-9037-7
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    ABSTRACT: Overproduction of collagen (I) by activated hepatic stellate cells is a critical step in the development of liver fibrosis. It has been established that these cells express interleukin (IL)-6 and respond to this cytokine with an increase in α(I) collagen. Pentoxifylline, a methylxanthine derivate, has been reported to have antifibrotic properties, but the mechanism responsible for this effect is unknown. The aim of this study was to determine the effect of pentoxifylline on acetaldehyde-induced collagen production in a rat hepatic stellate cell line (CFSC-2G cells). Cells were treated with 100 μM acetaldehyde and 200 μM pentoxifyline for 3 h. IL-6 and α(I) collagen messenger RNA (mRNA) were determined by reverse transcriptase polymerase chain reaction (RT-PCR) assay. NFκB activation was determined by electrophoretic mobility shift assay. To corroborate NFκB participation in pentoxifylline effect, cells were pretreated with 10 μM TPCK, a NFκB inhibitor. IκBα was determined by Western blot. IL-6 expression decreased significantly in acetaldehyde-pentoxifylline-treated cells. Acetaldehyde-treated cells pretreated with an anti-IL-6 monoclonal antibody did not show any increase in α (I) collagen expression. Acetaldehyde-treated cells increased 1.48 times NFκB activation, whereas acetaldehyde-pentoxifylline- treated cells decreased NFκB activation to control values. TPCK pretreated acetaldehyde cells did not present NFκB activation. To corroborate NFκB participation in pentoxifylline effect, IκBα was determined. IκBα protein level decreased 50% in acetaldehyde-treated cells, while acetaldehyde-pentoxifylline-treated cells showed IκBα control cells value. The data suggest that acetaldehyde induced α(I) collagen and IL-6 expression via NFκB activation. Pentoxifylline prevents acetaldehyde-induced α(I) collagen and IL-6 expression by a mechanism dependent on IκBα degradation, which in turn blocks NFκB activation.
    Cell Biology and Toxicology 08/2008; 24(4):303-14. DOI:10.1007/s10565-007-9039-5
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    ABSTRACT: Increased levels of particulate air pollution (PM10) have been implicated as a causal agent in pulmonary disease exacerbation and increased deaths from respiratory and cardiovascular disorders. The exact mechanism by which PM10 drives toxicity in the lung is still unknown, but studies have focused on inhibition of macrophage function and impaired alveolar clearance mechanisms. To assess the effects of PM10 on pulmonary macrophage clearance mechanisms ex vivo, Wistar rats were instilled with 125 or 250 microg of PM10 collected from the North Kensington, London. Control rats were instilled with sterile saline. The rats were sacrificed after 18 h and a bronchoalveolar lavage (BAL) was performed. Macrophages isolated from the BAL fluid were assessed for ability to migrate towards a positive chemoattractant (ZAS) ex vivo and to perform phagocytosis. Macrophages isolated from the PM10-exposed rats showed inhibition of potential to migrate. Macrophage phagocytic ability ex vivo was also significantly reduced by the presence of PM10 inside the cells. This study indicates that acute PM10 exposure diminishes macrophage motility and phagocytosis in a manner that could prove deleterious to particle clearance from the alveolar region of the lung. Decreased particle clearance promotes inflammation, and hence, warrants further investigation in relation to the effects of chronic PM10 exposure on macrophage clearance mechanisms and establishing the mechanisms behind decreased macrophage migration.
    Cell Biology and Toxicology 07/2008; 24(3):243-52. DOI:10.1007/s10565-007-9033-y