RESUMO
The adduction of the aldehydic end-products of lipid peroxidation to DNA induces bulky adducts, leading to genome instability. The bulky-DNA adducts are miscoding and thus play a fundamental role in mutagenesis and cancerogenesis. Special attention is given to the etheno- and propanoadducts, recognized as DNA modifiers. Such DNA lesions are repaired by different DNA repair mechanisms, mainly base excision repair (BER) and nucleotide excision repair (NER), as well as nucleotide incision repair (NIR) and transcription-coupled repair (TCR).
Assuntos
Dano ao DNA/fisiologia , Reparo do DNA , Peroxidação de Lipídeos/fisiologia , Animais , Adutos de DNA/fisiologia , Radicais Livres/metabolismo , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Mutagênese/genética , Espécies Reativas de Oxigênio/metabolismo , Transcrição GênicaRESUMO
The aim of this study was to verify hypothesis that protective effect of local temporary ischemia depends on dose of radiation. 56 male WAG-strain rats were used. Total body irradiation with 3 x 3 and 3 x 5 Gy was performed. Local temporary ischemia was induced by clamping the tail base. The biochemical parameters were the thiobarbituric acid-reactive substances (TBA-RS). In bone marrow smears the polychromatic erythrocyte (PCE) numbers were counted and the numbers of micronucleated PCEs were analyzed. In small intestines the numbers of crypts were calculated. The levels of TBA-RS in the serum of the animals irradiated with a 3 x 3 Gy dose were significantly different (P < 0.002). Also in animals irradiated with a dose of 3 x 3 Gy the numbers of intestinal crypts were different (P < 0.05). In animals irradiated with dose 3 x 5 Gy, for analyzed parameters differences did not achieve statistical significance. Local temporary ischaemia provides general protection against radiation damage for lower dose. This protective effect disappeared after applications of a higher dose of radiation.
