**4. Summary and conclusion**

Exposure to low dose radiation could be of significance in clinical evaluation of risk assessment, radiotherapy and radiation protection. Although a number of mechanisms such as enhanced DNA repair, alterations in stress proteins, immuno-modulation, and antioxidant defense system have been proposed to contribute to beneficial effects of low dose exposure, the understanding about the mechanisms inadequate. This is primarily because the reports are scattered, and among the available reports there is variability of dose response, the model systems as well as the experimental design followed in different laboratories. Our studies with a uniform experimental design on two different model systems viz. *Saccharomyces cerevisiae* and human PBMCs, has clearly demonstrated that irradiation with lower doses of ionizing radiation has a beneficial effect on the organism. Moreover, the effect of lower dose of radiation can not be predicted simply by extrapolating the effect of higher doses. The term 'Radiation induced radioresistance' or 'RIR' was suggested in our studies to refer a phenomenon where a single small dose radiation exposure could lead to better tolerance to the subsequently given lethal doses of radiation, and the effect was transient. Although, the RIR caused by low dose irradiation appears to be a complex interplay of many genes, this study shows that the genes of *MRX/MRN* complex, *HSP* family and also mitochondrial gene have a confirmed role in phenomenon leading to RIR. *KAR2* is an integral component of unfolded protein response (UPR) pathway. Up regulation of *KAR2* negatively regulated UPR pathway (Kimata et al., 2003), and, therefore may have caused accumulation of unfolded cytosolic proteins. If this is true then, after low dose irradiation, up regulation of *KAR2* helped the accumulation of proteins that might have unfolded due to radiation stress. The accumulation of unfolded proteins may have been responsible for increased levels of *SSA1* /*SSA2* /*SSA4* similar to that observed in *S. cerevisiae* cells after heat shock (Stone & Craig 1990). Also, it was observed the mitochondrial genes for maintaining the functional integrity of mitochondria; as well as to counter the reactive oxygen species that may have been produced because of oxidative stress produced after irradiation, were up-regulated. Further, the absence of mutation in representative sequences, decrease in revertants as well as tryptophan prototrophs, decrease in the micronuclei frequency together with enhanced levels of error-free DNA repair*,* strongly suggested that priming with low doses imparted transient radio-resistance to the cells culminating in the survival benefits via error-free mechanisms.
