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超高效液相色谱-质谱联用技术对长期低剂量镉染毒大鼠血清的代谢组学分析

Metabonomics analysis of serum from rats given long-term and low-level cadmium by ultra-performance liquid chromatography-mass spectrometry.

作者信息

Hu Liyan, Bo Lu, Zhang Meiyan, Li Siqi, Zhao Xiujuan, Sun Changhao

机构信息

a Department of Nutrition and Food Hygiene , Public Health College, Harbin Medical University , Harbin , China.

出版信息

Xenobiotica. 2018 Nov;48(11):1079-1088. doi: 10.1080/00498254.2017.1397811. Epub 2017 Nov 16.

Abstract
  1. This study evaluated the toxicity of chronic exposure to low-level cadmium (Cd) in rats using ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). Forty male Sprague-Dawley rats were randomly assigned to four groups, namely, the control group, low-dose group (0.13 mg/kg·bw), middle-dose group (0.8 mg/kg·bw) and high-dose group (4.89 mg/kg·bw). The rats continuously received CdCl via drinking water for 24 weeks. Serum samples were collected for metabonomics analysis. The data generated from the UPLC-MS was analysed using principal components analysis (PCA) and partial least-squares discriminant analysis (PLS-DA). PLS-DA model with satisfactory explanatory and predictive ability is capable of discriminating the treatment groups from the control group. 2. Finally, the 10 metabolites were identified and showed significant changes in some treatment groups compared with that in the control group (p < 0.0167 or p < 0.003). Exposure to Cd resulted in increased intensities of lysophosphatidic acid (P-16:0e/0:0), glycocholic acid, bicyclo-prostaglandin E2, lithocholyltaurine, sulfolithocholylglycine, lysophosphatidylethanolamine (20:5/0:0) and lysophosphatidylcholine (20:0), as well as decreased intensities of 3-indolepropionic acid, phosphatidylcholine (18:4/18:0) and 15S-hydroxyeicosatrienoic acid in rat serum. 3. Results suggest that exposure to Cd can cause disturbances in the lipid metabolism, amino acid metabolism, nervous system, antioxidant defence system, liver and kidney function.
摘要
  1. 本研究采用超高效液相色谱 - 质谱联用技术(UPLC-MS)评估大鼠长期暴露于低剂量镉(Cd)的毒性。40只雄性Sprague-Dawley大鼠随机分为四组,即对照组、低剂量组(0.13毫克/千克体重)、中剂量组(0.8毫克/千克体重)和高剂量组(4.89毫克/千克体重)。大鼠通过饮用水持续摄入氯化镉24周。收集血清样本进行代谢组学分析。使用主成分分析(PCA)和偏最小二乘判别分析(PLS-DA)对UPLC-MS产生的数据进行分析。具有满意解释和预测能力的PLS-DA模型能够区分治疗组和对照组。2. 最终,鉴定出10种代谢物,与对照组相比,某些治疗组中这些代谢物有显著变化(p < 0.0167或p < 0.003)。镉暴露导致大鼠血清中溶血磷脂酸(P-16:0e/0:0)、甘氨胆酸、双环前列腺素E2、石胆酰牛磺酸、磺基石胆酰甘氨酸、溶血磷脂酰乙醇胺(20:5/0:0)和溶血磷脂酰胆碱(20:0)的强度增加,以及3-吲哚丙酸、磷脂酰胆碱(18:4/18:0)和15S-羟基二十碳三烯酸的强度降低。3. 结果表明,镉暴露可导致脂质代谢、氨基酸代谢、神经系统、抗氧化防御系统、肝脏和肾脏功能紊乱。

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