Changes In Lysosomes Research Articles

Changes in liver lysosomes and cell junctions close to an invasive tumour.

The Journal of PathologyVolume 101, Issue 3 p. 227-232 Article Changes in liver lysosomes and cell junctions close to an invasive tumour S. T. G. Butterworth, S. T. G. Butterworth Department of Pathology, Western General Hospital, EdinburghSearch for more papers by this author S. T. G. Butterworth, S. T. G. Butterworth Department of Pathology, Western General Hospital, EdinburghSearch for more papers by this author First published: July 1970 https://doi.org/10.1002/path.1711010304Citations: 14AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume101, Issue3July 1970Pages 227-232 RelatedInformation

Lysosomal damage and its possible relationship with mitochondrial lesion in rat kidney under obstructive jaundice

Lysosomal lesions consisting of an increase of the unsedimentable activity of acid hydrolases (acid phosphatase and β-glucuronidase) have been demonstrated in early stages of rat cholemic tubulonephrosis. The release of lysosomal enzymes occurs earlier than the mitochondrial alterations, as shown by succinate and glutamate oxidation ratio. The demonstration of early changes in lysosomes, prior to evidence of mitochondrial injury, raises the possibility that lysosomal damage plays a role in initiating parenchymal lesions in rat kidney under obstructive jaundice.

Studies on poisoning by macrozamia communis—I : Biochemical disturbances in the liver

Oral administration to rats of kernels of Macrozamia communis induced changes in liver lysosomes and mitochondria prior to the onset of periacinar necrosis. Within 3 hr of poisoning with macrozamia the rate of release of β-glycerophosphate phosphatase from light mitochondrial fractions increased. This change was more pronounced after 6 hr. A similar change was induced by carbon tetrachloride and ethionine, but not by lasiocarpine or thioacetamide. Mitochondria isolated from livers of rats 6 hr after administration of macrozamia showed inhibition of NAD-dependent enzymes and an increased rate of swelling in the absence of substrate. Secretion of triglyceride from the liver of poisoned rats was inhibited, and triglyceride accumulated in the liver. Serum non-esterified fatty acid levels rose and serum triglyceride levels fell after poisoning with macrozamia. Protein synthesis was inhibited in the liver of rats treated with macrozamia. Density gradient centrifugation of post-mitochondrial and ribosomal fractions revealed a breakdown in polysomes after poisoning. The results are discussed in relation to the pathogenesis of lesions induced in the liver by macrozamia.

Formation of myeloid bodies in rat liver lysosomes after chloroquine administration

When single daily doses (120 mg/kg) of chloroquine sulphate were given to rats, histochemical and ultrastructural investigations demonstrated a sequence of changes in lysosomes of the liver cell. After the first dose, the liver showed an initial loss of particulate β-glucuronidase and acid phosphatase activities (at 1–3 hours) which was most distinct in the periportal area. By 6–24 hours numerous lysosomes with and without recognizable cytoplasmic organelles (autophagic vacuoles and myeloid bodies, were present. After the second and third doses of chloroquine, the lysosomes increased in size and the majority contained myelin figures. Considerable lysosomal enzyme activity was observed in the periphery of the organelle. Further daily doses produced an increasing amount of undegraded sequestrated material and loss of particulate enzyme staining. There was no demonstrable increase in neutral fat, but a progressive increase in what was probably phospholipid was observed, commencing in those areas of the hepatic lobule showing initial loss of lysosomal enzyme activity. The distributional changes of the phospholipid inclusions correspond closely with those seen for the lysosomal hydrolases. In the highest dosage administered, loss of glycogen occurred in the centrilobular cells, which also showed degenerative changes. We postulate that chloroquine initially labilizes the lysosomal membrane, releasing lysosomal enzymes and initiating autophagy thought responsible for sequenstration of cytoplasmic material. Multiple treatment induces stability of lysosomal membranes and probably impedes entry of enzymes into these organelles, resulting in accumulation of undegraded sequestrated material.

Lysosomal changes associated with hyperoxia in the isolated perfused rat liver

Changes in lysosomes associated with hyperoxia were studied in the isolated rat liver, perfused by the method of Mayes and Felts (1966). Increased PO2 in perfused blood resulted in the formation of enlarged lysosomes and autophagic vacuoles. Demonstration of acid phosphatase (both by light and electron microscopy), β-glucuronidase, aryl sulfatase, and E600-resistant esterase in these organelles identified them as lysosomes. Electron-microscopic observations show that except for changes in the lysosomes, none of the other cellular organelles are distinctly affected. The formation of autophagic vacuoles and the cell damage are prevented if perfusion is carried out with blood oxygenated with air or if the liver is derived from a rat treated with chloroquine. These findings are attributed to alteration in the permeability of the lysosomal membrane resulting from hyperoxia. In turn, this permeability change releases hydrolytic enzymes into the cytoplasm leading to cell death, particularly in the centrilobular areas of the liver in fed and fasted rats. A special role in this process is envisaged for the smaller pericanalicular lysosomes, as indicated by a reduction in their number and a change in their distribution.

Lysosomal Changes in Lytic and Nonlytic Infections With the Simian Vacuolating Virus (SV40)<xref ref-type="fn" rid="FN1">2</xref>

Lysosomal changes have been observed by histochemical methods in the BSC-1 green monkey kidney cell line and the 3T3 mouse cell line infected with high multiplicities of simian vacuolating virus (SV40) and in 3T3 cells infected with herpes simplex virus. BSC-1 cells infected with SV40 showed marked cytoplasmic vacuolation and lysis. The lysosomes were enlarged and aggregated and there was second-stage activation with release of enzyme into the cytoplasm. Possibly, some product of viral replication in the nucleus is released into the cytoplasm and brings about changes in lysosomes and other cytoplasmic organelles. Lysosomal enzymes probably contribute to the dissolution of cells and release of virus from nuclei. 3T3 cells infected with SV40 under these conditions do not lyse, but a large proportion may become transformed. First-stage activation of lysosomes was seen for at least 6 days. After 6 days these changes disappeared. The possible relationship of lysosomal changes to the events occurring in transformed cells is discussed. The cells infected with herpes simplex virus showed marked cytopathic effects associated with second-stage lysosomal activation.

The localisation of acid phosphatase activity changes in lysosomes in the adrenal zona fasciculata of intact and hypophysectomized rats following ACTH administration

In the cells of the zona fasciculata of intact adult rats lysosomes can be found in medium amounts, measuring 0.2–0.4 μ in diameter. After treatment with ACTH, the lysosomes in the zona fasciculata of the intact animals increase in number and size, and lysosome-lipid conglomerates are formed. In hypophysectomized animals, the lysosomes in the zona fasciculata decrease in number and size in proportion to the time elapsed. Treatment with ACTH given 2 to 4 weeks after hypophysectomy, resulted in the increase in number and size of the lysosomes. Under such circumstances lysosomes appear in conspicuously large numbers around lipid droplets, which frequently coalesce with them. The possible role of lysosomes is discussed.

UV-induced changes in lysosomes tagged with quinacrine

A description is given of the changes in intravital fluorescent morphology with incubation time and the effects of UV illumination on embryonic cells growing in quinacrine. These observations strongly suggest a direct relation between fluorescent granules and cytoplasmatic vacuoles. The discussion of these findings was based on the concept of lysosome as a cytoplasmatic particle entity.

A histochemical study of hypertrophy and ischaemic injury of rat liver with special reference to changes in lysosomes

A histochemical study of hypertrophy and ischaemic injury of rat liver with special reference to changes in lysosomes

CYTOCHEMICAL OBSERVATIONS ON THE RELATIONSHIP BETWEEN LYSOSOMES AND PHAGOSOMES IN KIDNEY AND LIVER BY COMBINED STAINING FOR ACID PHOSPHATASE AND INTRAVENOUSLY INJECTED HORSERADISH PEROXIDASE.

After incubation of formalin-fixed, frozen sections of kidney and liver from peroxidase-treated rats in an azo dye medium for acid phosphatase, and after subsequent incubation of the same sections with benzidine, phagosomes were stained blue and lysosomes were stained red in the same cells. It was observed that newly formed phagosomes were separate from preexisting lysosomes in the tubule cells of the kidney and in the Kupffer cells of the liver at early periods after treatment with peroxidase. At later periods, the color reactions for acid phosphatase and peroxidase occurred in the same granules. The reaction of peroxidase decreased gradually and disappeared from the phago-lysosomes after 2 to 3 days, whereas the reaction for acid phosphatase persisted. In the liver, most of the injected protein was concentrated in large phagosomes located at the periphery of the cells lining the sinusoids. The peribiliary lysosomes showed a relatively weak reaction for peroxidase in the proximity of the portal veins. After pathological changes of permeability, phagosomes and lysosomes lost their normal location and fused, in the interior of many liver cells, to form large vacuoles or spheres. The effects of a reduced load of peroxidase and the effects of the pretreatment with another protein (egg white) on the phago-lysosomes of the kidney were tested. The relationship of the fusion of phagosomes with lysosomes to the size of normal and pathological phago-lysosomes was discussed.

CHANGES IN EPITHELIAL CELL LYSOSOMES DURING EXPERIMENTAL ORAL CARCINOGENESIS.

THE general concept of lysosomes as separate cytoplasmic organelles was originated by de Duve1 in 1955, when he also demonstrated that acid phosphatase is characteristically present in these structures. Other workers2,3 have determined the cytological location of lysosomes by applying histochemical techniques for acid phosphatase to specially prepared tissue sections. This communication describes changes in the lysosomes of malignant epithelial cells, as shown by staining fresh frozen cryostat sections and exfoliated cell smears for acid phosphatase. The malignant tumours used in this experiment were produced in hamster cheek pouches in response to repeated applications of a chemical carcinogen, in a manner similar to that first described by Salley4.

Changes of Lysosomes in Fibroblasts Cultured Anaerobically

Changes of Lysosomes in Fibroblasts Cultured Anaerobically