Hydrogen peroxide oxidative stress

Exposure of normal human epidermal keratinocy tes (NHEKs) to UVB radiation induces intracellular release of hydrogen peroxide (oxidative stress) and phosphorylation of MARK cell signaling pathways. Pretreatment of NHEK with EGCG inhibits UVB-induced hydrogen peroxide production and its mediated phosphorylation of MARK signaling pathways. It has been demonstrated that tea polyphenols inhibit PKC, MARK, and AP-1 activities in NIH 3T3 cells. °... 

Key Words Abiotic stress acquired tolerance antioxidant breeding crop plants cross protection functional genomics heat shock heat shock factors heat shock proteins hydrogen peroxide oxidative stress reactive oxygen species signaling pathways stress tolerance transgenic plants. 

These include the mitochondrial respiratory chain, key enzymes in fatty acid and amino acid oxidation, and the citric acid cycle. Reoxidation of the reduced flavin in oxygenases and mixed-function oxidases proceeds by way of formation of the flavin radical and flavin hydroperoxide, with the intermediate generation of superoxide and perhydroxyl radicals and hydrogen peroxide. Because of this, flavin oxidases make a significant contribution to the total oxidant stress of the body. 

In their review some years ago, Reddy and Rao (1986) cited several lines of evidence for peroxisome-proliferation-mediated oxidative stress being associated with hepatocarcinogenesis. They mentioned the sustained increase in hydrogen peroxide production, the detectable increased levels of hydrogen peroxide in the livers of treated animals, increased lipid peroxidation associated with treatment and marked inhibition of hepatocarcinogenesis by antioxidant compounds. However, definitive studies remain to be carried out. 

It has been shown in many studies that protective effects of carotenoids can be observed only at small carotenoid concentrations, whereas at high concentrations carotenoids exert pro-oxidant effects via propagation of free radical damage (Chucair et al., 2007 Lowe et al., 1999 Palozza, 1998, 2001 Young and Lowe, 2001). For example, supplementation of rat retinal photoreceptors with small concentrations of lutein and zeaxanthin reduces apoptosis in photoreceptors, preserves mitochondrial potential, and prevents cytochrome c release from mitochondria subjected to oxidative stress induced by paraquat or hydrogen peroxide (Chucair et al., 2007). However, this protective effect has been observed only at low concentrations of xanthophylls, of 0.14 and 0.17 pM for lutein and zeaxanthin, respectively. Higher concentrations of carotenoids have led to deleterious effects (Chucair et al., 2007). 

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