Abstract
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.
Highlights
Vanadium (V) is an ultra-trace element that can affect the activities of intracellular enzymes and acts a crucial role in metabolism and normal cell function and development [1]
The ultrastructural observation of the myocardial cells showed that the structure of organelles and nucleus were clear in the control group, and mitochondrial swelling and vacuolization were observed under ultrastructure in the V group on 44 days (Figure 1A)
Previous studies have shown that V induced the impairment of mitochondrial electron transport by interacting with cysteine thiol, which in turn led to oxidative stress and mitochondrial dysfunction [32, 33]
Summary
Vanadium (V) is an ultra-trace element that can affect the activities of intracellular enzymes and acts a crucial role in metabolism and normal cell function and development [1]. Mitochondria are highly dynamic double-membraned organelles, especially abundant in cardiac tissue, which takes part in numerous cellular processes, such as ATP production, bioenergetics, metabolism, redox balance, and cell death [8]. They can produce ROS via transferring electrons in the mitochondrial respiratory chain to the oxygen atoms [9]. Most of the studies suggested that V induced the generation of excess ROS and impaired antioxidant defense systems, eventually causing oxidative stress and mitochondrial dysfunction [12, 13]. The maintenance of mitochondrial function depends on the normal operation of the mitochondrial quality control (MQC) system
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