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摘要
Aims: This study was performed to evaluate the therapeutic efficacy of nanocapsulated flavonoidal quercetin (QC) in combating arsenic-induced reactive oxygen species (ROS)-mediated oxidative damage in hepatocytes and brain cells in a rat model. Main methods: Hepatic and neuronal cell damage in rats was made by a single injection (sc) of sodium arsenite (NaAsO2, 13 mg/kg b. wt. in 0.5 ml of physiological saline). A single dose of 500 mu l of quercetin suspension (QC) (QC 8.98 mu mol/kg) or 500 mu l of nanocapsulated QC (NPQC) (QC 8.98 mu mol/kg) was given orally to rats at 90 min prior to the arsenite injection. Key findings: Inorganic arsenic depositions (182 /- 15.6 and 110 /- 12.8 ng/g protein) were found in hepatic and neuronal mitochondrial membranes. Antioxidant levels in hepatic and neuronal cells were reduced significantly by arsenic. NPQC prevented the arsenite-induced reduction in antioxidant levels in the liver and brain. Arsenic induced a substantial decrease in liver and brain cell membrane microviscosities. and NPQC treatment resulted in a unique protection against the loss. A significant correlation between mitochondrial arsenic and its conjugated diene level was observed both in liver and brain cells for all experimental rats. Significance: Arsenic-specific antidotes are used against arsenic-induced toxicity. However, the target site is poorly recognized and therefore achieving an active concentration of drug molecules can be a challenge. Thus, our objective was to formulate NPQC and to investigate its therapeutic potential in an oral route against arsenite-induced hepatic and neuronal cell damage in a rat model.
- 出版日期2009-1-16
