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CJ Newton, D Bilko, S Pappa, and SL Atkin

The oestrogen receptor is fundamental to the growth and survival of the rat pituitary tumour cell line, GH(3). Our previous studies have shown that antioestrogens such as RU 58668 and ZM 182780 will reduce the rate of cell division and also induce cell death. Death of these cells in response to antioestrogen treatment appears to be due to a heightened sensitivity to reactive oxygen species (ROS). As part of a study to determine the cross-talk between steroid receptor systems in these cells, we have observed that the glucocorticoid, dexamethasone (Dex), inhibits antioestrogen-induced cell death. Cell death induced by H(2)O(2) is enhanced by ZM 182780 and this effect is also blocked by Dex. As apoptotic cell death in a number of systems involves an early loss of mitochondrial membrane potential (DeltaPsi(m)), we have performed detailed studies on the time-course of DeltaPsi(m) loss in relation to the loss in cell membrane function. These studies have indicated that a loss of DeltaPsi(m) parallels a loss of cell membrane function - this is more characteristic of necrosis than of apoptosis. From microscopic observations of these cells in response to H(2)O(2), it has been noted that early cell membrane blebbing, induced by H(2)O(2), is blocked in the presence of ZM 182780. Cell membrane blebbing can precede necrosis as well as apoptosis and it is thought to involve cytoskeletal changes, for which localised glycolytic reactions provide ATP. These observations, together with those showing that removal of glucose, but not inhibition of mitochondrial function, enhances ROS-induced cell death, prompted studies on the glycolytic pathway. As a strong candidate mechanism, it would appear that, via an effect on one of the rate-limiting glycolytic enzymes, glyceraldehyde-3-phosphate dehydrogenase, Dex is able to overcome the antioestrogen-enhanced loss of glycolytic function following exposure of cells to ROS. This report contributes to the growing body of evidence showing that glucocorticoids provide a survival advantage to both normal and tumour cell types.

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C Riou, C Remy, R Rabilloud, B Rousset, and P Fonlupt

Apoptosis might be involved in the reduction of the thyroid cell population in physiopathological situations such as goitre involution and autoimmune deleterious processes. Up to now, little attention has been paid to the apoptotic phenomenon in the normal thyroid gland the specialized metabolism of which is expected to generate reactive oxygen species. Indeed, thyroid cells have the capacity to synthesize H2O2. In this study, we have analyzed the capacity of H2O2 to trigger apoptosis of pig thyrocytes in culture to try to determine whether thyrocytes exhibit a particular resistance to apoptosis induced by an oxidative stress. We show that exposure of thyrocytes cultured as monolayers to exogenous H2O2 induced cell death with characteristics of apoptosis. The effect of H2O2 was concentration-dependent; apoptotic cells were already observed after exposure to 50 micro M H2O2. At high concentrations (millimolar range), H2O2 exerted toxic effects leading to rapid cell disruption. Within the first hour after the onset of exposure to 50-300 micro M H2O2, early signs of apoptosis, i.e. DNA fragmentation, appeared in a low (0.1-1%) but definite fraction of thyrocytes. The proportion of adherent cells exhibiting DNA fragmentation remained fairly constant after 6, 15 and 24 h. During the 24-h period, an increasing number of cells detached from the culture dish and up to 30-40% of cells in suspension displayed apoptotic features. The fraction of cells that lost contact with the culture dish amounted to up to 25% 24 h after addition of 300 micro M H2O2. In conclusion, as reported for other cell types, low H2O2 concentrations are capable of triggering apoptosis in thyrocytes cultured as monolayers. Thyrocytes that undergo apoptosis secondarily lose contact with neighbour cells and the substratum; cell detachment from the monolayer probably happens within 1-2 h after initiation of DNA fragmentation. Our data show that the apoptotic commitment can take place many hours after initiation of the oxidative stress.

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G Şener, L Kabasakal, B M Atasoy, C Erzik, A Velioğlu-Öğünç, Ş Çetinel, G Contuk, N Gedik, and B Ç Yeğen

histological analysis, while additional samples were stored at −80 °C for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Formation of reactive oxygen species (ROS) in the tissue

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F González, N S Rote, J Minium, and J P Kirwan

. 1990 , Yki-Jarvinen 1992 ). It is recognized that these effects may be the exaggeration of normal regulatory responses to increases in circulating glucose. We have shown that in PCOS, hyperglycemia causes an increase in reactive oxygen species (ROS

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Javier Blanco-Rivero, Ana Sagredo, Gloria Balfagón, and Mercedes Ferrer

NO release. It is known that reactive oxygen species are involved in metabolising NO ( Gryglewski et al. 1986 , Ferrer et al. 2000 , 2001 ). Among all the reactive oxygen species, superoxide anion plays a critical role since it is a

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Charles A Ducsay and Dean A Myers

and receptors. Free sulfhydryl groups of cysteine are subject to oxidation by reactive oxygen species (widely used as a marker for oxidative stress) as well as nitrogen species such as NO. It is becoming recognized that NO-mediated S -nitrosylation of

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Nigel Turner, Gregory J Cooney, Edward W Kraegen, and Clinton R Bruce

with insulin signalling. Reduced or dysregulated FA oxidation in mitochondria could create a build-up of bioactive lipids and generate reactive oxygen species (ROS) that also activate kinases that interfere with insulin signalling. Lipid intermediates

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A Makker, F W Bansode, V M L Srivastava, and M M Singh

Introduction Aerobic metabolism is inextricably associated with the generation of reactive oxygen species (ROS). These species are extremely hazardous and so a complex system of tissue-/species-specific antioxidant defenses has

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Chisato Katoh, Tomohiro Osanai, Hirofumi Tomita, and Ken Okumura

secretory peptide, its secretion level appears to be compatible with the several fold increase in gene expression rather than the twofold increase in protein content (cell content). It was described that reactive oxygen species (ROS) are released from the

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Stephen G Hillier and Richard Lathe

Evidence for reactive reduced phosphorus species in the early Archean ocean . PNAS 110 10089 – 10094 . ( https://doi.org/10.1073/pnas.1303904110 ) 10.1073/pnas.1303904110 23733935 Pastar I Stojadinovic O Sawaya AP Stone RC Lindley LE Ojeh N Vukelic S