TGACTGTAC AC TGACATGTAC
TGACTGT GA ACTGACA CX£TGAC
I I I I i I I l^l I I I ' ' ' ' ' ■ ■ ■ r ■ ■ ■ ■
■rvTTVTVvvrvv* 'rvrvvTvi VVTVV*
TGACTGTACATG TGACTGTGAACA G
ACTGACATGTAC ACTGACACTGA C
Figure 7 Hypothetical mechanisms for DNA damage-induced frameshift mutation formation. (a) Deletion in newly synthesized DNA; (b) insertion in newly synthesized DNA.
of neoplasia ('cancer') is sex dependent, so that mutagenesis is perhaps modulated by estrogen or other hormones. Because cell division in embryonic, larval, and juvenile organisms is more rapid than in adults, the adults may be less susceptible to such damage. Also, persistent DNA lesions (mutations or chromosomal abnormalities) may accumulate over time, so that older individuals are more likely to exhibit neoplasia or other mutagenic effects. Additionally, variation between individuals may be due to different exposure histories or genetic variability in cellular uptake, excretion, xenobiotic metabolism, or DNA repair. Environmental factors that modulate DNA damage and mutagenesis include temperature (which may mediate carcinogen metabolism or DNA repair rates in these ectotherms), dissolved oxygen concentration in water (which may mediate oxidative stress), salinity or ionic composition of water, or food availability and chemical composition. Also, the amount of DNA damage in fish may vary with season, perhaps due to temperature or bioenergetic or hormonal status. Furthermore, concomitant exposure to other chemicals may promote DNA damage or promote mutagenesis. Thus, the amount of DNA damage induced by complex mixtures may be much more than that predicted by single-chemical genotoxic effects. Finally the degree of genotoxic or mutagenic effects may be mediated by intra-and interspecific interactions such as competition, predation, parasitism, trophic structure and complexity of the ecosystem, and population density of affected organisms.
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