Reactive oxygen species cell culture

Kundu K, Knight SF, Willett N, Lee S, Taylor WR, Murthy N (2009) Hydrocyanines a class of fluorescent sensors that can image reactive oxygen species in cell culture, tissue, and in vivo. Angew Chem Int Ed 48 299-303... 

The mitochondrial dysfunctionality seen in manganese neurotoxicity might be related to the accumulation of reactive oxygen species (Verity, 1999). Mitochondrial Mn superoxide dismutase (MnSOD) is found to be low or absent in tumour cells and may act as a tumour suppressor. It is induced by inflammatory cytokines like TNF, presumably to protect host cells. In a rat model, iron-rich diets were found to decrease MnSOD activity, although a recent study reported that in rat epithelial cell cultures iron supplementation increased MnSOD protein levels and activity, but did not compromise the ability of inflammatory mediators like TNF to further increase the enzyme activity (Kuratko, 1999). 

A study has been undertaken to clarify whether glucocorticoid excess affects endothelium-dependent vascular relaxation in glucocorticoid treated patients and whether dexamethasone alters the production of hydrogen peroxide and the formation of peroxynitrite, a reactive molecule between nitric oxide and superoxide, in cultured human umbilical endothelial cells (7). Glucocorticoid excess impaired endothelium-dependent vascular relaxation in vivo and enhanced the production of reactive oxygen species to cause increased production of peroxynitrite in vitro. Glucocorticoid-induced reduction in nitric oxide availability may cause vascular endothelial dysfunction, leading to hypertension and atherosclerosis. 

Inoguchi, T., P. Li, F. Umeda, H.Y. Yu, M. Kakimoto, M. Imamura, T. Aoki, T. Etoh, T. Hashimoto, M. Naruse, H. Sano, H. Utsumi, and H. Nawata. 2000. High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C-dependent activation of NAD(P)H oxidase in cultured vascular cells. Diabetes 49 1939-1945. 

In spite of the increased activities of SOD-1 and GPx and normal catalase activity, increased lipid peroxides in the blood plasma of DS patients have been reported (K10), as has as an increased accumulation rate of age pigments (i.e., lipofuscin and ceroid, known products of lipid peroxidation) (K9). In addition, an early study showed increased lipid peroxides in the cerebral cortex of DS fetal brains (B15). More recently, cortical neurons from fetal DS and age-matched normal brains were shown to differentiate normally early in cell cultures. However, DS neurons subsequently degenerated and underwent apoptosis, whereas the normal cells remained viable (B18). In addition, the DS neurons exhibited a three- to fourfold increase in reactive oxygen species and increased lipid peroxidation that preceded cell death. Importantly, DS neuron degeneration could be prevented by treatment with the free radical spin trap A-ferf-butyl-2-sulphophenylnitrone, the... 

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