Membrane lysosomal

Sialin was first identified as the product of the gene defective in sialidosis, a lysosomal storage disorder. The transporter mediates the movement of sialic acid out of lysosomes by coupling to the proton electrochemical gradient across the lysosomal membrane. Unlike the vesicular neurotransmitter transporters which are antiporters, sialin is a sympoiter with sialic acid and protons both moving out of the lysosome. 

Stabilizes lysosomal membrane and prevents the release of proteolytic enzymes released during the inflammatory process... 

In addition to effects mediated through glucocorticoid secretion (stress-related), a hypothetical mechanism for direct immunotoxicity of organophosphates is the inhibition of esterases and stabilization of the lysosomal membrane of lymphocytes, thus blocking release of lymphokines (Sharma and Reddy 1987). 

Neutral Red (NR) Live cells red lysosomes Lysosomal membrane No [33, 34]... 

Immunopathology Hematology (blood cell count), weight of spleen, thymus and liver, histology of spleen, thymus, and lymph nodes Histopathology, cell viability, lysosomal membrane stability... 

One consequence of the uptake of some contaminants is a reduction in the ability of lysosomes to retain the dye Neutral Red. As a consequence, the Neutral Red retention time has been developed as an index of lysosomal membrane fragility and thus of toxicity. The test has been used on the digestive cells involved with intracellular digestion of endocytosed food following administration of organic contaminants, such as polycyclic aromatic hydrocarbons [71]. The phenomenon has been reported many times after exposure to... 

Moore, M. N. and Viarengo, A. (1987). Lysosomal membrane fragility and catabolism of cytosolic proteins evidence for a direct relationship, Experientia, 15, 320-323. 

Grundy, M. M., Moore, M. N., Howell, S. M. and Ratcliffe, N. A. (1996). Phagocytic reduction and effects on lysosomal membranes by polycyclic aromatic hydrocarbons, in haemocytes of Mytilus edulis, Aquat. Toxicol., 34, 273-290. 

Fig. 11.2 (a) HAADF-STEM image of a stained cell section (40nm thick). A SWNT cluster within a lysosome invading the lysosomal cell membrane, (b) Corresponding high-resolution lattice image of SWNTs at the lysosomal membrane from boxed area. Cytoplasm (cy) and secondary... 

The test is based on an in vitro assay of the uptake of the dye, neutral red (NR), in Balb/c 3T3 fibroblasts. It was developed to detect the phototoxicity induced by the combined interaction of the test substance and light of the wavelength range from 315 to 400 nm, the so-called UVA. The cytotoxicity is evaluated in the presence (+UVA) or absence (-UVA) of UVA light exposure, after application of a nontoxic dose of the compound. The cytotoxicological impact is assessed via the inhibition of the fibroblasts to take up the vital dye NR (NR is a weak cationic dye, penetrating easily into the cell membrane by a nonionic diffusion and accumulates in the lysosomes) one day after the initial treatment. Normally, healthy cells may incorporate and bind NR. Alterations of the cell surface or the lysosomal membranes, however, lead to a decreased uptake and binding of the dye. 

Brunk, U.T., Dalen, H., Roberg, K.., and Hellquist, H.B., 1997, Photo-oxidative disruption of lysosomal membranes causes apoptosis of cultured human fibroblasts. Free Radio. 

Kahalalide F (217) Depsipeptide Kahalalide F (217) PM02734 (Irvalec 218) Oncology Oncology Alters lysosomal membrane function Alters lysosomal membrane function Phase n Phase I PharmaMar PharmaMar 956-961 962-965... 

Glucocorticosteroids are the most potent antiinflammatory agents available. They stabilize lysosomal membranes and reduce the concentration of proteolytic enzymes at the site of inflammation. They promote the synthesis of proteins called lipocortins which inhibit phospholipase-A2 and thus inhibit production of arachidonic acid, leukotrienes and prostaglandins. Furthermore, the expression of COX-II and through that the inflammatory effects of the licosanoids is inhibited. Glucocorticosteroids reduce the release of histamine from basophils, decrease capillary permeability and cause vasoconstriction. Glucocorticosteroids stimulate the loss of calcium with the urine and inhibit the resorption of calcium from the gut. 

NSAID treatment alone. They may be used concurrently with NS AIDS. It mostly takes 1-3 month for their anti-inflammatory action to become apparent. The pharmacodynamics of these antimalarials in RA is uncertain. Possible mechanisms include decreased leukocyte chemotaxis, stabilization of lysosomal membranes, inhibition of DNA and RNA synthesis and trapping of free radicals. 

Mectianism of Action An adrenocorticosteroid that controls the rate of protein synthesis, depresses migration of polymorphonuclear leukocytes, reverses capillary permeability, and stabilizes lysosomal membranes. Therapeutic Effect Prevents or controls inflammation. 

It appears to reduce immune responsiveness. It inhibits the migration of mononuclear cells in area of inflammation. It may also stabilise lysosomal membrane, hence damage to cartilage is prevented. 

Glucocorticoids inhibit the functions of leukocytes and tissues macrophages. They also stabilize lysosomal membranes, thereby reducing the concentration of proteolytic enzymes at the site of inflammation. 

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