Membrane-damaging toxins

Often, less intense reactions are encountered. The epidermolytic, exfoliative toxins A and B attack the epidermidis causing epidermal necrosis (e.g., Sap/tytococcMX-scalded skin syndrome) [9]. Membrane-damaging toxins at infection sites (e.g., a-toxin, a-hemolysin) are a major factor in tissue damage after bacterial adherence has occurred. Other exoproteins, such as proteases, collage-nase, hyaluronidase, and lipase, act as virulence enhancers but do not actively destroy host tissues. 

Membrane-damaging toxins actually destroy or damage tissues or organs, directly or indirectly through the release of mediators of disease. The effects of membrane-damaging toxins are less commonly reversible. 

While neurotoxins effectively stop nerve and muscle function without causing microscopic damage to the tissues, membrane-damaging toxins destroy or damage tissue directly. For these toxins, prophylaxis is important, because the point at which the pathological change becomes irreversible often occurs within minutes to a few hours after exposure. 

Trichothecene Mycotoxins. Only one class of easily produced, membrane-damaging toxins, the trichothecene mycotoxins, is dermally active. Therefore, they must be considered by standards different from those for all other toxins. Trichothecenes can cause skin lesions and systemic illness without being inhaled and absorbed through the respiratory system. Skin exposure and ingestion of contaminated food are the two likely routes of exposure of soldiers oral intoxication is unlikely in modern, well-trained armies. Nanogram quantities per square centimeter of skin cause irritation, and microgram quantities cause necrosis. If the eye is exposed, microgram doses can cause irreversible injury to the cornea. 

Mdllby R. Isolation and properties of membrane damaging toxins. In Easmon CSF, Adlam C, eds. Staphylococci and staphylococcal infections. 2 ed. London Academic Press, 1983 619-669. 

The concept of membrane damage as an effector mechanism of bacterial exotoxins arose during the 1970s, mainly through the work on alpha-toxin by Freer, Arbuthnott and Bernheimer (Bernheimer, 1974 Freer et al., 1968) and, subsequently, Thelestam and Mollby (1975). These studies gave rise to the idea that staphylococcal alpha-toxin produced permeability defects in membranes. However, it was... 

FOssle R, Bhakdi S, Sziegoleit A et ol. (1981) On the mechanism of membrane damage by S. aureus alpha-toxin. In J Cell Biol 91 83-94. 

Bacterial toxins can be classified as membrane-damaging. This group includes escherichia coli (hemolysins), aeromonas, pseudomonas, and staphylococcus alpha... 

Other bacterial toxins, classified generally as membrane-damaging, are derived from Escherichia coli (which produces hemolysins), Aeromonas, Pseudomonas, and Staphylococcus, (which also pro-... 

Bhakdi S, Muhly M, Fusslc R. Correlation between toxin binding and hemolytic activity in membrane damage by staphylococcal alpha-toxin. Infect Immun 1984 46 318-323. 

Bashford CL, Alder GM, Menestiina G, Micklem KJ, Murphy JJ, Pasternak CA. Membrane damage by hemolytic viruses, toxin, complement, and other cytotoxic agents. A comment mechanism blocked by divalent cations. J Biol Chem 1986 261 9300-9308,... 

Hepatotoxicity for most chemical toxins mechanistically proceeds via free radical formation which causes OS that induces lipid peroxidation, membrane damage, and altered enzyme activities, the generation of ROS and hydrophilic toxins. Ethanol,... 

Necrosis is often initiated by damage to membranes, either the plasma membrane of the cell or the membranes of organelles, particularly mitochondria (Zimmerman, 1999). Cell membrane damage is often caused by membrane phospholipid peroxidation. Plasma membrane damage interferes wi ion regulation, calcium homeostasis, energy production, and decrease in the ability of that organelle to sequester calcium. Inhibition of protein synthesis is an alternative mechanism that may cause cell necrosis. Toxins that act in this way include phalloidin and related mushroom toxins, which inhibit the action of ribonucleic acid (RNA) polymerase, and therefore mRNA synthesis (Pineiro-Carrero and Pineiro, 2004). 

While it would be difficult to enumerate all of the efforts in the area of implants where plastics are involved, some of the significant ones are (1) the implanted pacemaker, (2) the surgical prosthesis devices to replace lost limbs, (3) the use of plastic tubing to support damaged blood vessels, and (4) the work with the portable artificial kidney. The kidney application illustrates an area where more than the mechanical characteristics of the plastics are used. The kidney machine consists of large areas of a semi-permeable membrane, a cellulosic material in some machines, where the kidney toxins are removed from the body fluids by dialysis based on the semi-permeable characteristics of the plastic membrane. A number of other plastics are continually under study for use in this area, but the basic unit is a device to circulate the body fluid through the dialysis device to separate toxic substances from the blood. The mechanical aspects of the problem are minor but do involve supports for the large amount of membrane required. 

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