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镉暴露对河南华溪蟹鳃氧化状态和细胞死亡的影响。

The effects of cadmium exposure on the oxidative state and cell death in the gill of freshwater crab Sinopotamon henanense.

机构信息

School of Life Science, Shanxi University, Taiyuan, PR China.

出版信息

PLoS One. 2013 May 30;8(5):e64020. doi: 10.1371/journal.pone.0064020. Print 2013.

DOI:10.1371/journal.pone.0064020
PMID:23737962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3667791/
Abstract

We studied here the short-term toxicity effects of Cd on the oxidative state and cell death in the gill of freshwater crab Sinopotamon henanense. Crabs were exposed to Cd that resulted in Cd accumulation and a significant increase in the metallothionein (MT) level in the gill, but MT level increased disproportionally compared to the Cd accumulation with an extension of exposure time. Significant changes in the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were observed. An increase in the levels of reactive oxygen species (ROS) and lipid peroxidation (LPO) was detected that will cause oxidative stress. Histological abnormalities of the gills were discovered, including the expansion of gill cavity, a decrease in the numbers of connection of the upper and the lower of the gill lamellae and epithelial cells, and an increase in the number of hemocytes. The results of a TUNEL test and transmission electron microscope (TEM) showed that more gill cells had apoptotic characteristics after 48 h of Cd treatment compared to the control, but epithelial cell necrosis and inflammatory response appeared only after 72 h. It was concluded that (1) Cd induced the ROS production and accumulation through inhibiting antioxidant enzyme activities and exceeding the saturation values of MT binging; (2) Cd led to lipid peroxidation and histopathological alternations; and (3) Cd induced apoptotic response at short time exposure, followed by necrotic features and inflammatory reaction after longer time exposure.

摘要

我们研究了 Cd 对淡水蟹 Sinopotamon henanense 鳃中氧化状态和细胞死亡的短期毒性效应。螃蟹暴露在 Cd 中,导致 Cd 积累和鳃中金属硫蛋白 (MT) 水平显著增加,但随着暴露时间的延长,MT 水平的增加与 Cd 积累不成比例。超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 和谷胱甘肽过氧化物酶 (GPx) 的活性发生了显著变化。检测到活性氧 (ROS) 和脂质过氧化 (LPO) 水平的增加,这将导致氧化应激。发现鳃的组织学异常,包括鳃腔扩张、上下鳃片连接的数量减少和上皮细胞、以及血球数量增加。TUNEL 试验和透射电子显微镜 (TEM) 的结果表明,与对照组相比,Cd 处理 48 小时后,更多的鳃细胞具有凋亡特征,但只有在 72 小时后才出现上皮细胞坏死和炎症反应。结论是:(1)Cd 通过抑制抗氧化酶活性和超过 MT 结合的饱和值,导致 ROS 的产生和积累;(2)Cd 导致脂质过氧化和组织病理学改变;(3)Cd 在短时间暴露时引起凋亡反应,长时间暴露后则出现坏死特征和炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/dd3c3d015ca2/pone.0064020.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/f42fe421d946/pone.0064020.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/004e31578453/pone.0064020.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/e84aff7e9af9/pone.0064020.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/fd714a7dbf7a/pone.0064020.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/0f8b502246e8/pone.0064020.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/dd3c3d015ca2/pone.0064020.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/f42fe421d946/pone.0064020.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/004e31578453/pone.0064020.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/e84aff7e9af9/pone.0064020.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/fd714a7dbf7a/pone.0064020.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/0f8b502246e8/pone.0064020.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ae5/3667791/dd3c3d015ca2/pone.0064020.g006.jpg

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