Reactive oxygen species oxidative stress, contribution

Oxygen free radicals are required intermediates in many biological reactions but may damage macromolecules during oxidative stress 566 Reactive oxygen species generated during ischemia—reperfusion contribute to the injury 567... 

The toxicity of C60 has been found to be related to its ability to cause oxidative stress (Oberdorster, 2004 and Sayes et al., 2005, 2007). However, literature describing the toxicity of C60 is contradictoiy. The first report on C60 cytotoxicity originated from Tsuchiya et al. who found that C60 inhibited cell proliferation and differentiation dose-dependently in mouse midbrain cells treated at -400 pg/ml for six days. Tsuchiya et al. proposed that reactive oxygen species (ROS) contributed to C60 cytotoxicity. The ROS generation and embryo head abnormalities suggested that C60 may contribute to brain and neuronal diseases such as Down syndrome, Alzheimer s, and Parkinson s disease (Tsuchaiya, 1996). The research that... 

As well as the formation of radicals, oxidative stress may also contribute to the toxicity of electrophilic metabolites. This may result from depletion by electrophiles of the glutathione pool, one of the major defenses against damage by reactive oxygen species. 

The reaction that produces NAPQI generates superoxide anions as a by-product. Interactions of NAPQI with other cellular molecules also generate reactive oxygen species, leading to oxidative stress on the hepatocyte (Zimmerman, 1999 Dahm and Jones, 1996). The role of calcium and Kupffer cell activation have been impUcated as contributing factors for acetaminophen-induced liver injury by producing reactive nitrogen species (Treinen-Moslen, 2001). 

Lead-induced hyperuricemia may contribute to chronic lead nephropathy. Uric acid per se induces endothelial cell injury, renal microvascular disease, and hypertension, at least in part mediated by oxidative stress [38]. Independent of uric acid, reactive oxygen species induced by lead have been imphcated in endothelial cell injury, increased vascular reactivity, and the production of hypertension in humans and experimental animals [39]. 

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