Lysosome enzyme leakage

Erythema is the most common effect of UVR exposure. The exact mechanism of how UVR induces skin erythema is not fully understood however, it is believed that a number of mediators are involved in the inflammatory reaction (260). These include histamine, lysosomal enzymes, kinins, and at least one prostaglandin. These mediators produce vasodilatation, which is manifested in erythema. As the UV radiation penetrates into the epidermis, another inflammatory reaction involving a lymphocytic infiltrate develops. Swelling of the endothelium and leakage of red blood cells also occurs. The inflammatory effect of UVB radiation reaches its maximum in 12-24 h after exposure (260). 

Many other inhibitory substances have been tested for their effect on picornavirus cytopathology. Among these are actinomycin D tested for its effect on poliovirus-induced leakage of protein from HEp-2 cells (Bubel, 1967) or redistribution of lysosomal enzymes as... 

Differences in membrane damage caused by tricyclic compounds may be related to their surface activities and extent of adsorption on to cell membranes [190,192]. Although in experiments on enzyme leakage from isolated hepato-cytes the concentrations of tricyclic used was much higher than therapeutic plasma levels, this is perhaps reasonable as it has been found that the liver/plasma ratio of tricyclic antidepressants is of the order of 20-100 1 [192]. The order of toxicity of tricyclic compounds estimated by the extent of leakage of cytoplasmic and lysosomal enzymes from isolated hepatocytes, was in the order CPZ > amitryptiline > imipramine [191], which is the ranking of these compounds according to their surface activity and cell uptake. 

Glycosaminoglycans are degraded in lysosomes, which contain hydrolytic enzymes that are most active at a pH of approximately 5. [Note Therefore, as a group, these enzymes are called acid hydrolases.] The low pH optimum is a protective mechanism that prevents the enzymes from destroying the cell should leakage occur into the cytosol where the pH is neutral. With the exception of keratan sui-... 

The finding that prolonged ischemia causes such a small amount of cellular injury was somewhat unexpected, since findings in other tissues such as liver (D8) and heart (W21) indicate that ischemia causes considerable leakage of lysosomal and other intracellular enzymes. 

Lead exposure may cause kidney damage (Lim et al. 2001). In acute lead toxicity, there is proximal tubular damage, which may result in a reversible Fanconi syndrome-like condition with aminoaciduria, glucosuria, and hyperphosphaturia. Further, the tubular damage may cause leakage of enzymes (e.g., lysosomal NAG) from the cells into the urine (Skerfving 1993) at B-Pbs in the range 1.5-2.0 pmolL. This effect may be reversible. 

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