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酒石黄酸诱导大鼠脑区神经生化改变。

Tartrazine induced neurobiochemical alterations in rat brain sub-regions.

机构信息

Environmental Toxicology Laboratory, Department of Zoology, University of Rajasthan, Jaipur 302004, India.

Environmental Toxicology Laboratory, Department of Zoology, University of Rajasthan, Jaipur 302004, India.

出版信息

Food Chem Toxicol. 2018 Mar;113:322-327. doi: 10.1016/j.fct.2018.02.011. Epub 2018 Feb 7.

Abstract

Tartrazine is a synthetic lemon yellow azo dye primarily used as a food coloring. The present study aimed to screen the neurobiochemical effects of Tartrazine in Wistar rats after administering the Acceptable Daily Intake (ADI) level. Tartrazine (7.5 mg/kg b.w.) was administered to 21 day old weanling rats through oral gavage once daily for 40 consecutive days. On 41st day, the animals were sacrificed and brain sub regions namely, frontal cortex, corpus striatum, hippocampus and cerebellum were used to determine activities of anti-oxidant enzymes viz. Superoxide Dismutase (SOD), Catalase (CAT), Glutathione-Stransferase (GST), Glutathione Reductase (GR) and Glutathione Peroxidase (GPx) and levels of lipid peroxides using Thio-barbituric Acid Reactive Substance (TBARS) assay. Our investigation showed a significant decrease in SOD and CAT activity, whereas there occurred a decline in GST and GR activity with an increase in GPx activity to counteract the oxidative damage caused by significantly increased levels of lipid peroxides. The possible mechanism of this oxidative damage might be attributed to the production of sulphanilc acid as a metabolite in azofission of tartrazine. It may be concluded that the ADI levels of food azo dyes adversely affect and alter biochemical markers of brain tissue and cause oxidative damage.

摘要

食用黄色 5 号(柠檬黄)是一种人工合成的偶氮染料,主要用作食品着色剂。本研究旨在检测柠檬黄在 Wistar 大鼠亚慢性经口染毒(每日允许摄入量 ADI 水平)的神经生化毒性。21 天大的断奶 Wistar 大鼠经口灌胃给予柠檬黄(7.5mg/kg bw),每天 1 次,连续 40 天。第 41 天处死动物,取大脑皮质、纹状体、海马和小脑等脑区,测定超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽-S-转移酶(GST)、谷胱甘肽还原酶(GR)和谷胱甘肽过氧化物酶(GPx)活性以及丙二醛(TBARS)含量。结果表明,柠檬黄染毒可导致 SOD 和 CAT 活性显著降低,GST 和 GR 活性下降,而 GPx 活性升高,以对抗脂质过氧化水平的显著升高引起的氧化损伤。这种氧化损伤的可能机制可能归因于偶氮键断裂生成的磺胺酸作为代谢物的产生。综上,ADI 水平的食用偶氮染料可能会对脑组织的生化标志物产生不利影响,导致氧化损伤。

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