Gong Pin, Chen Fu-xin, Wang Lan, Wang Jing, Jin Sai, Ma Yang-min
College of Life Science and Technology, College of Chemistry and Chemical Engineering, Shaanxi University of Science and Technology, Xi'an 710021, China.
School of Chemistry and Chemical Engineering, Xi'an University of Science and Technology, Xi'an 710054, China.
Environ Toxicol Pharmacol. 2014 May;37(3):1015-27. doi: 10.1016/j.etap.2014.03.017. Epub 2014 Mar 30.
The oxidative status and morphological changes of mouse liver exposed to cadmium chloride (Cd(II)) and therapeutic potential of blueberry (Vaccinium corymbosum L.) extract against Cd(II)-induced hepatic injury were investigated. A variety of parameters were evaluated, including lipid peroxidation (LPO), protein carbonyl (PCO) level, DNA fragment, as well as antioxidative defense system (i.e., superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH)). Elemental analysis and evaluation of morphological changes and NO levels were also performed. Exposure to Cd(II) led to increased LPO and PCO as well as DNA fragment and a reduction of SOD and CAT activities, however, the content of GSH elevated probably due to biological adaptive-response. In contrast, co-treatment of anthocyanin (Ay) inhibited the increased oxidative parameters as well as restored the activities of antioxidative defense system in a dose-dependent manner. Ay administration regained these morphological changes caused by intoxication of Cd(II) to nearly normal levels. Moreover, the accumulation of Cd(II) in liver may be one of the reasons for Cd(II) toxicity and Ay can chelate with Cd(II) to reduce Cd(II) burden. The influence of Cd(II) on the Zn and Ca levels can also be adjusted by the co-administration of Ay. Exposure to Cd(II) led to an increase of NO and Ay reduced NO contents probably by directly scavenging. Potential mechanisms for the protective effect of Ay have been proposed, including its anti-oxidative and anti-inflammatory effect along with the metal-chelating capacity. These results suggest that blueberry extract may be valuable as a therapeutic agent in combating Cd(II)-induced tissue injury.
研究了氯化镉（Cd(II)）暴露下小鼠肝脏的氧化状态和形态变化，以及蓝莓（Vaccinium corymbosum L.）提取物对Cd(II)诱导的肝损伤的治疗潜力。评估了多种参数，包括脂质过氧化（LPO）、蛋白质羰基（PCO）水平、DNA片段，以及抗氧化防御系统（即超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、还原型谷胱甘肽（GSH））。还进行了元素分析以及形态变化和一氧化氮（NO）水平的评估。暴露于Cd(II)导致LPO和PCO增加以及DNA片段增加，同时SOD和CAT活性降低，然而，GSH含量可能由于生物适应性反应而升高。相比之下，花青素（Ay）的联合处理以剂量依赖的方式抑制了氧化参数的增加，并恢复了抗氧化防御系统的活性。Ay给药使Cd(II)中毒引起的这些形态变化恢复到几乎正常水平。此外，肝脏中Cd(II)的积累可能是Cd(II)毒性的原因之一，Ay可以与Cd(II)螯合以减轻Cd(II)负担。Ay的联合给药还可以调节Cd(II)对锌和钙水平的影响。暴露于Cd(II)导致NO增加，Ay可能通过直接清除作用降低NO含量。已经提出了Ay具有保护作用的潜在机制，包括其抗氧化和抗炎作用以及金属螯合能力。这些结果表明，蓝莓提取物作为一种治疗剂在对抗Cd(II)诱导的组织损伤方面可能具有价值。
