Study of gamma radiation induced damages and variation of oxygen enhancement ratio with radiation dose using Saccharomyces cerevisiae Rajesha K. Nairy • Nagesh N. Bhat • K. B. Anjaria • B. Sreedevi • B. K. Sapra • Yerol Narayana Received: 24 July 2014 / Published online: 24 August 2014 Ó Akade ´miai Kiado ´, Budapest, Hungary 2014 Abstract In the present study, an attempt has been made to quantify Oxygen Enhancement Ratio (OER) and variation of OER as a function of dose with experi- mental and theoretical formulations using Saccharomyces cerevisiae D7, X2180 and rad 52. The study confirms that, the variation of OER with dose depends upon type of cell and repair proficiency of cells. A theoretical model has been formulated to estimate OER values. With the help of this model, OER value for any dose can be calculated in the exponential region of the sur- vival curve without actually extending the experiment in that dose region. Keywords Saccharomyces cerevisiae  Oxygen enhancement ratio  Radiation dose  Cell survival Introduction Ionizing radiation, which deposits energy from its inter- action with biological material, is a potent inducer of DNA damage due to both free radical formation and direct DNA interactions [1–4]. In sparsely ionizing radiations like c-rays, X-rays and electron beams, most of the energy is deposited in tissues by secondary electrons. Physico- chemical interaction of radiation with cellular DNA pro- duces a variety of primary lesions, such as Single Strand Breaks (SSBs), Double- Strand Breaks (DSBs), Crosslinks and Base damage. The SSBs, Base damage and Abasic site damage are generally repaired by excision repair, whereas DSBs are the principal lesion [5] which if un-repaired or mis-repaired may lead to a gene mutation or chromosomal aberrations [6], which leads to deterministic and stochastic effects, i.e. mitotic or clonogenic cell death, apoptosis and cancer [7–12]. Oxygen is one of the best known modifiers of radiation sensitivity and the biological effects are greater in the presence of oxygen [13]. The reduced oxygen availability is sensed and triggers homeostatic responses, which impact on virtually all areas of biology and medicine [14]. Failure to achieve complete response following radiotherapy of large tumors is attributed to the presence of radioresistant hypoxic cells, therefore clarifying the mechanism of the oxygen effect is important. In brief, under normoxic con- ditions, oxygen is capable of reacting with electrons ejec- ted from macromolecules by the interacting photons (ionizations), preventing recombination, thereby essentially fixing the damage radiochemically [15]. The radiochemical damage fixation is through organic peroxides, formed during the interaction of oxygen with hydrogen and hydroxyl radicals produced by radiation. This organic peroxide is the reason for most of the lethal DNA damages and cell death. Hydrogen donation by thiols, particularly glutathione, can repair lesions, but such thiols compete inefficiently with the counteracting effects of oxygen [16–20]. The lack of oxygen in hypoxic cells results in a greater probability of radiochemical restitution or repair, and thus less induced damage. The time scale of this pro- cess is in milliseconds [21]. More recent evidence, how- ever, has suggested that biochemical, as well as radiochemical mechanisms may be affecting the radiore- sistance of hypoxic cells [15]. The factor of sensitization R. K. Nairy  Y. Narayana (&) Department of Studies in Physics, Mangalore University, Mangalagangotri, Mangalore 574199, India e-mail: narayanay@yahoo.com N. N. Bhat  K. B. Anjaria  B. Sreedevi  B. K. Sapra RP & AD, Bhabha Atomic Research Center, Mumbai 400085, India 123 J Radioanal Nucl Chem (2014) 302:1027–1033 DOI 10.1007/s10967-014-3408-3