Oxidative stress and

Savolainen, K. M., L,oikkanen, J., Eerikainen, S., and Naarala, J. (1998). Interactions of excita-rury neurotransmitrers and xenobiorics in excitoroxiciry and oxidative stress Gliiraroare and lead. Toxicol. Lett. 102-103, 363-367. 

Kruman 11, Nath A, Mattson MP (1998) HlV-1 protein Tat induces apoptosis of hippocampal neurons by a mechanism involving caspase activation, calcium overload, and oxidative stress. Exp Neurol 154(2) 276-288... 

Roc AC, Ances BM, Chawla S, Korczykowski M, Wolf RL, Kolson DL, Detre JA, Poptani H (2007) Detection of hnman immnnodeficiency virus induced inflammation and oxidative stress in lenticnlar nnclei with magnetic resonance spectroscopy despite antiretroviral therapy. Arch Nenrol 64(9) 1249-1257... 

Morphine and HlV-Tat increase nucrogUal-free radical production and oxidative stress possible role in cytokine regulation. J Neurochem 108 202-215... 

Hoffman DJ, Heinz GH. 1998. Effects of mercury and selenium on glutathione metabolism and oxidative stress in mallard ducks. Environ Toxicol Chem 17 161-166. 

While many biological molecules may be targets for oxidant stress and free radicals, it is clear that the cell membrane and its associated proteins may be particularly vulnerable. The ability of the cell to control its intracellular ionic environment as well as its ability to maintain a polarized membrane potential and electrical excitability depends on the activity of ion-translocating proteins such as channels, pumps and exchangers. Either direct or indirect disturbances of the activity of these ion translocators must ultimately underlie reperfiision and oxidant stress-induced arrhythmias in the heart. A number of studies have therefore investigated the effects of free radicals and oxidant stress on cellular electrophysiology and the activity of key membrane-bound ion translocating proteins. 

Jaeschke, H. (1990). Glutathione disulfide formation and oxidant stress during acetaminophen-induced hepatotoxicity in mice in vivo-, the protective effect of allopurinol. J. Pharmacol Exp. Ther. 255, 935-941. 

Ellis, EM, 2007. Reactive carbonyls and oxidative stress Potential for therapeutic intervention. Pharmacol Ther 115, 13-24. 

MWNTs were found to be cytotoxic in human skin fibroblasts (HSF42) and human epidermal keratinocytes (HEK) [42-44], whereas SWNTs were toxic in human keratinocyte (HaCaT) cultures [25, 26, 45]. Reduced cell proliferation and oxidative stress were reported also in epithelial (HeLa) cells [45] and murine epidermal cells (JB6 P + ) [46] upon incubation with SWNTs. 

At first glance, the in vitro studies on CNT toxicity appear to be confusing, inconclusive, or contradictory. However, if one considers interference with dye-based viability assays, agglomeration issues, and oxidative stress due to catalyst contamination, the data available to date seem to favor the conclusion that well-dispersed, purified, and/or functionalized CNTs exhibit relatively low toxicity. 

Shvedova, A.A. et al. (2007) Vitamin E deficiency enhances pulmonary inflammatory response and oxidative stress induced by single-walled carbon nanotubes in C57BL/6 mice. Toxicology and Applied Pharmacology, 221 (3), 339-348. 

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