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Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format Example of Toxicology in Vitro format
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open access Open Access

Toxicology in Vitro — Template for authors

Publisher: Elsevier
Categories Rank Trend in last 3 yrs
Toxicology #32 of 122 down down by 7 ranks
journal-quality-icon Journal quality:
Good
calendar-icon Last 4 years overview: 1042 Published Papers | 5837 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 09/07/2020
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Journal Performance & Insights

Impact Factor

CiteRatio

Determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

A measure of average citations received per peer-reviewed paper published in the journal.

2.959

4% from 2018

Impact factor for Toxicology in Vitro from 2016 - 2019
Year Value
2019 2.959
2018 3.067
2017 3.105
2016 2.866
graph view Graph view
table view Table view

5.6

12% from 2019

CiteRatio for Toxicology in Vitro from 2016 - 2020
Year Value
2020 5.6
2019 5.0
2018 5.9
2017 5.7
2016 5.9
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 4% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 12% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

0.834

4% from 2019

SJR for Toxicology in Vitro from 2016 - 2020
Year Value
2020 0.834
2019 0.799
2018 0.895
2017 0.931
2016 1.025
graph view Graph view
table view Table view

0.924

2% from 2019

SNIP for Toxicology in Vitro from 2016 - 2020
Year Value
2020 0.924
2019 0.905
2018 0.953
2017 1.0
2016 0.944
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 4% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 2% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Toxicology in Vitro

Guideline source: View

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Use of these names, trademarks and brands does not imply endorsement or affiliation. Disclaimer Notice

Elsevier

Toxicology in Vitro

Toxicology in Vitro publishes original research papers and reviews on the application and use of in vitro systems for assessing or predicting the toxic effects of chemicals and elucidating their mechanisms of action. These in vitro techniques include utilizing cell or tissue c...... Read More

Medicine

i
Last updated on
09 Jul 2020
i
ISSN
0887-2333
i
Impact Factor
High - 1.226
i
Acceptance Rate
39%
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
elsarticle-num
i
Citation Type
Numbered
[25]
i
Bibliography Example
G. E. Blonder, M. Tinkham, T. M. Klapwijk, Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion, Phys. Rev. B 25 (7) (1982) 4515–4532. URL 10.1103/PhysRevB.25.4515

Top papers written in this journal

Journal Article DOI: 10.1016/J.TIV.2005.06.034
In vitro toxicity of nanoparticles in BRL 3A rat liver cells
Saber M. Hussain1, K. L. Hess, J.M. Gearhart2, K.T. Geiss1, John J. Schlager1
01 Oct 2005 - Toxicology in Vitro

Abstract:

This study was undertaken to address the current deficient knowledge of cellular response to nanosized particle exposure. The study evaluated the acute toxic effects of metal/metal oxide nanoparticles proposed for future use in industrial production methods using the in vitro rat liver derived cell line (BRL 3A). Different si... This study was undertaken to address the current deficient knowledge of cellular response to nanosized particle exposure. The study evaluated the acute toxic effects of metal/metal oxide nanoparticles proposed for future use in industrial production methods using the in vitro rat liver derived cell line (BRL 3A). Different sizes of nanoparticles such as silver (Ag; 15, 100 nm), molybdenum (MoO(3); 30, 150 nm), aluminum (Al; 30, 103 nm), iron oxide (Fe(3)O(4); 30, 47 nm), and titanium dioxide (TiO(2); 40 nm) were evaluated for their potential toxicity. We also assessed the toxicity of relatively larger particles of cadmium oxide (CdO; 1 microm), manganese oxide (MnO(2); 1-2 microm), and tungsten (W; 27 microm), to compare the cellular toxic responses with respect to the different sizes of nanoparticles with different core chemical compositions. For toxicity evaluations, cellular morphology, mitochondrial function (MTT assay), membrane leakage of lactate dehydrogenase (LDH assay), reduced glutathione (GSH) levels, reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) were assessed under control and exposed conditions (24h of exposure). Results showed that mitochondrial function decreased significantly in cells exposed to Ag nanoparticles at 5-50 microg/ml. However, Fe(3)O(4), Al, MoO(3) and TiO(2) had no measurable effect at lower doses (10-50 microg/ml), while there was a significant effect at higher levels (100-250 microg/ml). LDH leakage significantly increased in cells exposed to Ag nanoparticles (10-50 microg/ml), while the other nanoparticles tested displayed LDH leakage only at higher doses (100-250 microg/ml). In summary the Ag was highly toxic whereas, MoO(3) moderately toxic and Fe(3)O(4), Al, MnO(2) and W displayed less or no toxicity at the doses tested. The microscopic studies demonstrated that nanoparticle-exposed cells at higher doses became abnormal in size, displaying cellular shrinkage, and an acquisition of an irregular shape. Due to toxicity of silver, further study conducted with reference to its oxidative stress. The results exhibited significant depletion of GSH level, reduced mitochondrial membrane potential and increase in ROS levels, which suggested that cytotoxicity of Ag (15, 100 nm) in liver cells is likely to be mediated through oxidative stress. read more read less

Topics:

Toxicity (51%)51% related to the paper
View PDF
1,820 Citations
Journal Article DOI: 10.1016/J.TIV.2005.06.048
Dietary flavonoids: effects on xenobiotic and carcinogen metabolism.
Young Jin Moon1, Xiaodong Wang1, Marilyn E. Morris1
01 Mar 2006 - Toxicology in Vitro

Abstract:

Flavonoids are present in fruits, vegetables and beverages derived from plants (tea, red wine), and in many dietary supplements or herbal remedies including Ginkgo Biloba, Soy Isoflavones, and Milk Thistle. Flavonoids have been described as health-promoting, disease-preventing dietary supplements, and have activity as cancer ... Flavonoids are present in fruits, vegetables and beverages derived from plants (tea, red wine), and in many dietary supplements or herbal remedies including Ginkgo Biloba, Soy Isoflavones, and Milk Thistle. Flavonoids have been described as health-promoting, disease-preventing dietary supplements, and have activity as cancer preventive agents. Additionally, they are extremely safe and associated with low toxicity, making them excellent candidates for chemopreventive agents. The cancer protective effects of flavonoids have been attributed to a wide variety of mechanisms, including modulating enzyme activities resulting in the decreased carcinogenicity of xenobiotics. This review focuses on the flavonoid effects on cytochrome P450 (CYP) enzymes involved in the activation of procarcinogens and phase II enzymes, largely responsible for the detoxification of carcinogens. A number of naturally occurring flavonoids have been shown to modulate the CYP450 system, including the induction of specific CYP isozymes, and the activation or inhibition of these enzymes. Some flavonoids alter CYPs through binding to the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, acting as either AhR agonists or antagonists. Inhibition of CYP enzymes, including CYP 1A1, 1A2, 2E1 and 3A4 by competitive or mechanism-based mechanisms also occurs. Flavones (chrysin, baicalein, and galangin), flavanones (naringenin) and isoflavones (genistein, biochanin A) inhibit the activity of aromatase (CYP19), thus decreasing estrogen biosynthesis and producing antiestrogenic effects, important in breast and prostate cancers. Activation of phase II detoxifying enzymes, such as UDP-glucuronyl transferase, glutathione S-transferase, and quinone reductase by flavonoids results in the detoxification of carcinogens and represents one mechanism of their anticarcinogenic effects. A number of flavonoids including fisetin, galangin, quercetin, kaempferol, and genistein represent potent non-competitive inhibitors of sulfotransferase 1A1 (or P-PST); this may represent an important mechanism for the chemoprevention of sulfation-induced carcinogenesis. Importantly, the effects of flavonoids on enzymes are generally dependent on the concentrations of flavonoids present, and the different flavonoids ingested. Due to the low oral bioavailability of many flavonoids, the concentrations achieved in vivo following dietary administration tend to be low, and may not reflect the concentrations tested under in vitro conditions; however, this may not be true following the ingestion of herbal preparations when much higher plasma concentrations may be obtained. Effects will also vary with the tissue distribution of enzymes, and with the species used in testing since differences between species in enzyme activities also can be substantial. Additionally, in humans, marked interindividual variability in drug-metabolizing enzymes occurs as a result of genetic and environmental factors. This variability in xenobiotic metabolizing enzymes and the effect of flavonoid ingestion on enzyme expression and activity can contribute to the varying susceptibility different individuals have to diseases such as cancer. As well, flavonoids may also interact with chemotherapeutic drugs used in cancer treatment through the induction or inhibition of their metabolism. read more read less

Topics:

Flavones (55%)55% related to the paper, Genistein (54%)54% related to the paper, Isoflavones (54%)54% related to the paper, Biochanin A (52%)52% related to the paper, Fisetin (52%)52% related to the paper
795 Citations
Journal Article DOI: 10.1016/J.TIV.2009.06.001
Oxidative stress-dependent toxicity of silver nanoparticles in human hepatoma cells
Soohee Kim1, Ji Eun Choi1, Jinhee Choi1, Kyu-Hyuck Chung2, Kwangsik Park3, Jongheop Yi1, Doug-Young Ryu1
01 Sep 2009 - Toxicology in Vitro

Abstract:

Cytotoxicity induced by silver nanoparticles (AgNPs) and the role that oxidative stress plays in this process were demonstrated in human hepatoma cells. Toxicity induced by silver (Ag(+)) ions was studied in parallel using AgNO(3) as the Ag(+) ion source. Using cation exchange treatment, we confirmed that the AgNP solution co... Cytotoxicity induced by silver nanoparticles (AgNPs) and the role that oxidative stress plays in this process were demonstrated in human hepatoma cells. Toxicity induced by silver (Ag(+)) ions was studied in parallel using AgNO(3) as the Ag(+) ion source. Using cation exchange treatment, we confirmed that the AgNP solution contained a negligible amount of free Ag(+) ions. Metal-responsive metallothionein 1b (MT1b) mRNA expression was not induced in AgNP-treated cells, while it was induced in AgNO(3)-treated cells. These results indicate that AgNP-treated cells have limited exposure to Ag(+) ions, despite the potential release of Ag(+) ions from AgNPs in cell culture. AgNPs agglomerated in the cytoplasm and nuclei of treated cells, and induced intracellular oxidative stress. AgNPs exhibited cytotoxicity with a potency comparable to that of Ag(+) ions in in vitro cytotoxicity assays. However, the toxicity of AgNPs was prevented by use of the antioxidant N-acetylcysteine, and AgNP-induced DNA damage was also prevented by N-acetylcysteine. AgNO(3) treatment induced oxidative stress-related glutathione peroxidase 1 (GPx1) and catalase expression to a greater extent than AgNP exposure, but treatment with AgNO(3) and AgNPs induced comparable superoxide dismutase 1 (SOD1) expression levels. Our findings suggest that AgNP cytotoxicity is primarily the result of oxidative stress and is independent of the toxicity of Ag(+) ions. read more read less

Topics:

Silver nanoparticle (52%)52% related to the paper, Superoxide dismutase (50%)50% related to the paper, Oxidative stress (50%)50% related to the paper
758 Citations
Journal Article DOI: 10.1016/J.TIV.2009.12.001
Silver nanoparticles induce cytotoxicity by a Trojan-horse type mechanism.
Eun-Jung Park1, Jongheop Yi2, Younghun Kim3, Kyunghee Choi4, Kwangsik Park1
01 Apr 2010 - Toxicology in Vitro

Abstract:

Silver nanoparticles (AgNPs) are widely applied in many household products and medical uses. However, studies on the effects of AgNPs on human health and environmental implications are in the beginning stage. Furthermore, most data on the toxicity of AgNPs have been generated using nanoparticles modified with detergents to pr... Silver nanoparticles (AgNPs) are widely applied in many household products and medical uses. However, studies on the effects of AgNPs on human health and environmental implications are in the beginning stage. Furthermore, most data on the toxicity of AgNPs have been generated using nanoparticles modified with detergents to prevent agglomeration, which may alter their toxicities. In this study, we studied toxicity using AgNPs prepared by dispersing them in fetal bovine serum (FBS), biocompatible materials. AgNPs (average size; 68.9 nm, concentrations; 0.2, 0.4, 0.8, and 1.6 ppm, exposure time; 24, 48, 72, and 96 h) showed cytotoxicity to cultured RAW264.7 cells by increasing sub G1 fraction, which indicates cellular apoptosis. AgNPs decreased intracellular glutathione level, increased NO secretion, increased TNF-α in protein and gene levels, and increased gene expression of matrix metalloproteinases (MMP-3, MMP-11, and MMP-19). When cells were treated with AgNPs, they were observed in the cytosol of the activated cells, but were not observed in the dead cells. It seemed that AgNPs were ionized in the cells to cause cytotoxicity by a Trojan-horse type mechanism suggested by previously reported studies. read more read less

Topics:

Silver nanoparticle (51%)51% related to the paper
626 Citations
Journal Article DOI: 10.1016/J.TIV.2009.05.015
Toxicity of nanoparticles of ZnO, CuO and TiO2 to yeast Saccharomyces cerevisiae.
Kaja Kasemets1, Angela Ivask1, Henri-Charles Dubourguier1, Anne Kahru1
01 Sep 2009 - Toxicology in Vitro

Abstract:

The aim of this study was to evaluate the toxic effect of nanosized ZnO, CuO and TiO(2) to Saccharomyces cerevisiae - a widely used unicellular eukaryotic model organisms in molecular and cell biology. The effect of metal oxide nanoparticles, their bulk forms and respective ionic forms were compared. The bioavailable Zn(2+) a... The aim of this study was to evaluate the toxic effect of nanosized ZnO, CuO and TiO(2) to Saccharomyces cerevisiae - a widely used unicellular eukaryotic model organisms in molecular and cell biology. The effect of metal oxide nanoparticles, their bulk forms and respective ionic forms were compared. The bioavailable Zn(2+) and Cu(2+) ions in the growth medium were quantified by recombinant microbial sensors. Nano and bulk TiO(2) were not toxic even at 20000 mg/l. Both, nano and bulk ZnO were of comparable toxicity (8-h EC(50) 121-134 mg ZnO/l and 24-h EC(50) 131-158 mg/l). The toxicity was explained by soluble Zn-ions as proved by the microbial sensor. However, nano CuO was about 60-fold more toxic than bulk CuO: 8-h EC(50) were 20.7 and 1297 mg CuO/l and 24-h EC(50) were 13.4 and 873 mg/l, respectively. The increase in toxicity of both CuO formulations at 24th hour of growth was due to the increased dissolution of copper ions from CuO over time. Comparison of EC(50) values of nano CuO, bulk CuO and Cu(2+) with bioavailable copper concentrations in the growth medium showed that the solubilized Cu-ions explained only about 50% of the toxicity of both, nano and bulk CuO. To our knowledge, this is the first study that evaluates the toxicity of ZnO, CuO and TiO(2) nanoparticles to S.cerevisiae. read more read less
498 Citations
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12. Is Toxicology in Vitro's impact factor high enough that I should try publishing my article there?

To be honest, the answer is no. The impact factor is one of the many elements that determine the quality of a journal. Few of these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Toxicology in Vitro?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Toxicology in Vitro. The table below indicates the level of access a journal has as per Sherpa Romeo's archiving policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

14. What are the most common citation types In Toxicology in Vitro?

The 5 most common citation types in order of usage for Toxicology in Vitro are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

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