Efecto de la roya del álamo sobre el crecimiento del año y del rebrote de la siguiente temporada en tres clones con distinta susceptibilidad y arquitectura del canopeo

El cultivo de álamos en el Delta del Paraná, la tercera cuenca de importancia forestal de Argentina, es una actividad económica relevante que provee materia prima para las industrias del aserrado, debobinado, tableros de partículas y pulpa para papel. La producción de madera de álamo está amenazada por enfermedades, cuyo desarrollo se encuentra favorecido por las condiciones ambientales y la estrecha base genética de sus plantaciones comerciales. Entre ellas la roya es considerada la de mayor importancia y en varias oportunidades obligó al reemplazo total de los clones en cultivo. El objetivo de esta tesis fue evaluar el efecto de la roya sobre el crecimiento del año y del rebrote de la siguiente temporada utilizando como modelo tres clones de Populus deltoides con distinta arquitectura del canopeo y nivel de tolerancia. Se evaluó además el efecto sobre la densidad básica de la madera dada su importancia en la determinación de la calidad. A fin de conocer las bases fisiológicas del daño causado por la roya se estudiaron los cambios en la dinámica foliar, la intercepción de la luz, la fotosíntesis el contenido de clorofila y el reciclado del nitrógeno. Los resultados obtenidos indican que la reducción del crecimiento y la calidad de la madera atribuible a la enfermedad se deben a una disminución de la capacidad fotosintética y consecuentemente de la capacidad de fijar y translocar carbono, tanto para continuar el crecimiento del año como para acumular reservas en la parte aérea y radical. La reducción del sistema radical limita la capacidad de explorar el suelo y adquirir agua y nutrientes durante esa temporada de crecimiento. Esto, sumado a una retranslocación incompleta de nitrógeno debido a que las hojas enfermas caen con mayor cantidad de nitrógeno, reduce las reservas de carbono y de nitrógeno para iniciar el crecimiento y la capacidad de adquirir recursos desde el suelo al inicio de la temporada siguiente

Vanadium Compounds : Their Action on Alkaline Phosphatase Activity

The direct effect of different vanadium compounds upon alkaline phosphatase (ALP) activity was investigated~ Vanadate and vanadyl inhibited both the soluble and particulate ALP activity from UMR.106 cells and front bovine intestinal ALP. We have also shown the inhibition of ALP activity in the soluble fraction of osteoblasts by peroxo and hydroperoxo vanadium compounds. ALP activity in the particulate fraction was not inhibited by these species; nor was the bovine intestinal ALP. Using inhibitors of Tyr-phosphatase (PTPases), the soluble ALP was partially characterized as a PTPase. The major activity in the particulate fraction represents the bone-specific ALPactivity. This study demonstrates that different forms of vanadium are direct inhibitors of ALP activity. This effect is dependent on the enzymatic activity investigated and on the origin of the ALP.Facultad de Ciencias Médica

Proliferative and morphological changes induced by vanadium compounds on Swiss 3T3 fibroblasts

Vanadium compounds are shown to have a mitogenic effect on fibroblast cells. The effects of vanadate, vanadyl and pervanadate on the proliferation and morphological changes of Swiss 3T3 cells in culture are compared. Vanadium derivatives induced cell proliferation in a biphasic manner, with a toxic-like effect at doses over 50 mM, after 24 h of incubation. Vanadyl and vanadate were equally potent at 2.5–10 mM. At 50 mM vanadate inhibited cell proliferation, whereas slight inhibition was observed at 100 mM of vanadyl. At 10 mM pervanadate was as potent as vanadate and vanadyl in stimulating fibroblast proliferation, but no effect was observed at lower concentrations. A pronounced cytotoxic-like effect was induced by pervanadate at 50 mM. All of these effects were accompanied by morphological changes: transformation of fibroblast shape from polygonal to fusiform; retraction with cytoplasm condensation; and loss of lamellar processes. The magnitude of these transformations correlates with the potency of vanadium derivatives to induce a cytotoxic-like effect: pervanadate > vanadate > vanadyl. These data suggest that the oxidation state and coordination geometry of vanadium determine the degree of the cytotoxicit

Efectos “in vivo” de Metformina sobre las alteraciones de la microarquitectura ósea asociadas al Síndrome Metabólico inducido por fructosa en ratas

El Síndrome Metabólico (SM) se ha asociado recientemente con una disminución en la densidad mineral ósea, y con un aumento en la incidencia de fracturas osteoporóticas. Recientemente encontramos que la Metformina por vía oral en ratas, promueve la diferenciación osteogénica de células progenitoras de médula ósea e incrementa la reparación de lesiones óseas. En este trabajo evaluamos los efectos del SM inducido por Fructosa sobre la microarquitectura ósea en ratas, y la modulación de estos efectos por Metformina administrada en forma oral. Utilizamos ratas Sprague Dawley macho jóvenes: C (control sin tratamiento), C+M (100mg/kg/día Metformina en el agua de bebida), F (10 % Fructosa en el agua de bebida) y F+M (Fructosa+Metformina en el agua de bebida). Los tratamientos se continuaron por 3 semanas luego de lo cual se tomaron muestras de sangre, previas al sacrificio de los animales. Se disecaron los fémures para evaluación histomorfométrica de la microarquitectura metafisaria por tinción con Hematoxilina-Eosina (H-E). Se observó un incremento en la glucemia y trigliceridemia en el grupo F versus el C, compatible con el desarrollo de SM. El análisis de las metáfisis femorales mostró un aumento en la densidad osteocítica trabecular para el grupo C+M (118 % del control, p<0,05). El tratamiento con Fructosa sola disminuyó la densidad osteocítica (79 % del control, p<0,05), mientras que el co-tratamiento Fructosa+Metformina (grupo F+M) revirtió parcialmente este descenso (88 % del control). Similarmente, el porcentaje de hueso trabecular en la metáfisis femoral aumentó luego del tratamiento sólo con Metformina (129 % respecto del control), se redujo en las ratas tratadas con Fructosa (89 % respecto del control), y fue intermedia en el grupo F+M (94 % respecto del control). Estos resultados muestran que el SM inducido por Fructosa en ratas altera la microarquitectura metafisaria femoral; y que estos efectos deletéreos pueden ser parcialmente prevenidos por un tratamiento oral con Metformina.Several clinical studies have demonstrated that the Metabolic Syndrome (MS) is associated with a decrease in bone mineral density, and with an increased risk for non-vertebral osteoporotic fractures. We have recently found that orally administered Metformin induces osteogenic effects in rats, promoting osteoblastic differentiation of bone marrow progenitor cells and increasing the repair of bone lesions. In the present work we have evaluated the effects of Fructose-induced MS on bone micro-architecture in rats, and the possiblemodulation of these effects by orally administered Metformin. We utilized young male Sprague-Dawley rats, divided into four groups: C (non-treated controls); C+M (100 mg/kg/day of Metformin in drinking water); F (10 % of Fructose in drinking water); and F+M (Fructose+Metformin in drinking water). After three weeks of all treatments blood samples were taken, after which animals were sacrificed by cervical dislocation under anaesthesia. Femurs were then dissected for evaluation of metaphyseal micro-architecture after Haematoxilin-Eosin staining of 5 μm histological slices of decalcified bone. In particular, osteocytic density and relative trabecular volume were determined. An increase in serum glucose and triglycerides was observed in Fructose-treated rats, in accordance with the development of MS. In rats treated with Metformin alone (group C+M), the analysis of femoral metaphyses showed an increase in trabecular osteocytic density (118 % of control [group C], p<0.05). Treatment with Fructose alone (group F) significantly decreased ostecytic density (79 % of control, p<0.05), while co-treatment with Fructose and Metformin partially reverted this decrease (group F+M, 88 % of control). Similarly, the relative trabecular volume of femoral metaphysic was increased by treatment with Metformin alone (129% of control), was reduced in Fructose-treated rats (89 % of control), and tended to revert back to control values after Fructose-Metformin co-treatment (94 % of control). These results show for the first time that (a) Fructose-induced MS in rats alters their femoral metaphysis micro-architecture; and that (b) these deleterious effects can be partially prevented by orally administered Metformin

Insulin-mimetic action of vanadium compounds on osteoblast-like cells in culture

Vanadium compounds mimic insulin actions in different cell types. The present study concerns the insulin-like effects of three vanadium(V) derivatives and one vanadium(IV) complex on osteoblast-like (UMR106 and MC3T3E1) cells in culture. The vanadium oxalate and vanadium citrate complexes hydrolyzed completely under the culture conditions, whereas more than 40% of the vanadium tartrate and nitrilotriacetate complexes remained. Vanadate, as well as vanadium oxalate, citrate, and tartrate complexes enhanced cell proliferation (as measured by the crystal violet assay), glucose consumption, and protein content in UMR106 and MC3T3E1 osteoblast-like cells. The vanadium nitrilotriacetate complex (the only peroxo complex tested) stimulated cell proliferation in UMR106 but not in MC3T3E1 cells. This derivative strongly transformed the morphology of the MC3T3E1 cells. All vanadium(V) compounds inhibited cell differentiation (alkaline phosphatase activity) in UMR106 cells. Our data are consistent with the interpretation that vanadium oxalate and citrate complexes hydrolyze to vanadate. Vanadium nitrilotriacetate would appear to be toxic for normal MC3T3E1 osteoblasts. In contrast, the vanadium tartrate complex induced a proliferative effect; however, it did not alter cell differentiation

Insulin-mimetic action of vanadium compounds on osteoblast-like cells in culture

Vanadium compounds mimic insulin actions in different cell types. The present study concerns the insulin-like effects of three vanadium(V) derivatives and one vanadium(IV) complex on osteoblast-like (UMR106 and MC3T3E1) cells in culture. The vanadium oxalate and vanadium citrate complexes hydrolyzed completely under the culture conditions, whereas more than 40% of the vanadium tartrate and nitrilotriacetate complexes remained. Vanadate, as well as vanadium oxalate, citrate, and tartrate complexes enhanced cell proliferation (as measured by the crystal violet assay), glucose consumption, and protein content in UMR106 and MC3T3E1 osteoblast-like cells. The vanadium nitrilotriacetate complex (the only peroxo complex tested) stimulated cell proliferation in UMR106 but not in MC3T3E1 cells. This derivative strongly transformed the morphology of the MC3T3E1 cells. All vanadium(V) compounds inhibited cell differentiation (alkaline phosphatase activity) in UMR106 cells. Our data are consistent with the interpretation that vanadium oxalate and citrate complexes hydrolyze to vanadate. Vanadium nitrilotriacetate would appear to be toxic for normal MC3T3E1 osteoblasts. In contrast, the vanadium tartrate complex induced a proliferative effect; however, it did not alter cell differentiation.Facultad de Ciencias Exacta

Insulin-mimetic action of vanadium compounds on osteoblast-like cells in culture

Vanadium compounds mimic insulin actions in different cell types. The present study concerns the insulin-like effects of three vanadium(V) derivatives and one vanadium(IV) complex on osteoblast-like (UMR106 and MC3T3E1) cells in culture. The vanadium oxalate and vanadium citrate complexes hydrolyzed completely under the culture conditions, whereas more than 40% of the vanadium tartrate and nitrilotriacetate complexes remained. Vanadate, as well as vanadium oxalate, citrate, and tartrate complexes enhanced cell proliferation (as measured by the crystal violet assay), glucose consumption, and protein content in UMR106 and MC3T3E1 osteoblast-like cells. The vanadium nitrilotriacetate complex (the only peroxo complex tested) stimulated cell proliferation in UMR106 but not in MC3T3E1 cells. This derivative strongly transformed the morphology of the MC3T3E1 cells. All vanadium(V) compounds inhibited cell differentiation (alkaline phosphatase activity) in UMR106 cells. Our data are consistent with the interpretation that vanadium oxalate and citrate complexes hydrolyze to vanadate. Vanadium nitrilotriacetate would appear to be toxic for normal MC3T3E1 osteoblasts. In contrast, the vanadium tartrate complex induced a proliferative effect; however, it did not alter cell differentiation.Facultad de Ciencias Exacta

Proliferative and morphological changes induced by vanadium compounds on Swiss 3T3 fibroblasts

Vanadium compounds are shown to have a mitogenic effect on fibroblast cells. The effects of vanadate, vanadyl and pervanadate on the proliferation and morphological changes of Swiss 3T3 cells in culture are compared. Vanadium derivatives induced cell proliferation in a biphasic manner, with a toxic-like effect at doses over 50 mM, after 24 h of incubation. Vanadyl and vanadate were equally potent at 2.5–10 mM. At 50 mM vanadate inhibited cell proliferation, whereas slight inhibition was observed at 100 mM of vanadyl. At 10 mM pervanadate was as potent as vanadate and vanadyl in stimulating fibroblast proliferation, but no effect was observed at lower concentrations. A pronounced cytotoxic-like effect was induced by pervanadate at 50 mM. All of these effects were accompanied by morphological changes: transformation of fibroblast shape from polygonal to fusiform; retraction with cytoplasm condensation; and loss of lamellar processes. The magnitude of these transformations correlates with the potency of vanadium derivatives to induce a cytotoxic-like effect: pervanadate > vanadate > vanadyl. These data suggest that the oxidation state and coordination geometry of vanadium determine the degree of the cytotoxicity.Facultad de Ciencias Exacta

Effect of vanadium compounds on acid phosphatase activity

The direct effect of different vanadium compounds on acid phosphatase (ACP) activity was investigated. Vanadate and vanadyl but not pervanadate inhibited the wheat germ ACP activity. These vanadium derivatives did not alter the fibroblast Swiss 3T3 soluble fraction ACP activity. Using inhibitors of tyrosine phosphatases (PTPases), the wheat germ ACP was partially characterized as a PTPase. This study suggests that the inhibitory ability of different vanadium derivatives to modulate ACP activity seems to depend on the geometry around the vanadium atom more than on the oxidation state. Our results indicate a correlation between the PTPase activity and the sensitivity to vanadate and vanadyl cation.Facultad de Ciencias Exacta

Oil seeps from the Patagonian shelf: their thermosteric fate

Radar images are commonly applied to recognize and monitor oil seeps on surface waters over continental shelves. In San Jorge Gulf, Patagonia, between 46° S and 48° S, oil slicks have been surveyed performing ellipse patterns in response to mesotidal dynamics. These effects were assigned to recent episodic increments of summer bottom temperatures at depths between 100 and 120 m, which are 2 °C warmer than those recorded during the 20th century. Slicks are assumed to have their origin from faults already known by the oil industry onshore. The effects here described should be envisaged in a climate-change scenario leading to temperature increases of the oceans’ shallow waters, together with other effects such as the human-induced global sea level rise. Under such warmer conditions seeps from continental shelf floors will become more frequent, and their contribution to the atmospheric C budget should be globally assessed