Oxidative stress, DNA damage and p53 expression in the larvae of Atlantic cod (Gadus morhua) exposed to ultraviolet (290-400 nm) radiation

Citation
Mp. Lesser et al., Oxidative stress, DNA damage and p53 expression in the larvae of Atlantic cod (Gadus morhua) exposed to ultraviolet (290-400 nm) radiation, J EXP BIOL, 204(1), 2001, pp. 157-164
Citations number
43
Categorie Soggetti
Biology,"Experimental Biology
Journal title
JOURNAL OF EXPERIMENTAL BIOLOGY
ISSN journal
00220949 → ACNP
Volume
204
Issue
1
Year of publication
2001
Pages
157 - 164
Database
ISI
SICI code
0022-0949(200101)204:1<157:OSDDAP>2.0.ZU;2-E
Abstract
nDecreases in stratospheric ozone levels from anthropogenic inputs of chlor inated fluorocarbons have resulted in an increased amount of harmful ultrav iolet-B (UVB, 290-320 nm) radiation reaching the sea surface in temperate l atitudes (30-50 degreesN). In the Gulf of Maine, present-day irradiances of ultraviolet-A (UVA, 320-400 nm) radiation can penetrate to depths of 23 m and WE radiation can penetrate to depths of 7-12 m, where the rapidly devel oping embryos and larvae of the Atlantic cod (Gadus morhua) are known to oc cur, Laboratory exposures of embryos and larvae of Atlantic cod to ultravio let radiation (UVR) equivalent to a depth of approximately 10 m in the Gulf of Maine resulted in significant mortality of developing embryos and a dec rease in standard length at hatching for yolk-sac larvae, Larvae at the end of the experimental period also had lower concentrations of UVR-absorbing compounds and exhibited significantly greater damage to their DNA, measured as cyclobutane pyrimidine dimer formation, after exposure to UVB radiation . Larvae exposed to WE radiation also exhibited significantly higher activi ties and protein concentrations of the antioxidant enzyme superoxide dismut ase and significantly higher concentrations of the transcriptional activato r p53. p53 is expressed in response to DNA damage and can result in cellula r growth arrest in the G1- to S-phase of the cell cycle or to programmed ce ll death (apoptosis), Cellular death caused by apoptosis is the most likely cause of mortality in embryos and larvae in these laboratory experiments, while the smaller size at hatching in those larvae that survived is caused by permanent cellular growth arrest in response to DNA damage, In addition, the sub-lethal energetic costs of repairing DNA damage or responding to ox idative stress may also contribute to poor individual performance in surviv ing larvae that could also lead to increases in mortality, The irradiances of WE radiation that elicit these responses in cod larvae can occur in many temperate latitudes, where these ecologically and commercially important f ish are known to spawn, and may contribute to the high mortality of cod emb ryos and larvae in their natural environment.