Oxidative stress liver

Enzymatic assays EROD Bg, Cc Liver Oxidative stress, dioxin-like compounds... 

Videla, L. A., Barros, S. B., Junqueira, V. B. Lindane-induced liver oxidative stress. Free Radic. Biol. Med 1990, 9, 169-179. 

Salo, D.C., Donovan, C.M., Davies, K.J, (1991). Hsp70 and other possible heat shock or oxidative stress proteins are induced in skeletal muscle, heart, and liver during exercise. Free Radic. Biol. Med 11,239-246. 

McMillian M, Nie A, Parker JB, Leone A, Kemmerer M, Bryant S, et al. Drug-induced oxidative stress in rat liver from a toxicogenomics perspective. Toxicol Appl Pharmacol 2005 207 171-8. 

Atkinson A, Meeks RG, Roy D. 1993. Increased oxidative stress in the liver of mice treated with trichloroethylene. Biochem Mol Biol Int 31 297-304. 

Augustin, W. et al.. Beta-carotene cleavage products induce oxidative stress by impairing mitochondrial functions brain mitochondria are more sensitive than liver mitochondria, Free Rad. Biol. Med., 33, S326, 2002. 

Bellomo, G., Richelmi, P., Hirabelli, F., Marioni, V. and Abbagnano, A. (1985). Inhibition of liver microsomal calcium ion sequestration by oxidative stress role of protein sul-phydryl groups. In Free Radicals in Liver Injury (eds. G. Poli, K.H. Cheeseman, M.U. Dianzani, and T.F. Slater) pp. 139-142. IRL Press, Oxford. 

Allopurinol has been shown to attenuate lipid peroxidation in ethanol-fed rats (Kato etal., 1990). However, this was not correlated with any possible effect on histological damage and, as discussed previously, the significance of lipid peroxidation is unclear. Despite the evidence suggesting that oxidative stress and increased oxidative metabolism may play a role in the pathogenesis of human alcoholic liver disease, it remains to be shown that treatment with specific antioxidants will modify this process. 

Metzger, J., Dore, S.P. and Layterberg, B.H. (1988). Oxidant stress during reperfusion of ischaemic liver no evidence for a role of xanthine oxidase. Hepatology 8, 580-584. 

Parks, D.A., Tan, S., Poplawski, S.C., Baldwin, S. and Sweeney, S.D. (1992). Uric acid oxidation products indicator of oxidant stress in human liver transplantation. Gastroenterology 102, A232. 

In their review some years ago, Reddy and Rao (1986) cited several lines of evidence for peroxisome-proliferation-mediated oxidative stress being associated with hepatocarcinogenesis. They mentioned the sustained increase in hydrogen peroxide production, the detectable increased levels of hydrogen peroxide in the livers of treated animals, increased lipid peroxidation associated with treatment and marked inhibition of hepatocarcinogenesis by antioxidant compounds. However, definitive studies remain to be carried out. 

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. 

Over the past years it has become apparent that the cell type is an important determinant of the extent of oxidative stress that may occur. Both the latent activities of cytoprotective enzymes in specific cell types, as well as the ability of the cell to respond rapidly to an oxidative insult by the upregulation of such enzymes, will be important predeterminants of the fate of the cell. Table 10.1 shows the concentrations of both antioxidants and cytoprotective enzymes in a variety of tissues. While the liver is well provided with antioxidant protection, the brain has very low levels, so the ability to respond rapidly to an oxidative insult by upregulation of gene transcription and translation will be an important determinant of survival or death. Cells such as hepatocytes have high levels of expression and... 

The progression of human immunodeficiency virus (HIV) towards its more advanced stages is accompanied by increasing body stores of iron. Iron accumulates in macrophages as well as microglia, endothelial cells and myocytes. The iron burden is especially intense in the bone marrow, brain white matter, muscle and liver. Such excesses of iron will enhance oxidative stress, impair several already compromised immune defence mechanisms and directly promote the growth of microbes (Boelaert et ah, 1996). 

As a rule, oxygen radical overproduction in mitochondria is accompanied by peroxidation of mitochondrial lipids, glutathione depletion, and an increase in other parameters of oxidative stress. Thus, the enhancement of superoxide production in bovine heart submitochondrial particles by antimycin resulted in a decrease in the activity of cytochrome c oxidase through the peroxidation of cardiolipin [45]. Iron overload also induced lipid peroxidation and a decrease in mitochondrial membrane potential in rat liver mitochondria [46]. Sensi et al. [47] demonstrated that zinc influx induced mitochondrial superoxide production in postsynaptic neurons. 

A battery of different biochemical quantitative assays was applied to many different tissues and species. DNA damage and lipid peroxidation assays measure the direct impact of genotoxics and oxidant pollutants [16,17] whereas alteration of GSH levels in liver is a marker for oxidative stress [18]. Mercury and other heavy metals are known to induce metallothionein levels in different tissues although this effect is variable in different species and organs [19-22]. 

GSH, GSSG quantitation Cc, Dp, Pc Liver (Cc), digestive gland (Dp, Pc) Oxidative stress, mercury poisoning... 

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