Xiong Zhiwei, Xing Chenghong, Xu Tianfang, Yang Yan, Liu Guohui, Hu Guoliang, Cao Huabin, Zhang Caiying, Guo Xiaoquan, Yang Fan
Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.
Jiangxi Agricultural Technology Extension Center, Nanchang, China.
Front Vet Sci. 2021 Oct 26;8:756534. doi: 10.3389/fvets.2021.756534. eCollection 2021.
Vanadium (V) is an ultra-trace element presenting in humans and animals, but excessive V can cause toxic effects. Mitochondrial quality control (MQC) is an essential process for maintaining mitochondrial functions, but the relationship between V toxicity and MQC is unclear. To investigate the effects of excessive V on oxidative stress and MQC in duck hearts, 72 ducks were randomly divided into two groups, including the control group and the V group (30 mg of V/kg dry matter). The cardiac tissues were collected for the histomorphology observation and oxidative stress status evaluation at 22 and 44 days. In addition, the mRNA and protein levels of MQC-related factors were also analyzed. The results showed that excessive V could trigger vacuolar degeneration, granular degeneration, as well as mitochondrial vacuolization and swelling in myocardial cells. In addition, CAT activity was elevated in two time points, while T-SOD activity was increased in 22 days but decreased in 44 days after V treatment. Meanwhile, excessive V intake could also increase the number of Drp1 puncta, the mRNA levels of mitochondrial fission-related factors (Drp1and MFF), and protein (MFF) level, but decrease the number of Parkin puncta and the mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM), mitochondrial fusion (OPA1, Mfn1, and Mfn2), and mitophagy (Parkin, PINK1, P62, and LC3B) related mRNA levels and protein (PGC-1α, Mfn1, Mfn2, PINK1) levels. Collectively, our results suggested that excessive V could induce oxidative stress and MQC disorder in the heart of ducks.
钒（V）是人和动物体内存在的一种超微量元素，但过量的钒会产生毒性作用。线粒体质量控制（MQC）是维持线粒体功能的一个重要过程，但钒毒性与MQC之间的关系尚不清楚。为了研究过量钒对鸭心脏氧化应激和MQC的影响，将72只鸭随机分为两组，即对照组和钒组（30 mg钒/千克干物质）。在第22天和第44天采集心脏组织进行组织形态学观察和氧化应激状态评估。此外，还分析了MQC相关因子的mRNA和蛋白水平。结果表明，过量的钒可引发心肌细胞空泡变性、颗粒变性以及线粒体空泡化和肿胀。此外，在两个时间点CAT活性均升高，而V处理后22天T-SOD活性升高，44天降低。同时，过量摄入钒还可增加Drp1斑点数量、线粒体分裂相关因子（Drp1和MFF）的mRNA水平以及蛋白（MFF）水平，但会减少Parkin斑点数量以及线粒体生物合成（PGC-1α、NRF-1和TFAM）、线粒体融合（OPA1、Mfn1和Mfn2）和线粒体自噬（Parkin、PINK1、P62和LC3B）相关的mRNA水平和蛋白（PGC-1α、Mfn1、Mfn2、PINK1）水平。总的来说，我们的结果表明过量的钒可诱导鸭心脏氧化应激和MQC紊乱。
