RESUMO
Saturated solutions of calcium l-lactate in water or in deuterium oxide continuously dissolve calcium l-lactate by addition of solid sodium d-gluconate and become strongly supersaturated in calcium d-gluconate due to no or slow precipitation. The quantification of total dissolved calcium allied with the calcium complexes equilibrium constants allowed an ion speciation, which shows an initial non-thermal and spontaneous supersaturation of more than a factor of 50 at 25 °C only slowly decreasing after initiation of precipitation of calcium d-gluconate after a lag phase of several hours. A mathematical model is proposed, based on numerical solution of coupled differential equations of dynamics of l-lactate and d-gluconate exchange during the lag phase for precipitation and during precipitation. A slow exchange of l-lactate coordinated to calcium with d-gluconate is indicated with a time constant of 0.20 h-1 in water and of 0.15 h-1 in deuterium oxide and a kinetic deuterium/hydrogen isotope effect of 1.25. Such spontaneous non-thermal supersaturation and slow ligand exchange with a pseudo first order equilibration process with a half-life of 3.5 h in water for calcium hydroxycarboxylates can help to understand the higher calcium bioavailability from calcium hydroxycarboxylates compared to simple salts.
Assuntos
Cálcio , Ácido Láctico , Gluconatos , Solubilidade , ÁguaRESUMO
Dissolution of amorphous calcium phosphate (ACP) in aqueous citrate at varying pH has been studied with perspective of increasing availability of calcium from sidestreams of whey protein, lactose and/or cheese production or on development of new functional foods. ACP formed as an initial precipitate in 0.10â¯molâ¯L-1 equimolar aqueous calcium chloride, sodium citrate, and sodium hydrogenphosphate was used as model for mineral residues formed during milk processing. Upon acidification of the ACP suspension by hydrochloric acid decreasing pH from 6.5 to 4.5, the transformations of ACP occurred through an 8â¯h period of supersaturation prior to a slow precipitation of calcium citrate tetrahydrate. This robust supersaturation, which may explain increased availability of calcium phosphates in presence of citrate, presented a degree of supersaturation of 7.1 and was characterized by precipitation rates for 0.10â¯molâ¯L-1 equimolar aqueous calcium chloride, sodium hydrogencitrate, and sodium hydrogenphosphate with pHâ¯5.5, and for 0.10â¯molâ¯L-1 equimolar aqueous calcium chloride, sodium hydrogencitrate, and sodium dihydrogenphosphate with pHâ¯4.1, with a degree of supersaturation of 2.7. The crystallization processes were similar according to Avrami's model with a half-life for precipitation of approximately 5â¯h independent of the degree of supersaturation. Ion speciation based on measurement of pH, and total concentrations of calcium, phosphate and citrate, and of conductivity and calcium ion activity during precipitation indicates a low driving force for precipitation with calcium citrate complex dominating at pHâ¯5.5 and calcium hydrogencitrate complex dominating at pHâ¯4.1. Calcium hydrogencitrate is suggested to be the species involved in the crystal growth followed by solid state transformation to calcium citrate tetrahydrate.
Assuntos
Citrato de Cálcio/metabolismo , Fosfatos de Cálcio/metabolismo , Ácido Cítrico/metabolismo , Citrato de Cálcio/química , Fosfatos de Cálcio/química , Ácido Cítrico/químicaRESUMO
This work evaluated the analgesic and anti-inflammatory activity of ruthenium(II) complexes trans-[Ru(NO(+))(NH3)4(L)](BF4)3 and [Ru(NH3)5(L)](BF4)3 containing the nonsteroidal anti-inflammatory drugs nicotinic acid (Hnic) and its isomer isonicotinic acid (ina) as ligands (L). The anti-nociceptive potential of these complexes and the free ligands (noncoordinated to ruthenium) was tested in different models with doses ranging from 1 to 100 µmol/kg. The ligands themselves were inactive; however, the ruthenium complexes containing Hnic and ina inhibited mechanical hyperalgesia induced by prostaglandin E2, carrageenan-induced hyperalgesia, and antigen-induced arthritis. Moreover, the ruthenium complexes inhibited overt nociception induced by formalin, acetic acid, capsaicin, and cinnamaldehyde. The mechanism involved in the anti-nociceptive effects of the ruthenium complexes suggested that ATP-sensitive K(+) channel pathways were not involved because glibenclamide did not affect their anti-nociceptive activities. However, the anti-nociceptive effect appears to be a consequence of the reduction in neutrophil migration and inhibition of the protein kinase C pathway.