Evidences showing ultraviolet-B radiation-induced damage of DNA in cyanobacteria and its detection by PCR assay

Abstract

Ultraviolet-B (UV-B) radiation is a biologically effective component of solar radiation which because of its absorption by important biomolecules such as nucleic acids, proteins, and lipids causes deleterious effects on biological systems [1], [2]. It has now been well documented that depletion of stratospheric ozone has led to an increase in the level of ultraviolet-B radiation (280–320 nm) reaching the earth’s surface [3], [4] and has caused a risk of exposure of living organisms on the Earth to this harmful radiation [1], [5], [6], [7], [8]. Several studies conducted under laboratory and natural conditions have revealed the harmful effects of UV-B radiation on growth, survival, motility, development, pigmentation, nutrient uptake, and various metabolic processes of cyanobacteria [2], [9]. These effects are in part due to the direct effect on membrane proteins, photosystem II, DNA, enzymes, growth regulators or due to indirect effect through the formation of reactive oxygen species. Amongst several targets of UV-B damage that have been identified, DNA and photosynthesis are recognized as the most predominant action sites [2], [6], [10].

Most of the information pertaining to induction of UV-induced DNA damage, their biological effects, and repair have been obtained by using short wavelength UV-C radiation (254 nm). In general during the course of UV irradiation, photons are absorbed by the DNA causing several types of damage involving single bases or interaction between adjacent bases or between DNA and protein [5], [10], [11], [12], [13]. The main class of UV-induced lesions consists of dimeric pyrimidine photoproducts which distort the DNA helix. These include cyclobutyl pyrimidine dimers arising from the cycloaddition of C5–C6 double bond of two adjacent pyrimidines and the pyrimidine (6-4) pyrimidone adducts which result from the addition of the 5′ end pyrimidine to the C4 carbonyl or imine group of the 3′ end pyrimidine [5], [12]. The latter are produced at a much slower rate but unlike the former cannot be excised and repaired by the usual photoreactivation mechanisms and thus they have the capacity for longer term damage. The dimers block the action of DNA polymerase and thereby prevent genome replication [14], [15], [16]. This may consequently lead to delayed cell division and growth inhibition and ultimately to death.