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慢性镉暴露对大鼠体内铜和锌的组织分布及氧化应激参数的影响。

Influence of chronic cadmium exposure on the tissue distribution of copper and zinc and oxidative stress parameters in rats.

作者信息

Erdem Onur, Yazihan Nuray, Kocak Mehtap Kacar, Sayal Ahmet, Akcil Ethem

机构信息

Department of Toxicology, Gulhane Military Medical Academy, Ankara, Turkey

Department of Pathophysiology, Faculty of Medicine, Ankara University, Ankara, Turkey.

出版信息

Toxicol Ind Health. 2016 Aug;32(8):1505-1514. doi: 10.1177/0748233714566875. Epub 2015 Jan 29.

Abstract

The aim of this study was to investigate the effect of oral cadmium (Cd) intoxication on the antioxidant response and its relationship with essential bioelements like copper (Cu) and zinc (Zn). The experimental group was chronically exposed to Cd daily for 8 weeks via consumption of water containing 15 ppm cadmium chloride. Cu, Zn, and Cd concentrations and oxidative stress parameters were analyzed in liver, kidney, and heart tissues. Exposure to Cd led to a significant decrease in the activities of superoxide dismutase in all considered samples while a significant increase in the activity of glutathione peroxidase except for the kidney. We found a significant increase in malondialdehyde concentration in the tissues except for heart. Also oral administration of Cd caused a significant reduction of Zn and Cu in the tissues. Our results allow us to hypothesize that higher Cd concentration in the tissues causes oxidative stress by increasing malondialdehyde as a means of altering antioxidant defense system and deterioration of bioelements in rat liver, kidney, and heart. In addition, further studies are needed to explain the effect of long-term, low-dose exposure to Cd on distribution of bioelements and its relationship with oxidative stress.

摘要

本研究的目的是调查口服镉(Cd)中毒对抗氧化反应的影响及其与铜(Cu)和锌(Zn)等必需生物元素的关系。实验组通过饮用含15 ppm氯化镉的水,连续8周每日慢性接触镉。分析了肝脏、肾脏和心脏组织中的铜、锌和镉浓度以及氧化应激参数。接触镉导致所有受试样本中超氧化物歧化酶活性显著降低,而除肾脏外谷胱甘肽过氧化物酶活性显著增加。我们发现除心脏外,各组织中丙二醛浓度显著增加。此外,口服镉还导致组织中锌和铜显著减少。我们的结果使我们能够假设,组织中较高的镉浓度通过增加丙二醛来引起氧化应激,从而改变大鼠肝脏、肾脏和心脏中的抗氧化防御系统并导致生物元素恶化。此外,需要进一步研究来解释长期低剂量接触镉对生物元素分布的影响及其与氧化应激的关系。

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