Reactive oxygen species, oxidative stress induced

It has been shown that the renal bioactivation of xenobiotics such as the herbicides paraquat and diquat [10, 111, 112], and of p-lactams such as cephaloridine and cefsulodin [10, 40, 41] or the antitumor agent adriamycin [113, 114] can induce the generation of reactive oxygen species (oxidative stress) which can be involved in alterations of the structure and functions of cell membranes, cytoskeletal injury, mutagenicity, carcinogenicity, and cell necrosis [115-117]. 

Oxidative stress induced by reactive oxygen species is described for many other brain disorders of inflammatory and noninflammatory nature. Some examples of such disorders are given below. Quick and Dugan [326] demonstrated superoxide-mediated damage of neurons... 

Hassoun, EA Creighton University Assess abilities of endrin to induce the formation of reactive oxygen species and lipid peroxidation and DNA single strand breaks that result in oxidative stress in fetuses of pregnant mice. The protective effects of some antioxidants will also be assessed using this model. 

Antonsson and Marinou 2000 Adams and Cory, 1998). Stress may also cause inaease, nitric oxide (NO), or reactive oxygen species (ROS) production which, in turn, triggers release of apoptotic proteins from the intermemhrane space (Kroemer and Reed, 2000 Vieira et at, 2000). Release of these proteins from mitochondria are required for stress induced killing hut are, with a few exceptions (Bergmann et al, 1994, Schulze- Osthoff et al, 1993), dispensible for CD95 and TNF-receptor transduced apoptosis. These other death processes require FADD and caspase-8 to be recruited into the death receptor complexes and cannot be blocked by Bcl-2 (Krammer, 2000 Scaffidi et al, 1998). 

Reactive oxygen species (ROS) are a common mediator of apoptosis. Induction of apoptosis by bile acids appears to be caused, at least in part, by oxidative stress and consequent DNA damage. Unrepaired DNA damage can trigger apoptosis. Table 3.3 lists studies indicating that bile acids induce production of ROS and reactive nitrogen species (RNS) in cells of the GI tract. Table 3.4... 

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. 

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. 

Alcohol-related liver diseases are complex, and ethanol has been shown to interact with a large number of molecular targets. Ethanol can interfere with hepatic lipid metabolism in a number of ways and is known to induce both inflammation and necrosis in the liver. Ethanol increases the formation of superoxide by Kupffer cells thus implicating oxidative stress in ethanol-induced liver disease. Similarly prooxidants (reactive oxygen species) are produced in the hepatocytes by partial reactions in the action of CYP2E1, an ethanol-induced CYP isoform. The formation of protein adducts in the microtubules by acetaldehyde, the metabolic product formed from ethanol by alcohol dehydrogenase, plays a role in the impairment of VLDL secretion associated with ethanol. 

Based on the evidence that several antioxidants inhibit angiotensin II-mediated phosphorylation of the EGF receptor (Ushio-Fukai et al. 2001) while H2O2 induces its phosphorylation, it has been postulated that oxidative stress is an early and necessary event in the transactivation of the EGF receptor (Zhang et al. 2005). A likely site of reactive oxygen species (ROS) action is the inhibition of a protein tyrosine... 

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