Clastogen

[1] These processes are a form of mutagenesis which if left unrepaired, or improperly repaired, can lead to cancer.

[1] Known clastogens include acridine yellow, benzene, ethylene oxide, arsenic, phosphine, mimosine, actinomycin D, camptothecin, methotrexate, methyl acrylate, resorcinol and 5-fluorodeoxyuridine.

Radiation was the earliest known clastogen that caused direct DNA damage, following the classic breaks theory.

The IVMN assay can pick up on fragments that were membrane bound to DNA that were split from nuclei throughout the process of cell division.

There can be uncertainty with telomeres that occur short term during the first round of cell division in which there can be chromosomal damage by clastogens.

[9] In plants and mice cells studies have found that purine receptor agonists adenosine, ATP, ADP, cyclohexyladenosine, phenylisopropyladenosine and dimethylaminopurine riboside can lower the amount of clastogen damage seen in chromosomes and reduce the amount of micronuclei affected brought on by ethyl methanesulfonate and cyclophosphamide.

Some ligands more than others can stop or reduce the clastogen activity of ethyl methanesulfonate such as adenosine, ADP or DAP.

Figure comparing the effects of exposure to genotoxic agents (aneugens and clastogens) on DNA. Aneugens induce mis-segregation of chromosomes into daughter cells while clastogens break the DNA and chromosome.
Summary of theories of the mechanisms of chromosomal aberrations: A, ‘classic’ breaks theory; B, ‘mis-repair of breaks’ theory; C, ‘repair-created breaks’ theory. Adapted from Bignold. [ 4 ]