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活性氧参与蓖麻毒素诱导的大鼠甲状腺毒性作用。

Reactive oxygen species involvement in ricin-induced thyroid toxicity in rat.

作者信息

Sadani G R, Soman C S, Deodhar K K, Nadkarni G D

机构信息

Radiation Medicine Centre, Bhabha Atomic Research Centre, Tata Memorial Centre Annexe, Parel, Bombay, India.

出版信息

Hum Exp Toxicol. 1997 May;16(5):254-6. doi: 10.1177/096032719701600503.

DOI:10.1177/096032719701600503
PMID:9192203
Abstract

Ricin is known to have diverse effects on the cells of different organs like liver, kidney, pancreas, intestines and parathyroid. Acute decrease in serum thyroid hormone level 24 h after ricin administration (1.5 micrograms/100 g) led us to suspect the toxic action of ricin on the thyroid. We monitored the lipid peroxidation (LP) and anti-oxidant status of the thyroid tissue to determine the role, if any, played by reactive oxygen species (ROS) in this pathology. An increase of 39% in LP and 47% in superoxide dismutase, along with a 8.5% decrease in catalase points to the imbalance in the antioxidant defence involving hydrogen peroxide and its univalent reduction product, the hydroxyl radical. Thyroid histopathology shows destruction of thyroid follicles and necrosis, which may be due to ROS and may partly explain the 50% reduction in circulating thyroid hormones seen after ricin administration.

摘要

已知蓖麻毒素对肝脏、肾脏、胰腺、肠道和甲状旁腺等不同器官的细胞有多种影响。给予蓖麻毒素(1.5微克/100克)24小时后,血清甲状腺激素水平急剧下降,这使我们怀疑蓖麻毒素对甲状腺的毒性作用。我们监测了甲状腺组织的脂质过氧化(LP)和抗氧化状态,以确定活性氧(ROS)在这种病理过程中是否起作用。LP增加39%,超氧化物歧化酶增加47%,同时过氧化氢酶减少8.5%,这表明涉及过氧化氢及其单价还原产物羟基自由基的抗氧化防御失衡。甲状腺组织病理学显示甲状腺滤泡破坏和坏死,这可能是由ROS引起的,并且可以部分解释蓖麻毒素给药后循环甲状腺激素减少50%的现象。

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