Metabolomics analysis of the effects of quercetin on renal toxicity induced by cadmium exposure in rats.

This study aims to explore the protective effects of quercetin against cadmium-induced nephrotoxicity utilizing metabolomics methods. Male Sprague-Dawley rats were randomly assigned to six groups: control, different dosages of quercetin (10 and 50 mg/kg·bw, respectively), CdCl2 (4.89 mg/kg·bw) and different dosages quercetin plus CdCl2 groups. After 12 weeks, the kidneys were collected for metabolomics analysis and histopathology examination. In total, 11 metabolites were confirmed, the intensities of which significantly changed (up-regulated or down-regulated) compared with the control group (p < 0.00067). These metabolites include xanthosine, uric acid (UA), guanidinosuccinic acid (GSA), hypoxanthine (Hyp), 12-hydroxyeicosatetraenoic acid (tetranor 12-HETE), taurocholic acid (TCA), hydroxyphenylacetylglycine (HPAG), deoxyinosine (DI), ATP, formiminoglutamic acid (FIGLU) and arachidonic acid (AA). When high-dose quercetin and cadmium were given to rats concurrently, the intensities of above metabolites significantly restored (p < 0.0033 or p < 0.00067). The results showed quercetin attenuated Cd-induced nephrotoxicity by regulating the metabolism of lipids, amino acids, and purine, inhibiting oxidative stress, and protecting kidney functions.

Metabonomics analysis of liver in rats administered with chronic low-dose acrylamide.

The current study aimed to investigate the hepatotoxicity of rats administered with chronic low-dose acrylamide (AA) by using metabonomics technology on the basis of ultraperformance liquid chromatography-mass spectrometry (UPLC-MS). A total of 40 male Wistar rats were randomly divided into the following four groups: control, low-dose AA (0.2 mg/kg bw, non-carcinogenic end-point based on the induction of morphological nerve changes in rats), middle-dose AA (1 mg/kg bw), and high-dose AA (5 mg/kg bw). The rats continuously received AA by administering it in drinking water daily for 16 weeks. After the treatment, rat livers were collected for metabonomics analysis and histopathology examination. Principal components analysis (PCA) and partial least-squares discriminant analysis (PLS-DA) were used to investigate the metabonomics profile changes in rat liver tissues and screen the potential biomarkers.Fourteen metabolites were identified with significant changes in intensities (increased or decreased compared with the control group) as a result of treatment (p < 0.05 or p < 0.01). These metabolites included tauro-b-muricholic acid, docosapentaenoic acid, sphingosine 1-phosphate, taurodeoxycholic acid, lysoPE(20:5), cervonyl carnitine, linoleyl carnitine, docosahexaenoic acid, lysoPC(20:4), lysoPE(18:3), PA(20:4), stearidonyl carnitine, alpha-linolenic acid, and lysoPA(18:0).Results showed that chronic exposure to AA at NOAEL (0.2 mg/kg bw) exhibited no toxic effect in rat livers at the metabolic level. AA induced oxidative stress to the liver and disrupted lipid metabolism. The results of liver histopathology examination further supported the metabonomic results.