Antimutagen

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 mutagenic compound into 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]

Examples of antimutagens

Micronutrients

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):

UV blockers

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

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]

References

  1. "The database and ontology of Chemical Entities of Biological Interest". EMBL-EBI, European Molecular Biology Laboratory, Wellcome Trust Genome Campus.
  2. 1 2 Bhattacharya, Sanjib. "Natural Antimutagens: A Review". Research Journal of Medicinal Plant 5. pp. 116–126. doi:10.3923/rjmp.2011.116.126.
  3. Renner, H.W.; Münzner, R. (April 1991). "The possible role of probiotics as dietary antimutagens". Mutation Research Letters 262 (4). Elsevier B.V. pp. 239–245. doi:10.1016/0165-7992(91)90090-q.
  4. "Natural antimutagenic agents". Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 350 (1). Elsevier B.V. pp. 143–152. doi:10.1016/0027-5107(95)00099-2. Retrieved 19 February 1996. Check date values in: |accessdate= (help)
  5. E. Wall, Monroe (1992). "Antimutagenic Agents from Natural Products". Journal of Natural Products 55 (11). ACS Publications. pp. 1561–1568. doi:10.1021/np50089a002.
  6. 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. PMID 23781504.
  7. 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.
  8. Maslin, DL (November 2014). "Do suncreens protect us?". International Journal of Dermatology 53 (11): 1319–23. doi:10.1111/ijd.12606. PMID 25208462.
  9. 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.
  10. Hausman, Geoffrey M. Cooper ; Robert E. (2003). The cell (3 ed.). Washington, DC: ASM Press [u.a.] ISBN 978-0878932146.
  11. 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.
  12. 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.

Further reading

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