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Approaches for Identification and Validation of Antimicrobial Compounds of Plant Origin: A Long Way from the Field to the Market
Published in Mahendra Rai, Chistiane M. Feitosa, Eco-Friendly Biobased Products Used in Microbial Diseases, 2022
Lívia Maria Batista Vilela, Carlos André dos Santos-Silva, Ricardo Salas Roldan-Filho, Pollyanna Michelle da Silva, Marx de Oliveira Lima, José Rafael da Silva Araújo, Wilson Dias de Oliveira, Suyane de Deus e Melo, Madson Allan de Luna Aragão, Thiago Henrique Napoleão, Patrícia Maria Guedes Paiva, Ana Christina Brasileiro-Vidal, Ana Maria Benko-Iseppon
As mentioned earlier, genotoxicity can be assessed in vitro and in vivo models [Guideline M3 (R2)]. For in vitro assessments, two tests are required: (1) Salmonella (Ames) test; and (2) a test using mammalian cells. The latter can be one of the three possibilities: (1) assay of gene mutation in mouse lymphoma; (2) chromosomal aberrations; and (3) micronucleus test (Sekizawa et al. 2017). In the development of antimicrobials, the Ames test is often unfeasible because it involves bacterial strains of Salmonella typhimurium. In this case, more than one analysis can be carried out strategically on mammalian cells. On the other hand, for in vivo tests, the following assays are recommended: (1) the bone marrow micronucleus test; (2) chromosomal aberrations of the bone marrow; and (3) the micronucleus test in peripheral blood cells of mice or rats (EMA 2013).
Consumer Safety Considerations of Cosmetic Preservation*
Published in Philip A. Geis, Cosmetic Microbiology, 2020
Corie A. Ellison, Alhaji U. N’jai, Donald L. Bjerke
Genotoxicity is a broader term and includes harmful effects on genetic materials such as DNA strand breaks and DNA adducts that do not necessarily lead to mutagenicity. Genotoxic effects can occur in both somatic and germ cells. Malformation, death, or a permanent heritable change in the resulting embryo can occur in germ cells, while somatic cell mutations could result in cancer since cancer often arises from a mutagenic occurrence. Thus, genotoxicity testing is important for evaluating the ability of a preservative to interact with genetic material and cause adverse effects that could produce cancer or heritable changes in the offspring.
Hazard Characterization and Dose–Response Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
Genotoxicity is the ability of substances to damage DNA and/or cellular components regulating the fidelity of the genome—such as the spindle apparatus, topoisomerases, DNA repair systems, and DNA polymerases. The oldest, least expensive, and least predictive test is the bacterial reverse mutation assay, or Ames Test. The in vitro micronucleus test uses mammalian cell lines or cultures of primary human cells and looks for micronuclei or chromosomal aberrations. Micronuclei are infrequent third nuclei formed during cell division that contain chromosome fragments. The dose-dependent frequency of micronuclei suggests potential genotoxicity. In vivo genotoxicity tests are most often performed in transgenic animals and look for specific effects depending on the transgenic species.157
Is a non-cytotoxic and non-genotoxic novel bioinspired dipeptide structure synthesis possible for theragnostic applications?
Published in Drug and Chemical Toxicology, 2023
Merve Bacanlı, Jülide Secerli, Burcu Karayavuz, Onur Erdem, Hakan Erdoğan
It is also important to investigate the genotoxic effects in evaluation of the toxic effects of the theragnostics synthesized with new approaches. Genotoxicity can cause irreversible damage to DNA, mutagenicity, and cancer formation. There are several assays available that can be used to detect genotoxicity. One of the most common DNA damage assays is the single-cell gel electrophoresis assay, commonly known as the Comet assay (Catalán et al.2014). The results of the genotoxic effects of Hg2+/Phe–Phe dipeptides in NIH/3T3 cells by the alkaline Comet assay are shown in Figure 5. At 4- and 24-h exposures, Hg2+/Phe–Phe dipeptides did not cause any significant changes in DNA damage in NIH/3T3 cells at concentrations of 1, 2, and 5 mg/mL. At the 48-h exposure, Hg2+/Phe–Phe dipeptide exposure at concentrations of 2 and 5 mg/mL caused a significant increase in DNA damage compared to the negative control. At 72 h of exposure, a significant increase in DNA damage was observed in NIH/3T3 cells compared to the negative control at all concentrations.
Analysis of cytotoxicity and genotoxicity in a short-term dependent manner induced by a new titanium dioxide nanoparticle in murine fibroblast cells
Published in Toxicology Mechanisms and Methods, 2022
Matheus Pedrino, Patrícia Brassolatti, Ana Carolina Maragno Fattori, Jaqueline Bianchi, Joice Margareth de Almeida Rodolpho, Krissia Franco de Godoy, Marcelo Assis, Elson Longo, Karina Nogueira Zambone Pinto Rossi, Carlos Speglich, Fernanda de Freitas Anibal
In general, genotoxicity is known to result from direct or indirect effectors. Here, we highlight the importance of an indirect genotoxic factor related to chronic inflammation caused by (i) immune system activation or (ii) a route of mitochondria damage that leads to increased ROS production and consequently impairs genetic material (Ali et al. 2016). The reactive oxygen species are involved in many cellular mechanisms including cell cycle regulation, proliferation and differentiation, cell self-renewal, and apoptosis (Kim et al. 2010; Gholinejad et al. 2019). In turn, cells developed defense mechanisms to maintain the intracellular oxidative balance as the tumor suppressor protein p53 that controls cell cycle arrest and allows DNA damage repair (Benchimol 2001). However, damages that cannot be repaired may lead to cell death by apoptosis.
Exploring graphene-based materials’ genotoxicity: inputs of a screening method
Published in Nanotoxicology, 2021
Salma Achawi, Ludovic Huot, Fabrice Nesslany, Jérémie Pourchez, Sophie Simar, Valérie Forest, Bruno Feneon
Primary genotoxicity can be direct or indirect. Direct genotoxicity is a consequence of a direct interaction between nanomaterial and DNA or chromosomes by direct binding with DNA or through mechanical effects. It is often considered that direct genotoxicity is a non-threshold effect, supposingly increasing the risk from the smallest dose (Jenkins et al. 2010). GBMs such as graphene quantum dots or GO have been shown to be able to penetrate cell nucleus (Wang et al. 2011, 2013), a direct contact with nuclear DNA can then be suspected. Some GBMs are known to interact with specific loci of the chromatin (Sun et al. 2018). GO, for example, was found to bind directly DNA, which affects the replication process (Liu et al. 2013). A direct interaction with DNA can also occur during interphase and may affect replication or transcription mechanisms, which can impact DNA structure and even cause cleavage (Ren et al. 2010). Furthermore, a direct interaction can also be observed between the GBMs and chromosomes during mitosis: in that case, loss of chromosome (aneugenicity) or chromosomal break (clastogenicity) can be observed. Lastly, carbon-based materials are well-known to instrinsically generate free radicals: GBMs are of no exception. Depending on their surface parameters (such as surface oxidation and suface defects), free radicals are released from the GO surface and can directly damage DNA (Dizdaroglu et al. 2002).