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D A Barrio

Publications and source records attributed to D A Barrio.

6 recordsLinked to original sources

Vanadium and bone development: putative signaling pathways.

Vanadium is a trace element present in practically all cells in plants and animals. It exerts interesting actions in living systems. At pharmacological doses, vanadium compounds display relevant biological actions such as mimicking insulin and growth factors as well as having osteogenic activity. Some vanadium compounds also show antitumoral properties. The importance of vanadium in bone arises from the studies developed to establish the essentiality of this element in animals and humans. Bone tissue, where the element seems to play an important role, accumulates great amounts of vanadium. This paper reviews the physiology of osteoblasts, the involvement of different growth factors on bone development, and the effects of vanadium derivatives on the skeletal system of animal models and bone-related cells. Two cellular lines are discussed in particular; one derived from a rat osteosarcoma (UMR106) and the other is a nontransformed osteoblast cell line (MC3T3-E1). The effects of different growth factors and their mechanisms of action in these cellular lines are reviewed. These models of osteoblasts are especially useful in understanding the intracellular signaling pathways of vanadium derivatives in hard tissues. Vanadium uses an intricate interplay of intracellular mechanisms to exert different biochemical and pharmacological actions. The effects of vanadium derivatives on some cellular signaling pathways related to insulin are compiled in this review. The comprehension of these intracellular signaling pathways may facilitate the design of vanadium compounds with promising therapeutic applications as well as the understanding of secondary side effects derived from the use of vanadium as a therapeutic agent.

Animals↗

Three new vanadyl(IV) complexes with non-steroidal anti-inflammatory drugs (Ibuprofen, Naproxen and Tolmetin). Bioactivity on osteoblast-like cells in culture.

The synthesis and spectral and magnetic characterization of VO(2+) complexes with Ibuprofen (2-(4-isobutylphenyl)propionic acid), Naproxen (6-methoxy-alpha-methyl-2-naphthalene acetic acid) and Tolmetin (1-methyl-5-(4-methylbenzoyl)-1H-pyrrole-2-acetic acid) were studied. The complexes [VO(Ibu)(2)] x 5CH(3)OH, [VO(Nap)(2)] x 5CH(3)OH and [VO(Tol)(2)] were obtained from methanolic solutions under nitrogen atmosphere. The biological activities of these complexes on the proliferation of two osteoblast-like cells in culture (MC3T3E1 and UMR106) were compared with that of the vanadyl(IV) cation. The complexes exhibited different effects depending on the concentration and the cellular type, while no effect was observed for their parent drugs.

Animals↗

Non-enzymatic glycosylation of a type I collagen matrix: effects on osteoblastic development and oxidative stress.

BACKGROUND: The tissue accumulation of protein-bound advanced glycation endproducts (AGE) may be involved in the etiology of diabetic chronic complications, including osteopenia. The aim of this study was to investigate the effect of an AGE-modified type I collagen substratum on the adhesion, spreading, proliferation and differentiation of rat osteosarcoma UMR106 and mouse non-transformed MC3T3E1 osteoblastic cells. We also studied the role of reactive oxygen species (ROS) and nitric oxide synthase (NOS) expression on these AGE-collagen mediated effects. RESULTS: AGE-collagen decreased the adhesion of UMR106 cells, but had no effect on the attachment of MC3T3E1 cells. In the UMR106 cell line, AGE-collagen also inhibited cellular proliferation, spreading and alkaline phosphatase (ALP) activity. In preosteoblastic MC3T3E1 cells (24-hour culture), proliferation and spreading were significantly increased by AGE-collagen. After one week of culture (differentiated MC3T3E1 osteoblasts) AGE-collagen inhibited ALP activity, but had no effect on cell number. In mineralizing MC3T3E1 cells (3-week culture) AGE-collagen induced a decrease in the number of surviving cells and of extracellular nodules of mineralization, without modifying their ALP activity. Intracellular ROS production, measured after a 48-hour culture, was decreased by AGE-collagen in MC3T3E1 cells, but was increased by AGE-collagen in UMR106 cells. After a 24-hour culture, AGE-collagen increased the expression of endothelial and inducible NOS, in both osteoblastic cell lines. CONCLUSIONS: These results suggest that the accumulation of AGE on bone extracellular matrix could regulate the proliferation and differentiation of osteoblastic cells. These effects appear to depend on the stage of osteoblastic development, and possibly involve the modulation of NOS expression and intracellular ROS pathways.

Animals↗

On the interaction of the vanadyl(IV) cation with lactose: inhibition effects of vanadyl(IV)/monosaccharide and disaccharide complexes upon alkaline phosphatase activity.

A new vanadyl(IV) complex of the disaccharide lactose was obtained in aqueous solution at pH = 13. The sodium salt of the complex, of composition Na4[VO(lactose)2].3H2O, has been characterized by elemental analysis and by ultraviolet-visible, diffuse reflectance, and infrared spectroscopies. Its magnetic susceptibility and thermal behavior were also investigated. The inhibitory effect on alkaline phosphatase activity was tested for this compound as well as for the vanadyl(IV) complexes with maltose, sucrose, glucose, fructose, and galactose. For comparative purposes, the free ligands and the vanadyl(IV) cation were also studied. The free sugars and the sucrose/VO complex exhibited the lowest inhibitory effect. Lactose-VO, maltose-VO, and the free VO2+ cation showed an intermediate inhibition potential, whereas the monosaccharide/VO complexes appeared as the most potent inhibitory agents.

Alkaline Phosphatase↗

Synthesis, characterization and bioactivity of a new VO2+/aspirin complex.

A new VO2+ complex with salicylic acid acetate (Aspirin) of formula C18H18Cl2O12V2 was synthesized and characterized. Its biological effects upon cell proliferation, differentiation and promotion of tyrosine protein phosphorylation have been tested in two lines of osteoblast-like cells in culture.

Animals↗

Maltol complexes of vanadium (IV) and (V) regulate in vitro alkaline phosphatase activity and osteoblast-like cell growth.

Vanadium compounds have been found to possess insulin- and growth factor-mimetic effects. In consequence, these derivatives are potentially useful as effective oral therapeutic agents in diabetic patients. However, their use has been limited by various toxic side-effects and by the low solubility of different derivatives. Recently, vanadium complex with maltol, a sugar used as a common food additive, have been synthesised and investigated in animals, showing possible insulin-mimetic effects with low toxic side-effects. In the present study we have investigated the effect of bis(maltolato)oxovanadium (IV) (BMOV) and bis(maltolato)dioxovanadium (V) (BMV) on bone cells in culture as well as their direct effect on alkaline phosphatase in vitro. A comparison was also made with the action of vanadate and vanadyl cation. Vanadium compounds regulated cell proliferation in a biphasic manner with similar potencies. Osteoblast differentiation, assessed by alkaline phosphatase activity, was found to be dose-dependent, with the inhibitory effect being stronger for vanadate and BMOV than for vanadyl and BMV. All vanadium compounds directly inhibited bovine intestinal ALP with a similar potency. Thus, maltol vanadium derivatives behave in a similar way to vanadate and vanadyl in osteoblast-like UMR 106 cells in culture.

Alkaline Phosphatase↗