The use of plants containing genotoxic carcinogens as foods and medicine

2018 ◽  
Vol 116 ◽  
pp. 27-39 ◽  
Author(s):  
Gerhard Prinsloo ◽  
Noluyolo Nogemane ◽  
Renee Street
Keyword(s):  
Genotoxic Carcinogens

Concentration-dependent effect of fumonisin B1 on apoptosis in oesophageal cancer cells

2017 ◽  
Vol 37 (7) ◽  
pp. 762-771 ◽  
Author(s):  
RB Khan ◽  
A Phulukdaree ◽  
AA Chuturgoon
Keyword(s):  
Cell Viability ◽  
Oesophageal Cancer ◽  
Caspase 3 ◽  
Quantitative Polymerase Chain Reaction ◽  
Fumonisin B1 ◽  
Annexin V ◽  
Tail Length ◽  
Bax Protein ◽  
Genotoxic Carcinogens ◽  
Parp 1

The geographical distribution of oesophageal cancer is linked to the exposure of fumonisin B1 (FB1), a mycotoxin produced by fungi that contaminates staple food worldwide. Non-genotoxic carcinogens like FB1 disturb homeostasis through increased cell proliferation or suppression of apoptosis. This study investigated the involvement of FB1 (0–20 μM) in spindle-shaped N-cadherin (+) CD45 (−) osteoblastic (SNO) cell death. Cell viability and death were assessed using the MTS and Annexin V-Fluos assays, respectively. Caspase activities were determined luminometrically and the comet assay assessed DNA damage. Induction of oxoguanine glycosylase 1 (OGG1) was measured using quantitative Polymerase Chain Reaction (qPCR), while cleaved poly (ADP-ribose) polymerase 1 (PARP-1) and Bax were determined by western blotting. Cell viability and PARP-1 cleavage were not affected by 1.25 μM FB1, but phosphatidylserine externalization, Bax protein expression, caspase activity, comet tail length and OGG1 transcripts were increased. The reduced cell viability in 10 μM FB1-treated cells was accompanied by corresponding increases in externalized phosphatidylserine, Bax, caspase-3/7 activity and cleaved PARP-1. The OGG1 transcripts were not significantly increased, but comet tails were increased. Bax, caspase-3/7 activities and cleaved PARP-1 were inhibited at 20 μM FB1. In addition, the OGG1 transcript levels were decreased ( p < 0.0001) along with comet lengths ( p < 0.0001). This study showed that FB1-induced apoptosis in SNO cells may be caspase-dependent or caspase-independent; the pathway used depends on the exposure concentration.

scholarly journals Rapid induction of more malignant tumors by various genotoxic carcinogens in transgenic mice harboring a human prototype c-Ha-ras gene than in control non-transgenic mice

1996 ◽  
Vol 17 (11) ◽  
pp. 2455-2461 ◽  
Author(s):  
Satoshi Yamamoto ◽  
Kunitoshi Mitsumori ◽  
Yukio Kodama ◽  
Naochika Matsunuma ◽  
Sunao Manabe ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Malignant Tumors ◽  
Ras Gene ◽  
Rapid Induction ◽  
Genotoxic Carcinogens

Bhas 42 Cell Transformation Assay for Genotoxic and Non-Genotoxic Carcinogens

2014 ◽  
pp. 343-362 ◽  
Author(s):  
Kiyoshi Sasaki ◽  
Anna Huk ◽  
Naouale El Yamani ◽  
Noriho Tanaka ◽  
Maria Dusinska
Keyword(s):  
Cell Transformation ◽  
Transformation Assay ◽  
Genotoxic Carcinogens

Chapter 7. Dissecting Modes of Action of Non-genotoxic Carcinogens

2016 ◽  
pp. 209-235
Author(s):  
Mirjam M. Schaap ◽  
Jan van Benthem ◽  
Miriam N. Jacobs ◽  
Annamaria Colacci ◽  
Anne S. Kienhuis ◽  
...  
Keyword(s):  
Modes Of Action ◽  
Genotoxic Carcinogens

Chemical carcinogens

2019 ◽  
pp. 79-90
Author(s):  
David H. Phillips
Keyword(s):  
Dna Repair ◽  
Cancer Incidence ◽  
Mammalian Cells ◽  
Human Exposure ◽  
Chemical Carcinogens ◽  
Regulatory Processes ◽  
Genotoxic Carcinogens ◽  
The Many ◽  
Transformation Methods ◽  
Insight Into

Large geographical and temporal differences in cancer incidence indicate that the causes of the majority of cases are a consequence of environmental and lifestyle factors. While many of these remain unknown, around half have known causes, and these include chemicals in air, water, and food, as well as products of industrial processes and of combustion. The major classes of chemical carcinogens and how they were discovered are described. A property shared by many of them is that they, or one or more of their metabolites, are electrophiles that can damage DNA in mammalian cells, leading to cellular responses including DNA repair, cytotoxicity, apoptosis, mutagenesis, and malignant transformation. Methods for predicting the carcinogenicity of new chemicals are part of the regulatory processes for safety assessment, and sensitive methods for monitoring human exposure to carcinogens provide insight into the aetiology of cancer. The mutational signatures that genotoxic carcinogens leave in the tumours they induce provide evidence of the chemicals that have caused them, and the approach has promise for shedding light on the many as-yet-unidentified cases of cancer worldwide.

scholarly journals Nickel Nanoparticles Induce the Synthesis of a Tumor-Related Polypeptide in Human Epidermal Keratinocytes

Nanomaterials ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 992
Author(s):  
Javier Jiménez-Lamana ◽  
Simon Godin ◽  
Gerard Aragonès ◽  
Cinta Bladé ◽  
Joanna Szpunar ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Nickel Nanoparticles ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Nickel Allergy ◽  
Skin Cells ◽  
Nickel Binding ◽  
Nickel Compounds ◽  
Linear Behavior ◽  
Genotoxic Carcinogens

Although nickel allergy and carcinogenicity are well known, their molecular mechanisms are still uncertain, thus demanding studies at the molecular level. The nickel carcinogenicity is known to be dependent on the chemical form of nickel, since only certain nickel compounds can enter the cell. This study investigates, for the first time, the cytotoxicity, cellular uptake, and molecular targets of nickel nanoparticles (NiNPs) in human skin cells in comparison with other chemical forms of nickel. The dose-response curve that was obtained for NiNPs in the cytotoxicity assays showed a linear behavior typical of genotoxic carcinogens. The exposure of keratinocytes to NiNPs leads to the release of Ni2+ ions and its accumulation in the cytosol. A 6 kDa nickel-binding molecule was found to be synthesized by cells exposed to NiNPs at a dose corresponding to medium mortality. This molecule was identified to be tumor-related p63-regulated gene 1 protein.

scholarly journals Mesenchyme-derived factors enhance preneoplastic growth by non-genotoxic carcinogens in rat liver

2017 ◽  
Vol 92 (2) ◽  
pp. 953-966 ◽  
Author(s):  
Marzieh Nejabat ◽  
Teresa Riegler ◽  
Tabea Reitinger ◽  
Sandra Subosits ◽  
Michael Römer ◽  
...  
Keyword(s):  
Rat Liver ◽  
Genotoxic Carcinogens
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