Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study presents erythrocytic inclusion bodies exhibiting histochemically a strong beta-glucuronidase activity. The unique occurrence of this enzyme in cells of the erythropoietic series has never been described before and characterizes a novel type of erythrocyte inclusions mainly observed in patients suffering from liver damage but also from myelodysplasia and congenital dyserythropoietic anemia type I. Since it is known that hepatocytes contain high activities of beta-glucuronidase, we supposed a relationship between an increased breakdown of liver cells and the appearance of beta-glucuronidase positive inclusions in the red cells. To prove this hypothesis, we determined the beta-glucuronidase plasma levels of 99 unselected patients suffering from various liver disorders in comparison with 19 healthy controls by use of the umbelliferone technique. Our results indicate that in cases with liver diseases beta-glucuronidase plasma levels are significantly increased as compared with normal persons. The availability of a sufficient amount of beta-glucuronidase, thus, seems to be one prerequisite for the appearance of these inclusions in erythrocytes. As demonstrated by our investigations on congenital dyserythropoietic anemia, in which the red cells also show beta-glucuronidase positive inclusions, another premise seems to be an elevated autophagolysosomal activity in the erythrocytes.
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PMID:The occurrence of beta-glucuronidase in erythrocyte inclusions. 196 28

Quantitative cytochemistry of components of blood neutrophil azurophilic granules (myeloperoxidase, chloroacetate esterase, beta-glucuronidase, and acid phosphatase) and specific granules (lactoferrin) has been performed by scanning and integrating microdensitometry in 13 patients with a myelodysplastic syndrome and 11 patients with chronic granulocytic leukaemia. Both patient groups showed a reduction of enzyme activity in azurophilic granules, and also of lactoferrin, consistent with abnormal development of neutrophil granules. These cytochemical changes in blood neutrophils are similar to those found in acute myeloid leukaemia, are consistent with a leukaemic maturation defect, and may be of diagnostic value.
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PMID:Quantitative cytochemistry of blood neutrophils in myelodysplastic syndromes and chronic granulocytic leukaemia. 609 32

The influence of a new dihydroquinoline type antioxidant on doxorubicin-induced hepatic toxicity was studied in mice (CFLP, LATI). Four groups of mice were studied: control, doxorubicin-treated, 5,6-methylen-bis (2,2,4/-trimethyl-1,2-dihydroquinoline/-disulphate (MDS)-treated, as well as doxorubicin and MDS-treated groups. Doxorubicin (15 mg/kg) was administered intraperitoneally, the MDS solution was given by a gastric tube. Liver function was assessed by the serum glutaminic-oxaloacetic-transaminase (SGOT) reaction. The lipid peroxidation in liver tissue was determined by the rate of malondialdehyd (MDA) production, the permeability of the liver lysosomal membrane was established by measuring beta-glucuronidase activity and its release from the cells. The MDS treatment proved to be effective in significantly reducing SGOT elevation, MDA production and lysosomal membrane damage in hepatic tissue. Clinical trials seem to be justified in using antioxidative substances to control doxorubicin toxicity.
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PMID:Inhibition of doxorubicin-induced liver toxicity by a new dihydroquinoline type antioxidant. 653 28