Chemicals can interact with genetic material either by causing damage that necessitates DNA repair or by inhibiting processes that repair DNA damage caused by other agents. Damage can be repaired by excision repair, which acts throughout the cell cycle and is considered an error free system, or by postreplication repair, which acts only during the DNA synthesis period and is considered error prone. The amount of excision repair that occurs under various conditions of chemical exposure is an indication of the amount of repairable damage, but it is only an indirect indication of the mutagenic potential of a chemical since the mutagenic potential and, by implication, the carcinogenic potential depend on the amount of damage that is not repaired. In addition, although most chemicals that damage DNA elicit excision repair, some, notably those that intercalate in DNA electrostatically, actually inhibit excision repair. But these and other inhibitory chemicals, including tumor promoters, inhibit all DNA functions to a similar extent; that is, they do not act specifically on excision repair. Measurements of excision repair or of its inhibition by chemicals thus bear a complex and currently unpredictable relation to the mutagenic and carcinogenic potential of any chemical and should be used with caution.
|Original language||English (US)|
|Title of host publication||IARC (International Agency for Research on Cancer) Scientific Publications|
|Number of pages||23|
|Publication status||Published - 1976|
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