Abstract
The goal of this study was to determine the short-term effects of the quality (UV-A/UV-B ratio) and quantity (irradiance) of natural ultraviolet radiation (UVR) on the apoptosis levels in Yellow perch (Perca flavescens) larvae. Apoptosis, or programmed cell death, is an essential event in many physiological processes as well as in pathological conditions. Western blots were used to measure the expression of several key proteins of the apoptotic cascade, such as p53, Bax, Bcl-2, and PARP-1, whereas specific apoptotic DNA fragmentation was measured by an ELISA assay. We predicted that higher UVR exposure would be related to higher levels of apoptosis. Our results showed that specific apoptotic DNA fragmentation was reduced by visible light + UV-A as well as by visible light + UV-A and UV-B treatments although it was not significantly affected by light quantity. However, the expression of p53, Bax/Bcl-2 ratio and PARP-1 were not significantly affected in larvae by the quantity or the quality of the light after two days of exposure. Altogether our results suggest that UVR may modulate the apoptotic process in Yellow perch larvae proposing an interesting role for this stressor on the early development of living organism under natural exposure condition.
Highlights
Ultraviolet radiation (UVR) is known to cause damages in aquatic organisms [1], eventually leading to increased mortality [2]
Based on the incident irradiance measured above the filters, we calculated that the cumulative UVR exposures received for the 313 nm (UV-B) and 340 nm (UV-A) wavelengths were of 0.67 and 3.35 W∙m−2∙nm−1, respectively
We studied the expression of p53, a tumor suppressor protein known to play an important role in evoking apoptosis, notably by encouraging the transcription of several pro-apoptotic genes such as Bax [34] and the expression of full-length PARP-1, a protein known to participate in the repair of damaged deoxyribonucleic acid (DNA) [41]
Summary
Ultraviolet radiation (UVR) is known to cause damages in aquatic organisms [1], eventually leading to increased mortality [2]. Most studies focused on UV-B (280 - 315 nm), showing that these wavelengths can cause cyclobutane pyrimidine dimers (CPD) formation in deoxyribonucleic acid (DNA) [4]-[6]. These damages may cause apoptotic cell death, known as programmed cell death, as reported in studies on Atlantic cod larvae [7]. Whereas a basal rate of apoptosis is normally observed in developing organisms such as fish larvae going through morphogenesis, external stressors such as UVR may affect developmental apoptosis by modulating specific rates of cellular death [7]
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