Browsing by Subject "Glutathione peroxidase"

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Open Access
Characterization of programmed cell death induced by oxidative stress in selenium - deficient hepatocellular carcinoma cells
(1999) İnce, Gülayşe
Selenium (Se) plays an important role in eliminating the reactive oxygen species generated during oxidative stress. Se-containing selenocysteine is an essential amino acid required for the synthesis of many selenoproteins, such as glutathione peroxidase. Se-dependent glutathione peroxidase is the major en2yme that metabolizes organic and hydrogen peroxides in the cell. It appears that Se manifests its antioxidant effect through the selenoproteins. Se deficiency causes a wide range of pathological conditions. Keshan disease, characterized by cardiomyocyte and liver cell death, defined as "necrosis", was found to be associated with Se deficiency. Se deficiency is also observed in liver cirrhosis, alcoholic liver disease, HIV positive and AIDS patients, thyroid hormone abnormalities, etc. Moreover, epidemiological studies show that Se deficiency increases the risk of many cancer types, including hepatocellular carcinoma (HCC). The molecular mechanisms of the pathologies associated with Se deficiency are mostly unknown. In this study, the in vitro responses of human hepatocellular carcinoma cells, to Se deficiency have been examined. Apoptotic changes (nuclear condensation, positive annexin V staining, genomic DNA breaks) are detected in Huh7, HepG2, and Mahlavu cells under Se-deficient culture conditions. Hydrogen peroxide addition into the culture medium aggravates apoptosis. Such changes are prevented by the supplementation of Se. The Se-dependent glutathione peroxidase enzyme is shown to be reduced in cells grown under Se-deficient conditions, explaining the build up of intracellular oxidative stress. It is proposed that the cell death observed in many pathologies associated with Se deficiency, is the result of the programmed cell death, triggered by an increase in intracellular oxidative stress, as opposed to necrotic cell death. Hep3B, Hep3B-TR, Hep40, PLC/PRF/5 and BC1/R14 cell lines have not displayed cell death when grown in Se-deficient conditions and were resistant to hydrogen peroxide, as well. The presence of such cell lines and the differential sensitivities manifested by HepG2, Huh7 and Mahlavu suggest a complete or partial gained resistance for apoptosis, which may contribute to the onset or progression of HCC, consistent with the increased risk of HCC in Se deficiency.
Open Access
Effect of high intensity interval training on elite athletes' antioxidant status
(Elsevier Masson, 2013) Ugras, A. F.
Objective: The effects of high intensity interval exercises on antioxidant defense system are not clear. Since there is an evident lack of studies focused on oxidative stress experienced following combat sports and high intensity interval training, we investigated oxidative stress markers (malondialdehyde [MDA], catalase [CAT], glutathione peroxidase [GPX], superoxide dismutase [SOD]) by completing high intensity interval training program (HIITP) and following International Muay Thai Championship (IMTC). Methods: The study was carried out on 21 elite players (15 males and six females) who had regular exercising and training habits. The participants were subjected to a daily 3-hour HIITP during brief training camp (10-day) before IMTC. They were instructed to maintain their normal dietary practices throughout the camp and during the study to take no antioxidant containing vitamin tablets. Results: There was a significant increase in MDA levels and significant decrease in CAT activities of players (P<. 0.05). The differences in SOD and GPX activities were not significant. Conclusion: These results suggested that high intensity interval training and competition could affect the oxidative status of Muay Thai (MT) athletes. © 2012 Elsevier Masson SAS.