Mechanism of Cadmium Exposure Induced Hepatotoxicity in the Mud Crab (Scylla paramamosain): Activation of Oxidative Stress and Nrf2 Signaling Pathway.
Mechanism of Cadmium Exposure Induced Hepatotoxicity in the Mud Crab (Scylla paramamosain): Activation of Oxidative Stress and Nrf2 Signaling Pathway.
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DOI：
10.3390/antiox11050978
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发表时间：
2022-05-17
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影响因子：
--
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镉是毒性最强的重金属之一，会对水生动物造成严重的氧化损伤。然而，泥蟹对镉暴露的反应机制仍不清楚。本研究调查了镉暴露对氧化应激和组织病理学变化的影响，并评估了 Nrf2 信号通路在调节泥蟹对镉诱导的肝毒性反应中的作用。青蟹暴露于0、0.01、0.05和0.125 mg/L镉中21 d。目前的结果表明，镉暴露增加了过氧化氢（H2O2）的产生、脂质过氧化和组织损伤，但降低了超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性，并引起脂质过氧化和组织损伤。综合生物标志物指数分析结果表明，镉的毒性与镉浓度呈正相关。镉暴露后，Nrf2 信号通路（Nrf2、金属硫蛋白和细胞色素 P450 酶）的表达水平上调。体内沉默 Nrf2 会降低抗氧化基因（SOD、CAT 和谷胱甘肽 S-转移酶）的表达，表明 Nrf2 可以调节抗氧化基因。镉暴露后，体内敲除 Nrf2 也会显着降低 SOD 和 CAT 的活性。此外，体内 Nrf2 的沉默会增加 H2O2 的产生，并降低镉暴露后青蟹的死亡率。本研究表明，镉暴露通过增加H2O2含量而引起青蟹肝毒性，从而降低抗氧化能力，导致细胞损伤。此外，在镉诱导青蟹肝毒性过程中，Nrf2被激活并与抗氧化反应元件结合，启动抗氧化酶基因的表达。
Cadmium, one of the most toxic heavy metals, can cause severe oxidative damage to aquatic animals. However, the mechanism whereby the mud crabs respond to cadmium exposure remains unclear. This study investigated the effects of cadmium exposure on oxidative stress and histopathology changes and evaluated the role of the Nrf2 signaling pathway in regulating responses to cadmium-induced hepatotoxicity were investigated in mud crabs. Mud crabs were exposed to 0, 0.01, 0.05, and 0.125 mg/L cadmium for 21 d. The present results indicated that cadmium exposure increased hydrogen peroxide (H2O2) production, lipid peroxidation and tissue damage, but decreased the activity of superoxide dismutase (SOD) and catalase (CAT), and caused lipid peroxidation and tissue damage. The results of an integrated biomarker index analysis suggested that the toxicity of cadmium was positively related to cadmium concentration. The expression levels of the Nrf2 signaling pathway (Nrf2, metallothionein, and cytochrome P450 enzymes) were up-regulated after cadmium exposure. Silencing of Nrf2 in vivo decreased antioxidant gene (SOD, CAT, and glutathione S-transferase) expression, suggesting that Nrf2 can regulate antioxidant genes. Knocking down Nrf2 in vivo also significantly decreased the activity of SOD and CAT after cadmium exposure. Moreover, silencing of Nrf2 in vivo enhanced H2O2 production and the mortality rates of mud crabs after cadmium exposure. The present study indicated that cadmium exposure induced hepatotoxicity in the mud crab by increasing H2O2 content, which decreased the antioxidant capacity, leading to cell injury. In addition, the Nrf2 is activated to bound with antioxidant response element, initiating the expression of antioxidant enzyme genes during cadmium induced hepatotoxicity in the mud crabs.
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