Tissue/cell damage

Conditions that cause tissue/cell damage... 

C12H20O4. M.p. 165°C. A plant growth hormone, which is produced in damaged plant tissue, and on diffusing into adjacent intact tissue cells stimulates them to divide. Traumatic acid has been isolated from the pods of green beans. 

Blood and lymph are approximately isotonic to a cell so that cells do not gain or lose liquid when bathed in these fluids. Pure water is hypotonic and may cause cells to swell and burst. During intravenous feeding, injections, and storage of cell tissue, a salt (saline) solution is used with a concentration of solutes that is essentially isotonic with blood (and hence, with the cell) to prevent cell damage. 

Since disinfectant itself might be toxic to the tissue culture or eggs, a toxicity test must also be carried out. Here, appropriate dilutions of disinfectant are mixed with inactivated horse serum and inoculated into tissue cells or eggs (as appropriate). These are examined daily for damage. 

Lecithinase is produced by Clostridium perfringens. This is a calcium-dependent lecithinase whose activity depends on the ability to split lecithin. Since lecithin is present in the membrane of many different kinds of cells, damage can occur throughout the body. Lecithinase causes the hydrolysis of erythrocytes and the necrosis of other tissue cells. 

Damage to the host may arise in two ways. First, multiplication of the microorganisms may cause mechanical damage to the tissue cells through interference with the normal cell metabolism, as seen in viral and some bacterial infections. Second, a toxin associated with the microorganism may adversely affect the tissues or organs of the host. Two types of toxins, called exotoxins and endotoxins, are associated with bacteria. 

There is a long-standing hypothesis that the microvasculature plays a pathological role in forms of chronic inflammatory polyarthritis, particularly RA (Rothschild and Masi, 1982). One of the proposed mechanisms of vascular damage in connective tissue disease is the direct action of a cytotoxic serum factor inducing endothelial cell damage. Blake et al. (1985) have su ested that the vascular abnormalities associated with RA may be linked to oxidized lipoproteins because they are cytotoxic to endothelial cells. 

Knowledge of the health of the cells after a stroke is fundamental if the cells are still alive, the use of neuroprotectant drugs can be useful to minimise brain damage otherwise, their utilisation is useless. A chemical parameter capable of assessing the state of health of tissue cells is pH. In fact, the death of tissue cells is followed by formation of lactic acid, which causes a decrease in blood pH. Normal values are around 7.4 a decrease below this value in the region in which a stroke has taken place is an index of the death of cells. 

High antioxidative activity carvedilol has been shown in isolated rat heart mitochondria [297] and in the protection against myocardial injury in postischemic rat hearts [281]. Carvedilol also preserved tissue GSL content and diminished peroxynitrite-induced tissue injury in hypercholesterolemic rabbits [298]. Habon et al. [299] showed that carvedilol significantly decreased the ischemia-reperfusion-stimulated free radical formation and lipid peroxidation in rat hearts. Very small I50 values have been obtained for the metabolite of carvedilol SB 211475 in the iron-ascorbate-initiated lipid peroxidation of brain homogenate (0.28 pmol D1), mouse macrophage-stimulated LDL oxidation (0.043 pmol I 1), the hydroxyl-initiated lipid peroxidation of bovine pulmonary artery endothelial cells (0.15 pmol U1), the cell damage measured by LDL release (0.16 pmol l-1), and the promotion of cell survival (0.13 pmol l-1) [300]. SB 211475 also inhibited superoxide production by PMA-stimulated human neutrophils. 

Ion pairs created by ionizing radiation eventually produce free radicals that disrupt the biochemistry of cells, break chemical bonds, and otherwise produce cell damage. Free radicals are highly reactive atoms that scavenge electrons from other atoms or molecules, causing a chain reaction that can produce cell and tissue damage. 

All plant diseases result from the invasion of plant tissue by microscopic organisms. These can be fungi, bacteria, or viruses. Taking their nourishment from the plant tissue as parasites, they cause cell damage and death, and sometimes distortions of growth rather like tumors or cancers. 

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. 

For pharmacological, toxicological and transport studies it is of utmost importance to assess not only the viability but also the functionality of the liver slices. This is essential both for end-point determination of toxic cell damage, and to assess the quality of the tissue during in-... 

Contact time the longer CNT contact with the cell membrane, the higher probability of cell damage. However, this factor also includes the mobility of nanoparticles, which can migrate to the surrounding tissue and be removed from the organism. 

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