Chloramphenicol succinate

Artemether (AM), a highly effective treatment for multidrug-resistant malaria and a component of artemisinin combination therapy, has been associated with some neurotoxicity following repeated high doses. This study was aimed at investigating the effect of AM on pentobarbitone sleep and electrical activities in rats. Wistar rats received AM i.p. at 3 dose levels: 1.5, 7.5, and 15 mg/kg, whereas control rats received 0.2 mL of the vehicle (3% v/v Tween 80). AM administered 20 min before pentobarbitone had no significant effect on the onset and duration of sleep. However, after a 7-day pretreatment, AM dose-dependently prolonged pentobarbitone sleep, as did chloramphenicol. Electroencephalogram and electromyogram recordings 20 min after pretreatment showed that AM (15 mg/kg) exhibited inhibitory activity similar to chlorpromazine as opposed to the excitatory effect of amphetamine. When pretreated for 7 days, rats receiving 1.5 mg/kg AM also showed inhibitory activity of the cortical centres, whereas desynchronization of the optic tectum and reticular formation was observed in rats pretreated with 7.

A highly selective and sensitive mesofluidic immunoassay system based on competitive immunoassay in polydimethylsiloxane (PDMS) channels was developed. This immunoassay system was successfully applied to quantificationally detect chloramphenicol (CAP) in animal foods. The glass beads (Ø 250 microm) were amino-silane modified, covalently precoated with chloramphenicol succinate, and then infused into the microchannels (Ø 300 microm); the CAP molecules of samples or standards in flow solution competed for CAP antibody with the CAP immobilized on the beads. The CAP antigen-antibody complex anchored on the beads was probed by Cy5-labeled secondary antibody, and the fluorescence intensities of beads were employed to determine the concentration of CAP. In this system, the detection limit of CAP is 0.008 microg/L. The method reveals good recovery rates from 90 to 108% and coefficients of variance (CV) from 4.72 to 6.52%. The experimental results demonstrate that the bead-based mesofluidic system has high sensitivity and excellent performance.

BACKGROUND: Emerging evidence suggests that "adaptive" induction of autophagy (the cellular process responsible for the degradation and recycling of proteins and organelles) may confer a cardioprotective phenotype and represent a novel strategy to limit ischemia-reperfusion injury. Our aim was to test this paradigm in a clinically relevant, large animal model of acute myocardial infarction.

The aim of this study was to determine the stability of three ester prodrugs, chloramphenicol succinate, enalapril and candesartan cilexetil, in human proximal small intestinal fluid (HIF), dog proximal small intestinal fluids (DIF) and simulated intestinal fluid (FaSSIF), with the addition of pancreatin. The total protein content in the proximal jejunal fluids was determined in HIF and DIF, respectively. Candesartan cilexetil was significantly degraded in HIF (initial t(1/2(0-5 min))=5.4 ± 0.5 min) and in DIF (initial t(1/2(0-5 min))=5.7 ± 0.1 min), while chloramphenicol succinate and enalapril were stable in both media. The degradation of candesartan cilexetil was shown to be mediated by enzymes following Michaelis-Menten enzyme kinetics and was inhibited by addition of esterase inhibitors. The enzymatic capacity reflected by V(max) was 4-fold higher in DIF than in HIF and correlated to its 2-fold higher protein concentration. The degradation of candesartan cilexetil in the FaSSIF-pancreatin solution was slower (t(1/2)=207 ± 34 min) than the degradation in both HIF and DIF.