Novel metal-organic framework combining with restricted access molecularly imprinted nanomaterials for solid-phase extraction of gatifloxacin from bovine serum.

Novel restricted access molecularly imprinted nanomaterials (RAMIPs) were successfully prepared on the surface of metal-organic frameworks (NH2-MIL-125) by surface-initiated atom transfer radical polymerization (SI-ATRP) technology. Then it was applied as a solid phase extraction (SPE) material in analysis of quinolones in bovine serum by HPLC detection. NH2-MIL-125@RAMIPs was empolyed as a sorbent for gatifloxacin (GTFX) and the resulted material has a good binding amounts (86.1 mg g-1), rapid binding kinetic (36 min). The results indicated that the prepared NH2-MIL-125@RAMIPs possess excellent specific recognition for GTFX. Combined with high-performance liquid chromatography (HPLC), the SPE column filled with NH2-MIL-125@RAMIPs was applied to selectively enrich GTFX antibiotic from bovine serum. The recovery of GTFX is between 96.8% and 105.6%, with relative standard deviations of 1.7-3.2% (n = 3). The research results illustrate that the method is successfully applied to the selective enrichment of GTFX in bovine serum. It provides a simple and efficient method for the direct detection of GTFX in bovine serum.

Based on reduced graphene oxide-copper sulfide-carbon nitride nanosheets composite electrochemiluminescence sensor for determination of gatifloxacin in mouse plasma.

A new method for determination of gatifloxacin hydrochloride (GAT) by reduced graphene oxide-copper sulfide (rGO-CuS) composite coupled with graphite-like carbon nitride nanosheets (g-C3N4 NSs) modified glassy carbon electrode was developed. In this work, rGO-CuS composite was synthesized by one-pot hydrothermal method and used for enhancing sensitivity of GAT. g-C3N4 NSs were synthesized as radiant agent. The sensor characteristics of electrochemistry and electrochemiluminescence (ECL) were investigated. The ECL intensity has enhanced four-fold after modifying with rGO-CuS composite. The results can be ascribed to the presence of rGO-CuS composite on the electrode surface that facilitates the electron transfer rate between the electroactive center of g-C3N4 NSs and the electrode. Under the optimum experimental conditions (photomultiplier tuber for 800 V, scan rate for 0.1 V/s, 0.1 mol/L PBS (pH 7.5) and 1.0 × 10-2 mol/L K2S2O8), the linear range for GAT was from 1.0 × 10-4 to 1.0 × 10-8 mol/L (R2 = 0.9991) with detection limit of 3.5 × 10-9 mol/L (S/N = 3). RSD for ECL intensity was 4.8% (n = 10). The recoveries of GAT in mouse plasma samples were from 98.36 to 104.7%. The sensor showed the advantages of low cost, high sensitivity and wide application in drug analysis.

Functional and Morphological Characteristics of Pancreatic Islet Lesions Induced by Quinolone Antimicrobial Agent Gatifloxacin in Rats.

We characterized pancreatic islet lesions induced by several quinolones using functional and morphological examinations of the pancreatic islets in male rats orally administered gatifloxacin, lomefloxacin, or levofloxacin at 300 mg/kg for 14 consecutive days. Consequently, in contrast to lomefloxacin or levofloxacin, gatifloxacin increased serum glucose and glycosylated albumin on day 14 and elevated serum glucose tended to decrease insulin in the intravenous glucose tolerance test. Microscopically, only gatifloxacin induced cytoplasmic vacuoles containing eosinophilic homogenous contents in islet cells. Immunohistochemical examination revealed that vacuolated islet cells were positively stained for insulin, demonstrating they were pancreatic ß cells. Electron microscopy showed that the cytoplasmic vacuoles represented dilated cisterna of the rough endoplasmic reticulum filled with electron-lucent materials in pancreatic ß cells. Moreover, insulin secretory granules were drastically decreased in vacuolated islet cells, suggesting impaired insulin synthesis and/or transport. This gatifloxacin-induced pancreatic toxicity in rats was considered to be associated with high pancreatic drug distribution. These results demonstrated that gatifloxacin provoked functional and morphological pancreatic ß cell alteration associated with impaired insulin synthesis and/or transport, leading to hyperglycemia.