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Li,Y.; Chen,L.J.; Jiang,F.; Yang,Y.; Wang,X.X.; Zhang,Z.; Li,Z.; Li,L.. |
Hormesis is an adaptive response to a variety of oxidative stresses that renders cells resistant to harmful doses of stressing agents. Caffeic acid (CaA) is an important antioxidant that has protective effects against DNA damage caused by reactive oxygen species (ROS). However, whether CaA-induced protection is a hormetic effect remains unknown, as is the molecular mechanism that is involved. We found that a low concentration (10 μM) of CaA increased human liver L-02 cell viability, attenuated hydrogen peroxide (H2O2)-mediated decreases in cell viability, and decreased the extent of H2O2-induced DNA double-strand breaks (DSBs). In L-02 cells exposed to H2O2, CaA treatment reduced ROS levels, which might have played a protective role. CaA also activated the... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Caffeic acid; Hormesis; Antioxidants; DNA double-strand breaks; Extracellular signal-regulated kinase. |
Ano: 2015 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015000600502 |
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Poplawski,Tomasz; Pastwa,Elzbieta; Blasiak,Janusz. |
DNA double-strand breaks (DSBs) are a serious threat to the cell, for if not or miss-repaired, they can lead to chromosomal aberration, mutation and cancer. DSBs in human cells are repaired via non-homologous DNA end joining (NHEJ) and homologous recombination repair pathways. In the former process, the structure of DNA termini plays an important role, as does the genetic constitution of the cells, through being different in normal and pathological cells. In order to investigate the dependence of NHEJ on DSB structure in normal and cancer cells, we used linearized plasmids with various, complementary or non-complementary, single-stranded or blunt DNA termini, as well as whole-cell extract isolated from normal human lymphocytes, chronic myeloid leukemia... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: DNA repair; Non-homologous DNA end joining; DNA double-strand breaks; Complementary and non-complementary DNA ends. |
Ano: 2010 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572010000200027 |
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