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Aflatoxin B₁ and ethanol co-exposure induces hepatic oxidative damage in mice.黄曲霉毒素B₁与乙醇共同暴露诱导小鼠肝脏氧化损伤。
Toxicol Ind Health. 2010 Nov;26(10):717-24. doi: 10.1177/0748233710377772. Epub 2010 Sep 13.
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Evaluation of status of cadmium, lead, and nickel levels in biological samples of normal and night blindness children of age groups 3-7 and 8-12 years.评价 3-7 岁和 8-12 岁正常儿童和夜盲儿童生物样本中镉、铅和镍水平的状况。
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Role of selenium on calcium signaling and oxidative stress-induced molecular pathways in epilepsy.硒在癫痫钙信号和氧化应激诱导的分子途径中的作用。
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Nickel, its adverse health effects & oxidative stress.镍及其对健康的不良影响与氧化应激
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Biochemistry of oxidative stress.氧化应激的生物化学
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Effect of nickel exposure on peripheral tissues: role of oxidative stress in toxicity and possible protection by ascorbic acid.镍暴露对周围组织的影响:氧化应激在毒性中的作用以及抗坏血酸可能的保护作用。
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Early cytotoxic effects of ochratoxin A in rat liver: a morphological, biochemical and molecular study.赭曲霉毒素A对大鼠肝脏的早期细胞毒性作用:一项形态学、生物化学和分子学研究。
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Intestinal glutathione: determinant of mucosal peroxide transport, metabolism, and oxidative susceptibility.肠道谷胱甘肽:黏膜过氧化物转运、代谢及氧化易感性的决定因素。
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日粮氯化镍诱导肉鸡氧化肠道损伤。

Dietary nickel chloride induces oxidative intestinal damage in broilers.

机构信息

Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an, China.

出版信息

Int J Environ Res Public Health. 2013 May 23;10(6):2109-19. doi: 10.3390/ijerph10062109.

DOI:10.3390/ijerph10062109
PMID:23702803
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3717726/
Abstract

The purpose of this study was to investigate the oxidative damage induced by dietary nickel chloride (NiCl2) in the intestinal mucosa of different parts of the intestine of broilers, including duodenum, jejunum and ileum. A total of 240 one-day-old broilers were divided into four groups and fed on a corn-soybean basal diet as control diet or the same basal diet supplemented with 300, 600 or 900 mg/kg NiCl2 during a 42-day experimental period. The results showed that the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) content were significantly (p < 0.05 or p < 0.01) decreased in the 300, 600 and 900 mg/kg groups in comparison with those of the control group. In contrast, malondialdehyde (MDA) content was significantly (p < 0.05 or p < 0.01) higher in the 300, 600 and 900 mg/kg groups than that in the control group. It was concluded that dietary NiCl2 in excess of 300 mg/kg could cause oxidative damage in the intestinal mucosa in broilers, which finally impaired the intestinal functions including absorptive function and mucosal immune function. The oxidative damage might be a main mechanism on the effects of NiCl2 on the intestinal health of broilers.

摘要

本研究旨在探讨日粮氯化镍(NiCl2)对肉鸡不同肠段(十二指肠、空肠和回肠)肠黏膜氧化损伤的影响。将 240 只 1 日龄肉鸡随机分为 4 组,分别饲喂基础玉米-豆粕日粮(对照组)或添加 300、600 或 900 mg/kg NiCl2 的基础日粮,试验期为 42 天。结果表明,与对照组相比,300、600 和 900 mg/kg 组肉鸡超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)活性以及羟自由基清除能力和谷胱甘肽(GSH)含量显著(p < 0.05 或 p < 0.01)降低,而丙二醛(MDA)含量显著(p < 0.05 或 p < 0.01)升高。综上可知,日粮中 NiCl2 含量超过 300 mg/kg 可导致肉鸡肠黏膜氧化损伤,进而损害肉鸡的肠道功能,包括吸收功能和黏膜免疫功能。氧化损伤可能是 NiCl2 影响肉鸡肠道健康的主要机制之一。