التفاصيل البيبلوغرافية
| العنوان: |
Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation. |
| المؤلفون: |
Liu, Yue, Ma, Wenxue, Liu, Qiaohan, Liu, Pinnan, Qiao, Senqiu, Xu, Lihua, Sun, Yue, Gai, Xiaoxue, Zhang, Ziwei |
| المصدر: |
Environmental Toxicology; Feb2023, Vol. 38 Issue 2, p436-450, 15p |
| مصطلحات موضوعية: |
THIOREDOXIN, BCL-2 proteins, CYTOCHROME c, HEART failure, SUPEROXIDE dismutase |
| مستخلص: |
Thioredoxin reductase 3 (Txnrd3) plays a crucial role in antioxidant and anti‐cancer activities, and sperm maturation. The damage of heavy metals, including Nickel (Ni), is the most prominent harm in social development, and hampering Txnrd3 might exacerbate Ni‐induced cardiac damage. In this study, a total of 160 8‐week‐old C57BL/N male mice with 25–30 g weight of Txnrd3+/+ wild‐type and Txnrd3−/− homozygote‐type were randomly divided into eight groups. The mice in the control and Ni groups were gavaged with distilled water and a freshly prepared 10 mg/kg NiCl2 solution. Melatonin (Mel) groups were administered at a concentration of 2 mg/kg for 21 days at the mice's 0.1 ml/10 g body weight. Ni exposure up‐regulated the messenger RNA (mRNA) levels of mitochondrial apoptosis (caspase‐3, caspase‐9, cytochrome c, p53, and BAX), autophagy (LC3, ATG 1, ATG 7, and Beclin‐1), and inflammation (TNF‐α, COX 2, IL‐1β, IL‐2, IL‐6, and IL‐7)‐related markers, but down‐regulated the mRNA levels of BCL‐2, p62 and mTOR (p <.05). Ni exposure decreased the expression of BCL‐2 and p62 protein but increased the expression levels of caspase‐3, caspase‐9, cytochrome c, p53, BAX, ATG 7, Beclin‐1, TNF‐α, COX 2, IL‐1β and IL‐2 protein (p <.05). Ni increased the contents of glutathione disulfide (GSSG) and malondialdehyde (MDA) and decreased the activities of catalase (CAT) and total superoxide dismutase (T‐SOD) (p <.05). Decreased Txnrd3 expression significantly exacerbated changes compared to the Ni exposure (p <.05). Mel significantly attenuated these changes, but the effect decreased when Txnrd3 was inhibited (p <.05). In conclusion, decreased Txnrd3 expression promoted Ni‐induced mitochondrial apoptosis and inflammation via oxidative stress and aggravated heart damage in mice. Decreased Txnrd3 expression significantly reduced the protective effect of Mel to Ni exposure. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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