**3.5 Homologous recombination and Non-homologous end-joining repair**

In mammalian cells double strand breaks (DSBs), one of the most deleterious damage, can be repaired by two different types of mechanism: 1) non-homologous end-joining (NHEJ) that rejoins the two broken ends in a template independent way with concomitant loss of sequence information. After overlapping of the two DNA ends, the ligase IV complex start the ligation process of the two broken ends; and 2) homologous recombination repair (HR) that uses a homologue undamaged DNA sequence (sister-chromatid or homologous chromosome) to repair the missing sequence between the two DNA ends. HR is an errorfree process (Dudas and Chovanec, 2004; Helleday *et al.*, 2007).

If not properly repaired DSB can cause loss of chromosomes and consequently generate mutations with or without induction of cell death (Dudas and Chovanec, 2004). Singlestrand breaks repair (SSBR) is a DNA repair pathway extremely important to avoid the deleterious effects of single-strand breaks (for more detail see the review Caldecott, 2007). Since DNA damage is recognized as the initial step in chemical carcinogenesis, inhibition of DNA damage and/or induction of repair would be the first line of defense against cancer caused by carcinogens. Chemoprevention by diet and dietary constituints against oxidative and alkylating agents will be covered by this review.
