Membrane structure damage

Many of the physical changes in membrane structure of cells are reversible and species differences in the degree of disruption of dry membranes may relate to differences in composition, protective mechanisms or to additional damage occurring during desiccation (see below). 

UV-induced ROS are extremely toxic to cells by causing oxidative damage to all biomolecules (Sies 1991). For instance, lipids, which are major compounds of all biological membranes, may be destroyed by ROS. After a first initiation reaction an unsaturated fatty acid is converted to a peroxyl radical, which in turn attacks another unsaturated fatty acid finally leading to free radical cascades. This photochemical peroxidation of unsaturated fatty acids may be particularly damaging for membrane structure and function (Bischof et al 2006a). 

Liver toxicity related to 1,2-dibromoethane depends on the metabolic pathway utilized and the amount of damage induced in cellular protein and membrane structures. Humans exposed to low levels of 1,2-dibromoethane are at potential risk of having toxic events occurring within hepatocytes whether these effects will be subcellular or result in cell necrosis may depend on internal dose and a variety of factors. Liver damage that is severe enough to cause clinical disease in humans from low-level exposure is unlikely. 

The outcome of oxidative stress is a depletion of cellular GSH, NADPH, NADH, and ATP, and also damage to lipid membranes, structural and enzymatic proteins, and DNA. 

The major secondary events are changes in membrane structure and permeability, changes in the cytoskeleton, mitochondrial damage, depletion of ATP and other cofactors, changes in Ca2+ concentration, DNA damage and poly ADP-ribosylation, lysosomal destabilization, stimulation of apoptosis, and damage to the endoplasmic reticulum. 

Secondary events result from primary events, for example, changes in membrane structure/permeability, mitochondrial damage, and lysosomal destabilization. Tertiary events are final observable manifestations, for example, fatty change and phospholipidosis, apoptosis, blebbing, and necrosis. 

Yatvin MB, Grummer MA (1987) Membrane structure and radiation and hyperthermic damage. Radiat Phys Chem 30 351-364... 

Amphotericin B imposes its antifungal effects by binding to the sterol moiety of the membrane and damaging its structural and functional integrity (Figure 45.1). 

The antimicrobial activity of eugenol may be associated with structural damage and alteration of the permeability mechanism of microsome, lysosome, and cell walls. The substance acts primarily on cytoplasm membranes, causing alteration of its permeability, and thus allowing leakage of essential bacterial cell constituents with subsequent death of the bacteria. 

In the Urushi matrix membrane, it is supposed that the solvent at the surface would be supplied from the porous bulk phase of the mechanically hard Urushi matrix membrane by capillary action, which was discussed in detail elsewhere (6), while in the PVC matrix membrane, the solvent of the surface would be supplied by the leaching process from the mechanically soft PVC matrix membrane, because the electron micrograph of the PVC matrix membrane indicates structural damage ( ). 

Several reports of the effects of ozone in vivo are presented in Table XII. It is impossible to decide whether the effects of ozone are primary reactions or the result of a series of reactions initiated by ozone. All results can be rationalized as enzyme inhibition of one sort or another. Effects on membrane structure are harder to observe, and in one case it was reported that the malonaldehyde which would be expected on fatty acid ozonolysis was only observed after symptoms were apparent (74). Results of electron microscope examination showed that the first observable damage was in the stroma of the chloroplasts (70). One can easily argue that earlier damage could not be detected by microscopic techniques. However, recent reports that the chloroplast polyribosomes are much more susceptible to degradation by ozone are important observations which are consistent with the microscopy experiments (76). Chloroplast polysomes are also more susceptible to sulfhydryl reagents than are cytoplasmic polysomes (77). This evidence indicates that ozone itself, or a toxic product from primary oxidation, can pass through the cytoplasm and have its effect in the chloroplast. 

ACAT transfers amino-acyl groups from one molecule to another. ACAT is an important enzyme in bile acid synthesis, and catalyses the intracellular esterification of cholesterol and formation of cholesteryl esters. ACAT-mediated esterification of cholesterol limits its solubility in the cell membrane and thus promotes accumulation of cholesterol ester in the fat droplets within the cytoplasm this process is important in preventing the toxic accumulation of free cholesterol that would otherwise damage ceU-membrane structure and function. Most of the cholesterol absorbed during intestinal transport undergoes ACAT-mediated esterification before incorporation into chylomicrons. In the liver, ACAT-mediated esterification of cholesterol is involved in the production and release of apo-B-containing lipoproteins. 

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