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Wyświetlanie 1-2 z 2
Tytuł:
Oxidative damage to DNA and antioxidant status in aging and age-related diseases
Autorzy:
Olinski, Ryszard
Siomek, Agnieszka
Rozalski, Rafal
Gackowski, Daniel
Foksinski, Marek
Guz, Jolanta
Dziaman, Tomasz
Szpila, Anna
Tudek, Barbara
Powiązania:
https://bibliotekanauki.pl/articles/1041102.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
ROS
aging
oxidative DNA damage
age-related diseases
BER
GO system
Opis:
Aging is a complex process involving morphologic and biochemical changes in single cells and in the whole organism. One of the most popular explanations of how aging occurs at the molecular level is the oxidative stress hypothesis. Oxidative stress leads in many cases to an age-dependent increase in the cellular level of oxidatively modified macromolecules including DNA, and it is this increase which has been linked to various pathological conditions, such as aging, carcinogenesis, neurodegenerative and cardiovascular diseases. It is, however, possible that a number of short-comings associated with gaps in our knowledge may be responsible for the failure to produce definite results when applied to understanding the role of DNA damage in aging and age-related diseases.
Źródło:
Acta Biochimica Polonica; 2007, 54, 1; 11-26
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Cu,Zn-superoxide dismutase deficiency in mice leads to organ-specific increase in oxidatively damaged DNA and NF-κB1 protein activity
Autorzy:
Siomek, Agnieszka
Brzoska, Kamil
Sochanowicz, Barbara
Gackowski, Daniel
Rozalski, Rafal
Foksinski, Marek
Zarakowska, Ewelina
Szpila, Anna
Guz, Jolanta
Bartlomiejczyk, Teresa
Kalinowski, Bartlomiej
Kruszewski, Marcin
Olinski, Ryszard
Powiązania:
https://bibliotekanauki.pl/articles/1042730.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Cu,Zn-SOD deficiency
NF-κB pathway
oxidative stress
Opis:
Earlier experimental studies have demonstrated that: i) Cu,Zn-superoxide dismutase deficiency leads to oxidative stress and carcinogenesis; ii) dysregulation of NF-κB pathway can mediate a wide variety of diseases, including cancer. Therefore, we decided, for the first time, to examine the level of oxidative DNA damage and the DNA binding activity of NF-κB proteins in SOD1 knockout, heterozygous and wild-type mice. Two kinds of biomarkers of oxidatively damaged DNA: urinary excretion of 8-oxodG and 8-oxoGua, and the level of oxidatively damaged DNA were analysed using HPLC-GC-MS and HPLC-EC. The DNA binding activity of p50 and p65 proteins in a nuclear extracts was assessed using NF-κB p50/p65 EZ-TFA transcription factor assay. These parameters were determined in the brain, liver, kidney and urine of SOD1 knockout, heterozygous and wild-type mice. The level of 8-oxodG in DNA was higher in the liver and kidney of knockout mice than in wild type. No differences were found in urinary excretion of 8-oxoGua and 8-oxodG between wild type and the SOD1-deficient animals. The activity of the p50 protein was higher in the kidneys, but surprisingly not in the livers of SOD1-deficient mice, whereas p65 activity did not show any variability. Our results indicate that in Cu,Zn-SOD-deficient animals the level of oxidative DNA damage and NF-κB1 activity are elevated in certain organs only, which may provide some explanation for organ-specific ROS-induced carcinogenesis.
Źródło:
Acta Biochimica Polonica; 2010, 57, 4; 577-583
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-2 z 2

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