Cytotoxic reaction

Because the cytotoxic effects of the energetic lithium-7 and alpha particles are spaciaHy limited to a range of only about one-ceU diameter, the destmctive effects are confined to only one or two cells near the site of the event. Thus BNCT involves the selective deUvery of sufficiendy high concentrations of B-containing compounds to tumor sites followed by the irradiation of these sites with a beam of relatively nondestmctive thermal neutrons. The resulting cytotoxic reaction can then in theory destroy the tumor cells that are intimately associated with B target. 

Perifascicular capillaries are closer to aggregates of antibody-secreting cells (B-lymphocytes) situated in perimysial connective tissue and therefore are most severely affected by antibody-dependent cytotoxic reactions. Immune-complex deposition occurs at a higher level in the vascular tree (i.e., at arteriolar level) and this may cause fluctuations in perfusion pressure. Perifascicular capillaries are most distal from the head of vascular pressure and therefore most likely to suffer from periodic anoxia. 

Cytotoxic reactions. The antibody and cell react, with resultant lysis of the cell. It was found that the presence of a third component, called complement, was necessary for this reaction to take place. 

Tidd DM and Paterson AR. A biochemical mechanism for the delayed cytotoxic reaction of 6-mercaptopurine. Cancer Res 1974 34 738-746. 

Soderhall, K. et al., The cytotoxic reactions of hemocytes from the freshwater crayfish Astacus astacus, Cell. Immunol., 94, 326,1985. 

IVpe 2, cytotoxic reaction. Drug-antibody (IgG) complexes adhere to the surface of blood cells, where either circulating drug molecules or complexes al-Lullmann, Color Atlas of Pharmacology 2000 Thieme All rights reserved. Usage subject to terms and conditions of iicense. 

The cytotoxicity is related to the direct contact the extracts show no significant cytotoxic reaction. 

Most anaphylactoid reactions are due to a direct or chemical release of histamine, and other mediators, from mast cells and basophils. Immune-mediated hypersensitivity reactions have been classified as types I-IV. Type I, involving IgE or IgG antibodies, is the main mechanism involved in most anaphylactic or immediate hypersensitivity reactions to anaesthetic drugs. Type II, also known as antibody-dependent hypersensitivity or cytotoxic reactions are, for example, responsible for ABO-incompatible blood transfusion reactions. Type III, immune complex reactions, include classic serum sickness. Type IV, cellular responses mediated by sensitised lymphocytes, may account for as much as 80% of allergic reactions to local anaesthetic. 

The importance of the plasma membrane as the site of action of im-munologically mediated cytotoxicity reactions involving humoral or cellular factors has recently become evident. In this regard, several studies have shown that humoral immune killing reactions involve a complex series of biochemical interactions between the attacker moieties and the cell surface membrane.One approach in studying and elucidating such interactions could therefore focus on the effects of the immune attack processes on the synthesis and/or turnover of cell surface macromolecules known to be structural and functional components of the plasma membrane (e.g., proteins and lipids). 

Both lines of research converged with the discovery that NO gas can account for the biological activity of EDRF (Palmer et al., 1987) and to mediate the some of the cytotoxic reactions of cytokine-activated macrophages. 

Cytotoxic Reaction This is an autoimmune response the results in hemolytic anemia, thrombocytopenia, or lupus erythematosus (blood disorders). In some cases, it takes months for the reaction to dissipate. 

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