Osjetljiva spektrofotometrijska metoda za određivanje sulfonamida u farmaceutskim pripravcima

A new, simple and sensitive spectrophotometric method for the determination of some sulfonamide drugs has been developed. The method is based on the diazotisation of sulfacetamide, sulfadiazine, sulfaguanidine, sulfamerazine, sulfamethazine, sulfamethoxazole and coupling with 8-hydroxyquinoline in alkaline media to yield red coloured products, with absorption maximum at 500 nm. The Beer’s law is obeyed from 0.17.0 µg mL1. The limits of quantification and limits of detection were 0.110.18 and 0.030.5 µg mL1, respectively. Intraday precision (RSD 0.10.5%) and accuracy (recovery 97.3100.8) of the developed method were evaluated. No interference was observed from common adjuvants. The method has been successfully applied to the assay of sulpha drug in the pharmaceutical formulations.U radu je opisana nova, jednostavna i osjetljiva spektrofotometrijska metoda za određivanje sulfonamida. Metoda se temelji na prevođenju sulfacetamida, sulfadiazina, sulfagvanidina, sulfamerazina, sulfometazina i sulfametoksazola u diazoderivate koji kondenzacijom s 8-hidroksikinolinom u alkalnom mediju daju crveno obojene produkte s maksimumom apsorpcije pri 500 nm. Beerov zakon vrijedi u koncentracijskom rasponu 0,17,0 µg mL1. Granice kvantifikacije i granice detekcije su 0,11-0,18, odnosno 0,03-0,05 µg mL-1. Za predloženu metodu procijenjene su intermedirska preciznost (RSD 0.1-0,5%) i točnost (analitički povrat 97,3-100,8). Uobičanjene pomoćne tvari u tabletama ne interferiraju tijekom određivanja. Metoda je uspješno primijenjena za analizu sulfonamida u farmaceutskim pripravcima

Chloroquine activates the p53 pathway and induces apoptosis in human glioma cells

Glioblastoma is the most common malignant brain tumor in adults. The currently available treatments offer only a palliative survival advantage and the need for effective treatments remains an urgent priority. Activation of the p53 growth suppression/apoptotic pathway is one of the promising strategies in targeting glioma cells. We show that the quinoline derivative chloroquine activates the p53 pathway and suppresses growth of glioma cells in vitro and in vivo in an orthotopic (U87MG) human glioblastoma mouse model. Induction of apoptosis is one of the mechanisms underlying the effects of chloroquine on suppressing glioma cell growth and viability. siRNA-mediated downregulation of p53 in wild-type but not mutant p53 glioblastoma cells substantially impaired chloroquine-induced apoptosis. In addition to its p53-activating effects, chloroquine may also inhibit glioma cell growth via p53-independent mechanisms. Our results clarify the mechanistic basis underlying the antineoplastic effect of chloroquine and reveal its therapeutic potential as an adjunct to glioma chemotherapy