The Effect of UV-B Radiation on Bufo arenarum Embryos Survival and Superoxide Dismutase Activity

J Herkovits,J L D´Eramo,O Fridman

doi:10.3390/ijerph2006030006

Abstract

The exposure of Bufo arenarum embryos to 300-310 nm UV-B at a dose of 4,104 Joule/m(2) resulted in 100% lethality within 24 hr while 820 Joule/m(2) was the NOEC value for short-term chronic (10 days) exposure. The dose response curves show that lethal effects are proportional with the dose and achieve its highest value within 48 hr post exposure. The superoxide dismutase (SOD) activity in amphibian embryos for sublethal UV-B exposures was evaluated by means of UV-B treatments with 273 (A), 820(B), 1368(C) and 1915(D) Joule/m(2) at 2 and 5 hours post irradiation. The SOD activity in units/mg protein in A, B, C and D at 2 hr after treatments were 80.72 +/- 14.29, 74.5 +/- 13.19, 39.5 +/- 6.99 and 10.7 +/- 1.89 respectively while for control embryos it was 10.88 +/- 1.31. At 5 hr after treatments the SOD values were similar to those found in control embryos. The results confirm the high susceptibility of amphibian embryos to UV-B and point out that the SOD activity is enhanced by low doses of UV-B irradiation achieving significantly higher values than in control embryos at 2 hr post exposure.

Highlights

Exposure to UV-B may result from both natural and artificial sources
The main purpose of this study is to report the dose response curves for UV-B exposure in Bufo arenarum embryos, the LC10, LC50 and LC90 plotted as Toxicity Profile (TOP) curves up to 10 days post irradiation, and the superoxide dismutase (SOD) activity in control and UV-B treated embryos
The dose-response and isotoxicity - TOP curves - [20] of UV-B treated Bufo arenarum embryos point out a proportional increase in mortality as the irradiation is increased with a cumulative lethal effect observed mainly within the initial 48 hr post exposure

Summary

Introduction

Exposure to UV-B may result from both natural and artificial sources. The sun is the principal source of exposure for most people and wildlife. Decreases in stratospheric ozone levels from anthropogenic inputs of chlorinated fluorocarbons have resulted in an increased amount of harmful ultraviolet-B (UV-B, 280-315 nm) radiation, having serious consequences for living organisms. The ion superoxide induce peroxidation of fatty acids, affecting membrane lipids [2], provoke monobasic damage, strand breaks and reading frame shifting on DNA [3], e.g. denaturalization and/or degradation of proteins [4], and depolarization of polysaccharides [5]. The cellular consequences of damage due to UV radiation include changes in membrane permeability and membrane transport systems, activation of genes, mutation, inhibition of cell division, activation of viruses, etc., resulting in cellular death [6]. At high dose UV-B radiation enhance lipid peroxidation, a widely accepted general mechanism for cellular injury and death [7,8,9]. Photoreactivating enzymes activities (photolyase) are a common mechanism of protection against UV-B exposure [8, 9]; in some organisms, photoreactivation is the most important mechanism for the repair of cyclobutane pyrimidine dimers (CBPDs) [10], which are major cytogenic and mutagenic photoproducts in the DNA

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