RESUMO
A new chemical structure, the 4,2',4",2'''-tetrahydroxy-6',6'''-dimethoxy-4'-O-4'''- bichalcone, named achyrobichalcone was isolated and identified from an Achyrocline satureioides spray-dried powder (SDP80). The thermal and photo stability of this new compound as well as that of the main polyphenols present in the spray dried powder, quercetin, luteolin, 3-O-metylquercetin and the corresponding kinetics of degradation are reported. In the long-term testing (30 +/- 2 degrees C/75 +/- 5% RH, 12 months), the total polyphenols contained in SDP80 demonstrated to be stable, remaining higher than 90% after a 12 month exposure. The photo stability testing revealed that all polyphenols were stable for 48 h when SDP80 was conditioned in amber or transparent flasks and exposed to UV-C radiation (light express LE UV, 254 nm, 30W). In contrast, when unprotected, the polyphenols demonstrated to be sensitive to both, thermal stress testing (80 +/- 2 degrees C), for 14 days and to UV-C radiation. Luteolin showed to be the most stable against UVC light and 3-O-methylquercetin against temperature. The achyrobichalcone demonstrated to be the more unstable against both, temperature and light. The kinetics of polyphenol thermal degradation (80 +/- 2 degrees C, 49 days) and photodegradation (UV-C radiation, 96 h) followed, 2nd and 1st order reaction, respectively.
Assuntos
Achyrocline/química , Chalconas/análise , Chalconas/efeitos da radiação , Cromatografia Líquida de Alta Pressão , Dessecação , Estabilidade de Medicamentos , Etanol , Temperatura Alta , Cinética , Luz , Espectroscopia de Ressonância Magnética , Fenóis/análise , Fenóis/efeitos da radiação , Extratos Vegetais/análise , Pós , Padrões de Referência , SolventesRESUMO
Methylmalonic acidemias are metabolic disorders caused by a severe deficiency of methylmalonyl-CoA mutase activity, which are characterized by neurological dysfunction, including convulsions. It has been reported that the accumulating metabolite, L-methylmalonic acid (MMA), inhibits succinate dehydrogenase leading to ATP depletion in vitro, and that the intrastriatal injection of MMA induces convulsions through secondary NMDA receptor stimulation. In this study we investigated the effect of creatine (1.2, 3.6 and 12.0 mg/kg, (i.p.), [DOSAGE ERROR CORRECTED] succinate (1.5 micromol/striatum) and MK-801 (3 nmol/striatum) on the convulsions and on the striatal lactate increase induced by MMA (4.5 micromol/striatum) in rats. The effect of creatine on the striatal phosphocreatine content and on MMA-induced phosphocreatine depletion was also evaluated. Creatine, succinate and MK-801 pretreatment decreased the number and duration of convulsive episodes and the lactate increase elicited by MMA. Creatine, but not succinate, prevented the convulsions and the lactate increase induced by the direct stimulation of NMDA receptors. Acute creatine administration increased the total striatal phosphocreatine content and prevented MMA-induced phosphocreatine depletion. Our results suggest that MMA increases lactate production through secondary NMDA receptor activation, and it is proposed that the anticonvulsant effect of creatine against MMA-induced convulsions may be due to an increase in the phosphocreatine content available for metabolic purposes.