title: Streptozotocin-induced alterations in rat liver Golgi complexes are ameliorated by BMOV [Bis(maltolato)oxovanadium(IV)] activity.
abstract: Twenty years ago, we detected the interdependence between structure and function of rat liver Golgi complexes that are characteristic for streptozotocin diabetes, which served us in further investigations as a useful indicator of the effectiveness of drugs we were testing. This work presented results obtained in eight groups of rats (four control and four diabetic) that were administered orally either bis(maltolato)oxovanadium(IV) [BMOV] or maltol alone. The activities of the rat liver Golgi marker enzyme, galactosyltransferase [GalT], as well as the morphology of Golgi complexes were studied in situ using an electron microscope; parallel estimations of vanadium concentration and phospholipid percentage were made in Golgi-rich preparations isolated from the liver. Our main findings were normalization in diabetic animals orally treated with 1.8 mmol BMOV in 0.09 mol NaCl solutions over seven days, which demonstrated an accompanying increase in phosphatidic acid (PA) percentage (p < 0.05) compared to controls. In the diabetic groups, Pearson's test showed a positive double correlation between GalT activity, vanadium concentration, and PA percentage in Golgi-rich membrane preparations from the liver. Additionally, a negative correlation was found between vanadium concentration and phosphatidylcholine percentage in the fractions.
authors.affiliation: Department of General Biochemistry, Faculty of Biotechnology, Jagiellonian University, Krakow, Poland. anna@piryt.net
authors.forename: A M
authors.initials: AM
authors.lastname: Kordowiak
authors.forename: D
authors.initials: D
authors.lastname: Dziga
authors.forename: W
authors.initials: W
authors.lastname: Dabroś
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005700:Galactosyltransferases / Q000378:metabolism; D006056:Golgi Apparatus / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000648:ultrastructure*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D008854:Microscopy, Electron; D009994:Osmolar Concentration; D010743:Phospholipids / Q000378:metabolism; D011753:Pyrones / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D012965:Sodium Chloride / Q000494:pharmacology; D014638:Vanadates / Q000494:pharmacology*; D014639:Vanadium / Q000493:pharmacokinetics
chemical_list: D007004:Hypoglycemic Agents; D010743:Phospholipids; D011753:Pyrones; D014639:Vanadium; C074212:bis(maltolato)oxovanadium(IV); C008316:maltol; D014638:Vanadates; D012965:Sodium Chloride; D005700:Galactosyltransferases