Oxidative stress increases

Nie, Z., Mei, Y., Ford, M. et al. (1998). Oxidative stress increases Al adenosine receptor expression by activationg nuclear factor kappa B. Mol Pharmacol. 53 (4), 663-9. 

Fuhrman, B., Volkova, N., and Aviram, M., Oxidative stress increases the expression of the CD36 scavenger receptor and the cellular uptake of oxidized low-density lipoprotein in macrophages from atherosclerotic mice Protective role of antioxidants and of paraoxonase, Atherosclerosis, 161, 307, 2002. 

Figure 1 Proposed mechanisms of anticancer effects of DR. Three main mechanisms proposed to expiain the antic-arcinogenic effects of DR inciude decreased oxidative stress, increased seiective apoptosis of initiated ceiis, and decreased metaboiism of carcinogens.

The data indicate that zinc-induced metallothionein binds mercury in the renal cortex and shifts the distribution of mercury from its site of toxicity at the epithelial cells of the proximal tubules. Thus, the renal content of mercury is increased, yet less is available to cause toxicity. In contrast, the renal toxicity of mercuric chloride is exacerbated in zinc-deficient animals (Fukino et al. 1992). In the zinc-deficient state, less mercury accumulates in the kidneys, but the toxicity is greater. The mechanism of the protection appears to involve more than simply a redistribution of renal mercury, because in the absence of mercury exposure, zinc deficiency increases renal oxidative stress (increased lipid peroxidation, decreased reduced ascorbate). When mercury exposure occurs, the oxidative stress is compounded (increased lipid peroxidation and decreased glutathione and glutathione peroxidase). Thus, zinc appears to affect the biochemical protective mechanisms in the kidneys as well. 

Oxidative stress increases the release of GSSG from cells and tissues, in-... 

Oxidative stress can be caused by a wide variety of factors, including inflammatory responses to infections or immune activation, exposure to heavy metals or toxic substances (Carpenter et al., 2002), and oxidative stress increases during the natural course of aging (Junqueira et al., 2007). When oxidative stress is induced by environmental exposures it represents a significant component of the toxicity syndrome, and most xenobiotics share the ability to cause oxidative stress. As a consequence, the effects of multiple exposures are additive at the level of oxidative stress. Metabolic changes associated with oxidative stress can be considered to be adaptive responses that increase prospects for survival during these stressful episodes. 

Inflammatory reactions, oxidative stress (increase in production of reactive oxygen species, ROS), and nitrosative stress (increased generation of reactive nitrogen species, RNS) are major components of secondary injury. All these processes play a major role in regulating the pathogenesis of acute and chronic TBI (Fig. 6.1). 

Oxidative stress increases during the formation of Ap. The secretion and storage of Ap into the damaged neurons in the course of AD is de facto the compensatory measure to protect cells against the cmisequence of oxidative stress [30]. The intensity of this process depends on the level of antioxidant defense mechanisms of cells (tissue) and the intracellular concentration of ROS. AD is one of the diseases in which course ROS contribute highly negatively. Oxidative stress leads to mitochondrial damage, cytochrome c release, activation of caspase system, and apoptosis. 

Almeida, M., E. Ambrogini, L. Han et al. Increased lipid oxidation causes oxidative stress, increased peroxisome proliferator-activated receptor-gamma expression, and diminished pro-osteogenic Wnt signaling in the skeleton. 284(40), 2009 27438-48. 

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