Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1389183 (autodigestion)
 317 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Strain L (Earle) cells in suspension tissue culture exhibit a logarithmic growth period followed by a stationary or plateau phase. Lipid to cell and lipid to protein ratios were found to be at minimal levels during logarithmic growth and increased 13 per cent and 42 per cent, respectively, in cultures in the stationary phase. The lipid accumulation was due to elevated cellular levels of phospholipid and cholesterol, which each increased in nearly the same ratio. Cellular triglyceride and free fatty acid content was not significantly altered. There was a loss of cellular protein in the older cultures that largely accounted for the greater increase in the lipid to protein ratio. Electron microscopic examination of cells from the stationary phase revealed numerous autophagic vacuoles and dense bodies, many of which contained membranous debris and other cytoplasmic components in different stages of autodigestion. These varied and complex membrane-bound structures localized acid phosphatase activity on cytochemical examination, establishing them as autophagic lysosomes. The present correlative biochemical and morphologic studies indicate that the observed elevation of phospholipid and cholesterol in stationary phase cells occurred as a result of autophagocytosis and demonstrate the role of cell injury in the accumulation of lipid of this type.
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PMID:Lipid accumulation in the stationary phase of strain L cells in suspension culture. 83 29

Several substances with lysosomotropic activity were investigated in toxicological studies. AR-L 115 BS (sulmazol, a cardiotonic agent) was tested on beagle dogs; HX-CH 44 BS (a beta-blocker) and SX-AB 1316 SE (an antithrombotic agent) were tested on rats, and AF-CX 1325 XX (an antiepileptic agent) was tested on both rats and beagle dogs. All organ systems were examined morphologically by light and/or electron microscopy. When an increase in the number of lysosomes occurred this was confirmed by the pigment scheme according to Krutsay (1971) as well as by the detection of acid phosphatase and compared with earlier histochemical results. At higher dosages, all substances caused very marked proliferation of lysosomes in the liver and/or kidneys. HX-CH 44 BS also caused such proliferation in striated muscles and in the lungs. A brown discolouration of the kidneys was found with sulmazol and AF-CX 1325 XX. This finding corresponded to the microscopically detectable occurrence of numerous lipofuscin granules. The reticulum cells in the lymph nodes of dogs were also affected by AF-CX 1325 XX. It is concluded that the proliferation of lysosomes in various organs after administration of the above-mentioned substances is due to an excess of substance. The increased substance in the body is then stored in the lysosomes. With HX-CH 44 BS, lysosomal autodigestion of mitochondria in the skeletal musculature and in the alveolar macrophages of the lungs was found. The selective lysosomal incorporation of mitochondria has not been described up to now and in our opinion, this constitutes a special feature. The results otherwise largely correspond to those already described in the literature. Systemic phospholipidosis such as occurs with some other substances was not detectable. The incorporation of the substance causes several types of lysosomal inclusion. Uptake of the substance in lysosomes either leads to overt autodigestion of organelles such as mitochondria (HX-CH 44 BS) or peroxisomes or to residual lysosomes of dense structure which histochemically resemble lipofuscin. SX-AB 1316 SE serves as an example of a substance which is stored directly by lysosomes in crystalline form. Above all, in the liver the substance is taken up not only by the sinusoidal stellate cells but also by hepatocytes.
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PMID:Drug-induced lysosomal disorders in laboratory animals: new substances acting on lysosomes. 134 5

A needle wound was made in the adult rat cerebral cortex. Responses of neurons and oligodendrocytes at the site of injury were followed over a period of 450 days and correlations made between morphological and enzyme cytochemical changes to clarify some phenomena previously unresolved. Evidence from acid phosphatase activity in degenerating neurons showed no increase in the number of cytochemically stained lysosomal profiles nor changes in the subcellular localization of the acid phosphatase reaction product. Our observations indicated that the majority of dying neurons were not digested by their own acid phosphatase 'autodigestion' but by the process of heterodigestion. The time-course study revealed that not all the traumatized neurons were eliminated but some persisted permanently in an attenuated 'atrophic' state. The atrophic neurons were small in size with low cytoplasmic-nuclear ratios and exhibited low levels of glucose-6-phosphatase and cytochrome oxidase activities. The acid phosphatase activity was slightly increased as evidenced by cytochemically stained hypertrophic Golgi cisternae and a slight increase in the number of lysosomes. The low level of enzyme activities concerned with carbohydrate metabolism reflected the low metabolic activity in atrophic neurons whilst an increase in Golgi-lysosomal enzyme activity suggested some anabolic process necessary for their survival. Oligodendrocytes displayed only minor changes in morphology, and their glucose-6-phosphatase and cytochrome oxidase activities were normal, suggesting that these cells have little or no involvement in the repair of a cerebral wound. The absence of significant changes in lysosomal acid phosphatase activity indicated a minimal role, if any, of oligodendrocytes in the process of phagocytosis.
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PMID:Neuronal and oligodendrocytic response to cortical injury: ultrastructural and cytochemical changes. 632 3