Oxygen toxic products

Pasteur effect Yeast and other cells can break down sugar in the presence of oxygen (eventually to CO2 and H2O) or in its absence (to CO2 and ethanol). The decomposition of sugar is often greater in the absence of oxygen than in its presence, i.e. the Pasteur effect. With oxygen, less toxic products (alcohol) are produced and the breakdown is more efficient in terms of energy production. 

Bronchial Asthma. Figure 2 Mechanisms of bronchial hyperresponsiveness. Toxic products from eosinophils [cationic peptides, reactive oxygen species (ROS)] cause epithelial injury. Nerve endings become easily accessible to mediators from mast cells, eosinophils [eosinophil-derived neurotoxin (EDN)], and neutrophils, and to airborne toxicants such as S02. Activation of nerve endings stimulates effector cells like mucosal glands and airway smooth muscle either directly or by cholinergic reflexes. 

Overall, DEHA is a low toxicity product, performs extremely well as a rapid oxygen scavenger and metal passivator, and is an excellent replacement for hydrazine. In addition, it is competitively priced and consequently a very popular product. 

Williams, J.G. and Hallett, M.B. (1989).Effect of sulphasalazine and its active metabolite, 5-aminosalicylic acid, on toxic oxygen metabolite production by neutrophils. Gut 30, 1581-1587. 

Only a limited number of reliable prediction tools are currently available for photoinduced toxicity. This is not surprising since establishing phototoxic potential is a complex task. Phototoxicity can be the consequence of various mechanisms such as photogeneration of reactive oxygen species, production of toxic photoproducts or sensitization of DNA damage by energy transfer. In addition, so far, there are no available universal descriptors (indicators) to predict the photodynamic potency of chemicals. 

Various defense mechanisms have evolved to protect humans and other animals from the thousands of chemicals present in food, drinks, and the environment. Of particular interest are cytochrome P450 (CYP) enzymes, which catalyze the final step in the incorporation of oxygen into organic molecules. They frequently convert xenobi-otics, including human-made chemicals and drugs, into less toxic products but can also transform nontoxic chemicals into toxic or carcinogenic-reactive species. 

The relationship between EC-SOD expression and NO production in cells is of a great physiological and pathophysiological significance. In 1992, Oury et al. [35] demonstrated that EC-SOD increased oxygen toxicity in central nervous system (CNS) by the inhibition of superoxide-mediated inactivation of nitric oxide. This conclusion is obviously erroneous one because, as it is well known that the interaction of superoxide and nitric oxide results in the formation of a very toxic peroxynitrite. Indeed, the same authors recently showed that EC-SOD promoted nitric oxide vasodilation by dismuting superoxide [36]. On the other hand, it has been found that nitric oxide can downregulate the synthesis of EC-SOD by smooth muscle cells [37]. 

G-CSF activates neutrophils, transforming them into cells capable of respiratory burst and release of secretory granules. It also modulates the expression of adhesion molecules on neutrophils as well as CD1 lb/CD18 and plasma elastase antigen levels. G-CSF induces proliferation of endothelial cells, phagocytic activity of neutrophils, reactive oxygen intermediate production by neutrophils and antibody-dependent cellular toxicity by neutrophils. 

Reactive oxygen species production is largely catalyzed by transition metals (especially copper and iron), and oxidative stress plays a critical role in AD pathogenesis. In one study, the association of metal levels and Ap toxicity was demonstrated by (i) the effect on cell viability by metal alone and in the combination with APP and Ap, (ii) Ap-induced neurotoxicity relevant to oxidative stress indicated by ROS production, and (iii) APPsw cells expressed APP and generated Ap, so that Ap Cu2+ and APP Cu2+ can catalyze more ROS generation than APP cells that only expressed APP. 

Hyperoxia was found to encourage the accumulation of primary and end-products of lipid peroxidation together with a significant lowering of the vitamin E content of rat brain tissue [152]. The consequence of hyperoxia was epileptiform seizures, which were prevented by vitamin E or synthetic antioxidant pre-injection. Other workers [153] have found that protection against hyperoxia is directly related to the level of vitamin E or selenium supplementation. However, some [ 154] have indicated no beneficial effects for vitamin E in reducing oxygen toxicity. 

Various proteins have been identified as markers for general stress in microorganisms or for specific stress like temperature, pH, toxic products, oxygen deficiency for strict aerobes, or oxygen toxicity for anaerobes, etc. most of them are rather small in size. Most work was done with E. coli (for a review see e.g. [53] and with B. subtilis [54]). 

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