Antimutagens are the agents that interfere with the mutagenicity of a substance.[1] The interference can be in the form of prevention of the transformation of a promutagenic compound into actual active mutagen, inactivation, or otherwise the prevention of Mutagen-DNA reaction.[2]
Antimutagens can be classified into: Desmutagens, that inactivate the chemical interactions before the mutagen attacks the genes and Bio-antimutagens, that stop the mutation process once after the genes are damaged by mutagens.[2] There are a number of naturally occurring anti-mutagens that show their efficient action.[3][4][5]
Nutrients such as vitamins and minerals are examples of micronutrients that are necessary for the proper maintenance of metabolism homeostasis in humans and other species. Micronutrients are also pointed to perform a role in genome stability acting as potential antimutagenic agents [6](see the examples below):
Carotenoids: Induction of single break DNA repair by a rejoining mechanism and elimination of 8-oxoguanine which is usually resulted from oxidative stress in cells;
Vitamins:[citation needed][clarification needed] Can induce cell programmed death via activation of p53 and increase of cellular mechanisms against strand breaks;
Flavonoid polyphenolics: Found to perform antimutagenic activity through the increase of OGG1 expression, which is an enzyme responsible to remove 8-oxoguanine a mutagenic product created after cell's exposure to oxidative stress; Increase of single break repair by rejoining and induction of genes related to base and nucleotide excision repair such as XPA and XPC;
Selenium: Induces programmed cell death via many signalling pathways as well as protects the cells against cell damage caused by oxidative stress.
Magnesium: Essentially necessary for the process of nucleotide excision repair where in cells treated in absence of this micronutrient the repair was impaired.[7]
Sunscreens are products commonly known by their capacity of protecting skin against sunburns. The active components present in sunscreens can vary, thus affecting the mechanism of protection against UV light, which can be done through absorption or reflection of UV energy.[8] As UV light can cause mutations by DNA damaging, sunscreen is considered an antimutagenic compound as it blocks the action of the UV light to induce mutagenesis in cells, basically the sunscreen inhibit the penetration of the mutagen.[9]
These genes have the function of protecting cells against tumor-like behaviour, such as higher proliferative rates and unlimited growth. It is common to find those genes down regulated or even inactivated in tumor cells. Thus, tumor suppressor genes can be recognized as antimutagenic agents.[10]
TP53: This gene encodes for the p53 protein, which is known to act on the apoptotic signalling pathway and is also described to be important in the break excision repair of cells that had their DNA damaged. p53 is a transcription factor that is involved in the transcription of many genes, some of which related to the process of cell response against DNA damage. Some types of cancer show a high prevalence of lower or even absent levels of expression of this protein, sustaining its importance against mutagenesis.[11]
PTEN: PTEN is another gene considered a tumor suppressor and acts through the inactivation of the PI3K-AKT pathway that leads to cell growth and survival. In other words, this gene is important to cause the cell growth arrest avoiding posterior effects and consequences of mutagenesis.[12]
Referencesedit
^"The database and ontology of Chemical Entities of Biological Interest". EMBL-EBI, European Molecular Biology Laboratory, Wellcome Trust Genome Campus.
^ abKada, Tsuneo; Inoue, Tadashi; Ohta, Toshihiro; Shirasu, Yasuhiko (1986). "Antimutagens and their Modes of Action". Antimutagenesis and Anticarcinogenesis Mechanisms. Vol. 39. pp. 181–196. doi:10.1007/978-1-4684-5182-5_15. ISBN978-1-4684-5184-9. PMID 3533041. {{cite book}}: |journal= ignored (help)
^Renner, H.W.; Münzner, R. (April 1991). "The possible role of probiotics as dietary antimutagens". Mutation Research Letters. 262 (4): 239–245. doi:10.1016/0165-7992(91)90090-q. PMID 1708108.
^Mitscher, Lester A.; Telikepalli, Hanumaiah; McGhee, Eva; Shankel, Delbert M. (1996-02-19). "Natural antimutagenic agents". Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 350 (1): 143–152. doi:10.1016/0027-5107(95)00099-2. PMID 8657175.
^E. Wall, Monroe (1992). "Antimutagenic Agents from Natural Products". Journal of Natural Products. 55 (11): 1561–1568. doi:10.1021/np50089a002. PMID 1479376.
^Arigony, AL; de Oliveira, IM; Machado, M; Bordin, DL; Bergter, L; Prá, D; Henriques, JA (2013). "The influence of micronutrients in cell culture: a reflection on viability and genomic stability". BioMed Research International. 2013: 597282. doi:10.1155/2013/597282. PMC3678455. PMID 23781504.
^Collins, AR; Azqueta, A; Langie, SA (April 2012). "Effects of micronutrients on DNA repair". European Journal of Nutrition. 51 (3): 261–79. doi:10.1007/s00394-012-0318-4. PMID 22362552. S2CID 23866597.
^Maslin, DL (November 2014). "Do suncreens protect us?". International Journal of Dermatology. 53 (11): 1319–23. doi:10.1111/ijd.12606. PMID 25208462.
^De Flora, S (18 June 1998). "Mechanisms of inhibitors of mutagenesis and carcinogenesis". Mutation Research. 402 (1–2): 151–8. doi:10.1016/s0027-5107(97)00292-3. PMID 9675264.
^Hausman, Geoffrey M. Cooper ; Robert E. (2003). The cell (3 ed.). Washington, DC: ASM Press [u.a.] ISBN978-0878932146.{{cite book}}: CS1 maint: multiple names: authors list (link)
^Zurer, I; Hofseth, LJ; Cohen, Y; Xu-Welliver, M; Hussain, SP; Harris, CC; Rotter, V (January 2004). "The role of p53 in base excision repair following genotoxic stress". Carcinogenesis. 25 (1): 11–9. doi:10.1093/carcin/bgg186. PMID 14555612.
^Song, MS; Salmena, L; Pandolfi, PP (4 April 2012). "The functions and regulation of the PTEN tumour suppressor". Nature Reviews. Molecular Cell Biology. 13 (5): 283–96. doi:10.1038/nrm3330. PMID 22473468. S2CID 28514977.
Further readingedit
Ramel, Class; et al. (1986). "Inhibitors of mutagenesis and their relevance to carcinogenesis: Report by ICPEMC expert group on antimutagens and desmutagens". Mutation Research/Reviews in Genetic Toxicology. 168 (1): 47–65. doi:10.1016/0165-1110(86)90021-7. PMID 3520303.
Stavric, B (1994). "Antimutagens and anticarcinogens in foods". Food and Chemical Toxicology. 32 (1): 79–90. doi:10.1016/0278-6915(84)90040-1. PMID 8132169.
Hartman, Philip E.; Shankel, Delbert M. (1990). "Antimutagens and anticarcinogens: a survey of putative interceptor molecules". Environmental and Molecular Mutagenesis. 15 (3): 145–182. doi:10.1002/em.2850150305. PMID 2185012. S2CID 23902598.
April 11, 2024
antimutagen, agents, that, interfere, with, mutagenicity, substance, interference, form, prevention, transformation, promutagenic, compound, into, actual, active, mutagen, inactivation, otherwise, prevention, mutagen, reaction, classified, into, desmutagens, t. Antimutagens are the agents that interfere with the mutagenicity of a substance 1 The interference can be in the form of prevention of the transformation of a promutagenic compound into actual active mutagen inactivation or otherwise the prevention of Mutagen DNA reaction 2 Antimutagens can be classified into Desmutagens that inactivate the chemical interactions before the mutagen attacks the genes and Bio antimutagens that stop the mutation process once after the genes are damaged by mutagens 2 There are a number of naturally occurring anti mutagens that show their efficient action 3 4 5 Contents 1 Examples of antimutagens 1 1 Micronutrients 1 2 UV blockers 1 3 Tumor suppressor genes 2 References 3 Further readingExamples of antimutagens editMicronutrients edit Nutrients such as vitamins and minerals are examples of micronutrients that are necessary for the proper maintenance of metabolism homeostasis in humans and other species Micronutrients are also pointed to perform a role in genome stability acting as potential antimutagenic agents 6 see the examples below Carotenoids Induction of single break DNA repair by a rejoining mechanism and elimination of 8 oxoguanine which is usually resulted from oxidative stress in cells Vitamins citation needed clarification needed Can induce cell programmed death via activation of p53 and increase of cellular mechanisms against strand breaks Flavonoid polyphenolics Found to perform antimutagenic activity through the increase of OGG1 expression which is an enzyme responsible to remove 8 oxoguanine a mutagenic product created after cell s exposure to oxidative stress Increase of single break repair by rejoining and induction of genes related to base and nucleotide excision repair such as XPA and XPC Selenium Induces programmed cell death via many signalling pathways as well as protects the cells against cell damage caused by oxidative stress Magnesium Essentially necessary for the process of nucleotide excision repair where in cells treated in absence of this micronutrient the repair was impaired 7 UV blockers edit Main article UV filter Sunscreens are products commonly known by their capacity of protecting skin against sunburns The active components present in sunscreens can vary thus affecting the mechanism of protection against UV light which can be done through absorption or reflection of UV energy 8 As UV light can cause mutations by DNA damaging sunscreen is considered an antimutagenic compound as it blocks the action of the UV light to induce mutagenesis in cells basically the sunscreen inhibit the penetration of the mutagen 9 Tumor suppressor genes edit Main article Tumor suppressor gene These genes have the function of protecting cells against tumor like behaviour such as higher proliferative rates and unlimited growth It is common to find those genes down regulated or even inactivated in tumor cells Thus tumor suppressor genes can be recognized as antimutagenic agents 10 TP53 This gene encodes for the p53 protein which is known to act on the apoptotic signalling pathway and is also described to be important in the break excision repair of cells that had their DNA damaged p53 is a transcription factor that is involved in the transcription of many genes some of which related to the process of cell response against DNA damage Some types of cancer show a high prevalence of lower or even absent levels of expression of this protein sustaining its importance against mutagenesis 11 PTEN PTEN is another gene considered a tumor suppressor and acts through the inactivation of the PI3K AKT pathway that leads to cell growth and survival In other words this gene is important to cause the cell growth arrest avoiding posterior effects and consequences of mutagenesis 12 References edit The database and ontology of Chemical Entities of Biological Interest EMBL EBI European Molecular Biology Laboratory Wellcome Trust Genome Campus a b Kada Tsuneo Inoue Tadashi Ohta Toshihiro Shirasu Yasuhiko 1986 Antimutagens and their Modes of Action Antimutagenesis and Anticarcinogenesis Mechanisms Vol 39 pp 181 196 doi 10 1007 978 1 4684 5182 5 15 ISBN 978 1 4684 5184 9 PMID 3533041 a href Template Cite book html title Template Cite book cite book a journal ignored help Renner H W Munzner R April 1991 The possible role of probiotics as dietary antimutagens Mutation Research Letters 262 4 239 245 doi 10 1016 0165 7992 91 90090 q PMID 1708108 Mitscher Lester A Telikepalli Hanumaiah McGhee Eva Shankel Delbert M 1996 02 19 Natural antimutagenic agents Mutation Research Fundamental and Molecular Mechanisms of Mutagenesis 350 1 143 152 doi 10 1016 0027 5107 95 00099 2 PMID 8657175 E Wall Monroe 1992 Antimutagenic Agents from Natural Products Journal of Natural Products 55 11 1561 1568 doi 10 1021 np50089a002 PMID 1479376 Arigony AL de Oliveira IM Machado M Bordin DL Bergter L Pra D Henriques JA 2013 The influence of micronutrients in cell culture a reflection on viability and genomic stability BioMed Research International 2013 597282 doi 10 1155 2013 597282 PMC 3678455 PMID 23781504 Collins AR Azqueta A Langie SA April 2012 Effects of micronutrients on DNA repair European Journal of Nutrition 51 3 261 79 doi 10 1007 s00394 012 0318 4 PMID 22362552 S2CID 23866597 Maslin DL November 2014 Do suncreens protect us International Journal of Dermatology 53 11 1319 23 doi 10 1111 ijd 12606 PMID 25208462 De Flora S 18 June 1998 Mechanisms of inhibitors of mutagenesis and carcinogenesis Mutation Research 402 1 2 151 8 doi 10 1016 s0027 5107 97 00292 3 PMID 9675264 Hausman Geoffrey M Cooper Robert E 2003 The cell 3 ed Washington DC ASM Press u a ISBN 978 0878932146 a href Template Cite book html title Template Cite book cite book a CS1 maint multiple names authors list link Zurer I Hofseth LJ Cohen Y Xu Welliver M Hussain SP Harris CC Rotter V January 2004 The role of p53 in base excision repair following genotoxic stress Carcinogenesis 25 1 11 9 doi 10 1093 carcin bgg186 PMID 14555612 Song MS Salmena L Pandolfi PP 4 April 2012 The functions and regulation of the PTEN tumour suppressor Nature Reviews Molecular Cell Biology 13 5 283 96 doi 10 1038 nrm3330 PMID 22473468 S2CID 28514977 Further reading editRamel Class et al 1986 Inhibitors of mutagenesis and their relevance to carcinogenesis Report by ICPEMC expert group on antimutagens and desmutagens Mutation Research Reviews in Genetic Toxicology 168 1 47 65 doi 10 1016 0165 1110 86 90021 7 PMID 3520303 Stavric B 1994 Antimutagens and anticarcinogens in foods Food and Chemical Toxicology 32 1 79 90 doi 10 1016 0278 6915 84 90040 1 PMID 8132169 Hartman Philip E Shankel Delbert M 1990 Antimutagens and anticarcinogens a survey of putative interceptor molecules Environmental and Molecular Mutagenesis 15 3 145 182 doi 10 1002 em 2850150305 PMID 2185012 S2CID 23902598 Retrieved from https en wikipedia org w index php title Antimutagen amp oldid 1183382077, wikipedia, wiki, book, books, library,
