Oxidative tissue damage

Quintanilha, A.T. and Packer, L. (1983). Vitamin E, physical exercise and tissue oxidative damage. In Biology of Vitamin E (eds. R. Porter and J. Whelan), pp. 56-69. Ciba Foundation Symposia Series No. 101. Pitman, London. 

Sadrzadeh, S.M.H. and Eaton, J.W. (1992). Hemt obin-induced oxidant damage to the central nervous system. In Free Radical Mechanisms of Tissue Injury (eds. M.T. Moslen and C.V. Smith) pp. 24—32. CRC Press, Boca Baton. 

The most damning evidence of APIs impact on wildlife comes from smdies on fish. Fluoxetine has been detected in tissues of fish species living in a municipal effluent at levels of 0.1 ng g Redox properties of some medicinal products can influence the oxidative metabolism in hepatocytes of rainbow trout leading to oxidative damage [115]. 

Several diaryl teUurides exhibit protection against TBH-induced cell death in lung fibroblast cultures. Besides, the same compounds prevent leucocyte-mediated cell damage in Caco-2 cells and protect rat kidney tissue against oxidative damage caused by anoxia and reoxygenation. 

P-carotene is only one of many antioxidants, which can be detected in the skin. Other carotenoids, for example, lutein and zeaxanthine, are preferentially found in the macula lutea, the so-called yellow spot in the eye. Here, carotenoids are subject to a metabolism typical for that tissue, which cannot be found in other tissues (e.g., formation of meso-zeaxanthine). In addition, they can specifically be absorbed into the macula. In the macula, they protect the retinal pigment epithelial cells against oxidative damage from UV light. Indeed, these two carotenoids can be protective against age-dependent macula degeneration. 

Metronidazole is a nitro-imidazole. It is a mixed amoebicide, i.e. it acts at all sites of infection. It has to be activated in the parasite. By reduction in the amoeba of its nitro group reactive intermediates are formed, resulting in oxidative damage and ultimately cell kill. It is effective against many parasitic intestinal and tissue infections such as trichomoniasis, giardiasis and amoebiasis. It is the drug of choice for amoebic dysentery and amoebic liver abscess. 

The inflammatory response changes with time and can be divided into phases. The rapid phase occurs within seconds to minutes and consists of vasodilation, increased blood flow, edema, and pain. The acute phase is characterized by induction of inflammatory genes by NF-kB and other transcription factors. During this phase, moderate amounts of inflammatory mediators are produced. The chronic phase occurs over months to years and is marked by dramatically increased production of inflammatory mediators. The secondary chronic phase of inflammation occurs after years of oxidative damage has degraded blood vessels and tissues. Such chronic inflammation appears to play a role in many disease states, such as arteriosclerosis and cancer. 

Buko, V. et al.. Inhibition of oxidative damage of red blood cells and liver tissue by genistein-8-C-glucoside, Adv. Exp. Med. Biol, 500, 271, 2001. 

The aim of the present study was to evaluate the effect of LLLT on oxidative markers in serum and tissue biopsies of healing ulcers before and after the 8th session of an LLLT course of chronic leg ulcer treatment. Oxidative damage was assessed in terms of lipid peroxidation reflected by serum malondialdehyde (MDA) level, protein oxidation was measured in terms of tissue protein carbonyls (PCb), and DNA damage was measured in terms of DNA fragmentation. Antioxidative activity was estimated by measuring activity of SOD, GPX and CAT enzymes. 

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