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Fenugreek in Management of Female-Specific Health Conditions
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
For regulatory purposes, a chemical’s mutagenicity potential has mainly been evaluated using in vitro assays, such as the Bacterial Reverse Mutation Test, AMES test (Mortelmans and Zeiger 2000). Mutagens are agents that can cause heritable changes in DNA, and their capacity to cause mutations is defined as mutagenicity (Cvetković, Takić Miladinov, and Stojanović 2018). As all information for the proper development, functioning, and reproduction of organisms is coded in DNA, mutations can result in harmful effects and play a role in genetic disorders (Verheyen 2017), especially for food-related products (Mandal et al. 2018; Weisburger 1999). The structural chromosomal abnormalities such as chromosomal aberration (a missing, extra, or irregular portion of chromosomal DNA) result from breakage and incorrect rejoining of chromosomal segments and result in many genetic diseases disorders such as cancer (Nguyen 2020). The standardized fenugreek seed extracts with markers such as furostenol saponins, glycosides, or low molecular galactomannans such as FENU-FG, SFSE-G, and LMWGAL-TF, were found safe and devoid of mutagenicity (OECD Test No. 471) and genotoxicity (Mammalian Chromosomal Aberration, OECD Test No. 473) potential during these studies (Deshpande, Mohan, and Thakurdesai 2016a; Deshpande, Mohan, Ingavale et al. 2017).
Consumer Safety Considerations of Cosmetic Preservation*
Published in Philip A. Geis, Cosmetic Microbiology, 2020
Corie A. Ellison, Alhaji U. N’jai, Donald L. Bjerke
Mutagenicity or mutation is defined as a permanent change in the content or structure of the genetic material of an organism that may result in a heritable change in the characteristics of the organism. These changes may involve many aspects of the genetic structure including a gene or gene segment, a block of genes, or whole chromosomes.
Quick Methods: Structure-Activity Relationships and Short-Term Bioassay
Published in Samuel C. Morris, Cancer Risk Assessment, 2020
To give some examples of results of SAR analysis, Craig and Enslein (1981) reported on a study of 416 compounds. Since no uniform endpoint was available, the analysis aimed to predict the probability that a substance was mutagenic. The relationship of various structural properties of these compounds were compared to the qualitative finding of mutagenicity for the compound. The most important properties predicting mutagenicity (in terms of their statistical significance) were: one benzene ring, branching terminal nitro group, generic halogen chain fragment, more than two carbocyclic or aromatic rings, more than one single heterocyclic ring un-fused to any other ring, three-branch nitrogen atom, single occurrence of carbonyl in more than one ring, two benzene rings, single occurrence of carbonyl in a ring, one single heterocyclic ring unfused to any other ring, and a generic halogen substitute fragment. In all, 48 properties were included in the predictive equation. A score was calculated for mutagenicity and one for nonmutagenicity and the probability of mutagenicity was calculated from these scores. Taking a predicted probability of over 60% as mutagenic, a probability of less than 40% as nonmutagenic, and a predicted probability between 40 and 60% as indeterminate, the model had a false positive rate of 11% and a false negative rate of 8%.
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
Briefly, aneugenicity, clastogenicity or mutagenicity are major genotoxicity mechanisms. For aneugenicity, genotoxicants act primarily on non-DNA targets (microtubule, centrosome or kinetochore (More et al. 2021)) or cause damage to the mitosis apparatus, leading to improper chromosome segregation (Parry et al. 1996, 2002). For clastogenicity, structural chromosome aberrations such as chromatid/chromosome breaks occur (Bignold 2009). Clastogenic agents can covalently bind to DNA or enzymes, leading to chromosome breakage. Mutagenicity corresponds to the induction of DNA mutations (Kumar et al. 2018), either by direct interaction with DNA or chromatin or by indirect mechanisms, such as through generation of reactive oxygen species or inflammation (DeMarini 2019). Genotoxicity is associated to serious health effects, the first one being cancer (Phillips and Arlt 2009): some genotoxic agents can indeed cause mutations that can eventually lead to malign tumor. Hence, most carcinogenic chemicals are genotoxic (Hayashi 1992), which make the measurement of this endpoint critical for hazard assessment.
Biomedical application of chondroitin sulfate with nanoparticles in drug delivery systems: systematic review
Published in Journal of Drug Targeting, 2021
Abebe Feyissa Amhare, Jian Lei, Huan Deng, Yizhen Lv, Jing Han, Lei Zhang
Cytotoxicity is referring to the quality of being toxic to cells. If cells are treated with the cytotoxic compound, it may lose membrane integrity and even rapidly die (undergo necrosis) due to cell lysis. The cells can stop actively growing and decrease in cell viability [62]. The cytotoxicity test is one of the biological evaluations by using cells in vitro to observe cell growth and morphological changes by developed drugs [63–65]. It has a series of advantages along with the preferred and mandatory items [64]. Cytotoxicity testing is important in ensuring safety ranging from environmental exposures to medical devices [66]. The previous study reported that cytotoxic drugs can kill cancer cells but they can also damage normal cells which are considered as the side effects of most chemotherapy drugs [67]. So, precautions are recommended specifically to avoid carcinogenicity and mutagenicity.
The 2-year rodent bioassay in drug and chemical carcinogenesis testing: Sensitivity, according to the framework of carcinogenic action
Published in Toxicology Mechanisms and Methods, 2020
Jose D. Suarez-Torres, Fausto A. Jimenez-Orozco, Carlos E. Ciangherotti
Alternatively, substances were acknowledged as threshold-based when they were (a) negative to in vitro mutagenicity in both bacterial systems and mammalian systems, or (b) negative to in vitro mutagenicity in bacterial or mammalian systems plus negative to in vivo (rodent) mutagenicity. On the other hand, chemicals were recognized as non-threshold-based when (a) there was evidence in the literature concerning their capability of covalent binding to the DNA, or their ability to yield non-oxidative DNA-adducts, and when (b) according to the frameworks for genotoxicity testing advanced by the EFSA (2011) or the U.K. COM (2011), the chemical could be regarded as genotoxic. Alternatively, substances were acknowledged as non-threshold-based when they were positive to (a) in vitro mutagenicity in both bacterial and mammalian systems, or (b) in vitro mutagenicity in bacterial or mammalian systems plus in vivo (rodent) mutagenicity.