Oxidative stress nitrogen species

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... 

A number of NO-derived reactive species can initiate lipid peroxidation, including nitrogen dioxide and, most notably, ONOO , which displays unique properties as a mediator of lipid oxidation. On a molecular basis, ONOO is a more potent lipid oxidant than hydrogen peroxide and, unlike H2O2, it does not require metal catalysis. The one-electron oxidants such as metals, as well as heme proteins and peroxynitrite, are assumed to play an important role in many diseases associated with oxidative stress. Heme proteins such as horseradish peroxidase (HRP) can produce alkylperoxyl radicals through two sequential... 

Fig. 3.4 Oxidative stress and increase in reactive oxygen species (ROS) and reactive thiol species (RTS) decreases constitutive NO in MMP/TIMP/NO ternary complex and generates reactive nitrogen species (RNS) and nitrotyrosine. This process oxidizes the TIMP and liberates active MMP.

The impairment of glucose utilization could result from the modification of the glycolytic enzymes under oxidative stress effects. Oxidative stress is an important factor leading to the pathophysiologcal alterations in conformational diseases. Oxidative stress is manifested in protein oxidation, lipid peroxidation, DNA oxidation, and advanced glycation end-products, as well as reactive oxygen species (ROS), and reactive nitrogen species (RNS) formation. Either the oxidants or the products of oxidative stress could modify the proteins or activate other pathways that may lead to additional impairment of cellular functions and to neuronal loss [57, 58]. 

Protein thiols can interact with glutathione by several mechanisms that permit glu-tathionylation to participate in the regulation and antioxidant protection of specific protein thiols. These reactions are involved in the consequences of oxidative stress caused by reactive species of oxygen and nitrogen and include the formation of protein sulfenic acids and their participation in regulatory processes. 

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). 

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