Cellular destruction

Cytotoxins obtained from cobra venom (Naja naja atra). Hydrophobic solids that cause irreversible depolarization of cell membrane and cellular destruction as well as contraction of skeletal and smooth muscle, including the heart. 

The sole biochemical function of 2 -5A (and hence 2 -5 A synthetase) appears to be as an activator of a dormant endo-RNase, which is expressed constitutively in the cell. This RNase, known as RNase L or RNase F, cleaves all types of single-stranded RNA (ssRNA). This inhibits production of both viral and cellular proteins, thus paralyzing viral replication. Presumably, cellular destruction of the invading ssRNA will be accompanied by destruction of any additional viral components. Removal of dsRNA would facilitate deactivation of the endo-RNase, allowing translation of cellular mRNA to resume. A 2-5 phosphodiesterase represents a third enzymatic... 

The IL-2 portion of the fusion protein facilitates product interaction with cells displaying cell surface IL-2 receptors, found in high levels on some leukaemia and lymphoma cells, including CTCL cells. Binding appears to trigger internalization of the receptor-fusion protein complex (Figure 9.B1). Sufficient quantities of the latter escape immediate cellular destruction to allow diphtheria toxin-mediated inhibition of cellular protein synthesis. Cell death usually results within hours. 

Some aspects of multiple sclerosis are reflected in the animal model experimental autoimmune encephalomyelitis, which is induced by immunization of susceptible animals with appropriate encephalogenic proteins or peptides. In these animals, if cultured adult stem cell neurospheres are injected into the bloodstream, injected cells can find their way to damaged portions of the nervous system and improve function in mice. How the injected cells augmented the recovery process is unclear. One possibility is that cells recruited to the lesions differentiated into oligodendrocytes and generated new myelin sheaths, but this seems unlikely in the face of ongoing cellular destruction. 

Medical Management There is no known antidote for mustard exposure, and the process of cellular destruction is irreversible. It is essential to remove the mustard agent as quickly as possible. Vesicants rapidly penetrate the skin causing both localized cellular damage and systemic damage. The deadly nature of such agents effect is that a person... 

Fig. 1. Overview of intravascular heme catabolism. Hemoglobin, myoglobin, and other heme proteins are released into the circulation upon cellular destruction, and the heme moiety is oxidized by O2 to the ferric form (e.g., methemoglobin and metmyoglobin). Haptoglobin can bind a substantial amount of hemoglobin, but is readily depleted. Ferric heme dissociates from globin and can be bound by albumin or more avidly by hemopexin. Hemopexin removes heme from the circulation by a receptor-mediated transport mechanism, and once inside the ceU heme is transported to heme oxygenase for catabolism.

Cytotoxicity Issues. In-vivo hemolysis has been observed with parenteral administration of all of the parent CDs. In-vitro studies with human erythrocytes have demonstrated that the damaging effect of the CDs is in the order p-CD > ot-CD > y-CD. This cellular destruction has also been observed in studies with human skin fibroblasts and intestinal cells, P388 murine leukaemic cells, E. coli bacterial cells, and immortalized human corneal epithelial cells.f " Mechanistic studies suggest that CDs extract either cholesterol (p-CD and y-CD) or phospholipids (a-CD) from the cell membrane causing small pores which allow leakage and eventually lead to cell lysis. 

The formed colloidal gel also produces a sorption gradient for soluble components within the serous exudate thereby allowing the removal of toxic compounds arising from bacterial or cellular destruction. However, during use, the dressing in contact with the wound liquefies to produce a pus-like liquid with a somewhat strong odor. 

Ionizing. This is the high frequency area of the spectrum where chemical bonds are broken and direct damage to cellular destruction occurs. Examples are gamma radiation and x-rays. 

The serum potassium concentration may also be falsely elevated in some conditions, and not reflect the actual in vivo potassium concentration. This is termed pseudohyperkalemia. Pseudohyperkalemia occurs most commonly in the setting of extravascular hemolysis of red blood cells. When a blood specimen is not processed promptly and cellular destruction occurs, intracellular potassium is released into the serum. Pseudohyperkalemia can also occur in conditions of thrombocytosis or leukocytosis. If severe hyperkalemia is found in a patient who is asymptomatic with an otherwise normal laboratory report, the hyperkalemia is most likely pseudohyperkalemia, and a repeat blood sample should be evaluated. Elevated potassium concentrations are normally associated with other laboratory abnormalities. 

The final mechanism for an immune-mediated reaction is the production of autoantibodies to a spoiled membrane. The offending drug alters the neutrophil membrane, which induces the formation of autoantibodies (antibodies that attach directly to the neutrophil). Their attachment to the neutrophil causes cellular destruction by the phagocytic system. 

This increased conversion of pyruvate to lactate decreases the pH in areas of the brain that have rapid ATP turnover rates and leads to cellular destruction. 

Roberts WG, Liaw LH, Berns MW. In vitro photosensitization II. An electron microscopy study of cellular destruction with mono-L-aspartyl chlorin e6 and photofrin II. Lasers Surg Med 1989 9 102-108. 

Lipid peroxidation leads to cellular destruction and death. Herbicides that divert photosynthetic electron transport, such as the bipyridyls paraquat and diquat, yield the superoxide anion. Superoxide levels produced overtax the normal defense mechanisms. More toxic species such as hydroxyl free radicals are also probably produced which instigate lipid peroxidation and lead to cellular disorganization and death. 

Possible DPE Effects on Phenolics. Phenolic levels were significantly increased in AFM treated tissue (unpublished results). This may be an indication of a wound response. However, it is also possible these herbicides may regulate the activity of one of the light-activated enzymes involved in phenolic acid synthesis. The resultant increase in high levels of free radical intermediates known to occur in these pathways, could be the ultimate cause of cellular destruction. Treatment of cucumber with fluorodifen [ -nitrophenyl (a,a,a-trifluoro-2-nitro- -tolyl)urea] has been shown to increase phenylalanine ammonia lyase (PAL) activity in vivo (21). 

A. HF is able to penetrate tissues deeply, where the highly cytotoxic fluoride ion is released and cellular destruction occurs. 

To minimize cellular destruction by ice crystals, the tissues must be cryoprotected prior to sectioning. The presence of high concentrations of sucrose results in the slow formation of small ice crystals, rather than the rapid formation of large ice crystals. 

Apoptosis and necrosis are the two extensively studied modalities of cell deadi that often exhibit similar initiator/effector molecules, signaling pathway s and involving of same organelles [86]. Both types of cell death can co-operate in cellular destruction or can be prevented by autophagy. It has been reported some anti-cancer alkaloids that induce eell death by activation of apoptosis or necrosis, where autophagy participates as a survival and protective pathway (anti-apoptotic or anti-necrotic effect). In these eases, mitoehondria participate at least as a modality of cell death. 

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