PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “THORIUM DIOXIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Uptake of colloidal thorium dioxide by the mouse connective tissue mast cell.

The ability of the mouse mast cell to phagocytize colloidal thorium dioxide, Thorotrast, was investigated employing the mouse connective tissue air pouch. The connective tissue mast cell of mouse was found to have limited capability to ingest the particulate Thorotrast in comparison to the rat peritoneal mast cell which ingested this material readily. Fibroblasts and macrophages in the connective tissue removed injected Thorotrast very rapidly in contrast to mast cells that demonstrated limited phagocytic capabilities. The tissue mast cell of the mouse, therefore, should not be considered a part of the reticuloendothelial system.

Animals↗

Uptake of colloidal thorium dioxide by mast cells.

Mast cells from the peritoneal cavity of the rat were obtained at various times following in situ injection of a colloidal thorium dioxide preparation (Thorotrast). They were prepared for electron microscopy by aldehyde fixation, osmium tetroxide postfixation, and embedding in Epon. Thorotrast was rapidly taken up by mast cells through enhanced or newly elicited surface specializations. It was confined at first to large vesicles which moved to the Golgi area. Subsequently, in a matter of a few hours only, it became associated with progressively more mature granules, including "fully" mature ones. In addition to demonstrating a further phagocytic or pinocytotic activity of mast cells, the findings suggest that mast cell granules share a common membranous investment, and that substances from the tissue environment may theoretically percolate over and interact with the granules. Mast cell function could thus be served primarily by absorptive rather than secretory processes.

Animals↗

Thorium dioxide granuloma of the neck with resultant fatal hemorrhage.

A 46-year-old man had a granuloma in the neck that was caused by extravasation of thorium dioxide (Thorotrast) by an angiographic procedure performed about 30 years previously. His chief complaints were dysphagia and dyspnea with mild hoarseness. Parital resection of the tumor was performed, but his symptoms were not ameliorated. The immediate postoperative course was unfavorable. The patient died four months after the operation from massive hemorrhages from the right common carotid artery.

Carotid Arteries↗

Hepatoma induced by thorium dioxide.

A 74-year-old man complained of anorexia and weight loss. Twenty-six years earlier he had received an injection of Thorotrast. A needle biopsy of the liver showed thorium dioxide granules and periportal fibrosis. On laparotomy, a hepatoma of the left lobe of the liver was discovered. Hepatic malignancy should be suspected in any patient with abnormal results of liver function tests, particularly an elevated level of alkaline phosphatase, who previously has had an injection of Thorotrast.

Aged↗

Pinocytotic uptake and intracellular distribution of colloidal thorium dioxide by cultured sensory neurites.

Sensory ganglia from 9-day chick embryos were grown on collagen coated coverslips for36 h in the presence of nerve growth factor, producing a profuse neuritic outgrowth. The cultures were then incubated for varying periods in a colloidal suspension of thorium dioxide, and the pinocytotic uptake of this marker was followed by electron microscopy. Following brief exposures (3 min), most of the labelled organelles consisted of smooth surfaced vesicles and vacuoles; with longer exposures, the bulk of the marker accumulated first in cup-shaped pre-multivesticular bodies and ultimately in multivesicular bodies. The marker was also taken up into coated vesicles, dense-cored and electron lucent tubules,dense-cored vesicles and dense bodies of the multi-layered myelin body configuration. In addition, evidence suggestive of exocytosis was also obtained; views of apparent fusion of labelled multivesicular bodies with the plasmalemma involving extrusion of vesiclesand marker particles into the extracellular space were regularly encountered following long exposures.

Animals↗

[Radiological signs of a disease that is dying out: hepato-splenic atrophy and cholangiocarcinoma after administration of thorium dioxide (Thorotrast)].

The cases of two patients with radio-opaque residues of contrast medium (Thorotrast) in the abdomen, at the level of the liver, the spleen and certain lymph node groups of the hepatic hilum and the pancreas are reported. In one of the two patients (both of whom had undergone examination with this contrast medium in the '40s) necropsy showed the existence of cholangiocarcinoma. It is therefore considered useful to recall the X-ray signs typical of this pathology, which is dying out after the abandonment of thorium dioxide as an X-ray contrast medium.

Adenoma, Bile Duct↗

Cumulative genetic damage in hematopoietic stem cells in a patient with a 40-year exposure to alpha particles emitted by thorium dioxide.

Thorotrast, a colloidal suspension of the long-lived radionuclide, thorium-232, was widely used as a radiographic contrast medium for several decades. Due to the poor excretion of the sol, however, Thorotrast would deposit in the liver, bone marrow and other tissue, and patients would receive alpha-particle irradiation for life. To gauge the cumulative genetic damage to hematopoietic stem cells due to chronic exposure to alpha particles, we conducted a multi-end-point evaluation in a 72-year-old man who had been administered a 32-ml bolus of Thorotrast during cerebral angiography performed over 40 years ago in 1950. Peripheral T lymphocytes were cultured to quantify the frequencies and cellular distributions of asymmetrical and symmetrical types of chromosome aberrations in first-division metaphases and micronuclei in cytokinesis-arrested interphase II cells. Aberrations were scored using classical chromosome group analysis methods and chromosome painting techniques. Assays of glycophorin-A (GPA) mutations in red blood cells were also performed to obtain a relative measurement of damage sustained by the erythroid stem cell population. Results revealed that approximately 30% of the lymphocytes in this patient contained one or more chromosome aberrations, the majority of which were of the "stable" type. About one-third of the lymphocytes with chromosome damage carried multiple aberrations, suggesting that significant numbers of stem cells survive exposures to alpha-particle radiation that induce complex genomic alterations. Increased frequencies of GPA mutations were observed, demonstrating that genomic damage is also induced in erythroid progenitors. The numbers of micronuclei in lymphocytes were only moderately increased compared to expected values for persons of comparable age, and thus this end point was not useful for quantifying exposure level. Despite the relatively severe burden of somatic cell damage induced by 40 years of internal alpha-particle irradiation, the patient remains surprisingly free of any serious illness.

Alpha Particles↗