Reactive oxygen species, arsenic

Botrytis cinerea is responsible for gray mold disease in more than 200 host plants. This necrotrophic fungus displays the capacity to kill host cells through the production of toxins and reactive oxygen species and the induction of a plant-produced oxidative burst. Thanks to an arsenal of degrading enzymes, B. cinerea is then able to feed on various plant tissues (Choquer and others 2007). 

Arsenic has been shown to induce oxidative stress (Shi, Shi and Liu, 2004 Hughes and Kitchin, 2006). Oxidative stress is a result of an imbalance between reactive oxygen species and the ability of a cell s antioxidant defense apparatus to respond. Oxidative stress can result in the damage of proteins, lipids, RNA, and deoxyribonucleic acid (DNA). In addition, since oxidant species have a role in cell signaling, a state of oxidative stress could potentially alter signaling within and between cells. 

Hei, T.K., Liu, S.U.X. and Waldren, C. (1998) Mutagenicity of arsenic in mammalian cells role of reactive oxygen species. Proceedings of the National Academy of Sciences of the United States of America, 95(14), 8103-7. 

Nesnow, S., Roop, B.C., Lambert, G., Kadiiska, M., Mason, R.P., Cullen, W.R., Mass, M.J. (2002). DNA damage induced by methylated trivalent arsenicals is mediated by reactive oxygen species. Chem. Res. Toxicol. 15 1627-34. 

The therapeutic efficacy of oral administration of seed powder of M. oleifera (500 mg/kg, orally, once daily) post arsenic exposure (100 ppm in drinking water for 4 months) in rats has been investigated (49). Animals exposed to arsenic(lll) shows a significant inhibition of 8-aminolevulinic acid dehydratase (ALAD) activity, decrease in reduced glutathione (GSH) level and an increase in reactive oxygen species (ROS) in blood. On the other hand, a significant decrease in hepatic ALAD, and an increase in 8-aminolevulinic acid synthetase (ALAS) activity is observed after arsenic exposure. These changes... 

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