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Cadmium induced time-dependent kidney injury in common carp via mitochondrial pathway: Impaired mitochondrial energy metabolism and mitochondrion-dependent apoptosis

文献类型： 外文期刊

作者： Cui, Jiawen 1 ; Liu, Yuhao 1 ; Hao, Zhiyu 1 ; Liu, Yuhang 1 ; Qiu, Minna 1 ; Kang, Lu 2 ; Teng, Xiaohua 1 ; Tang, You 3 ;

作者机构： 1.Northeast Agr Univ, Coll Anim Sci & Technol, Harbin 150030, Peoples R China

2.Xinjiang Acad Agr Sci, Inst Agr Qual Stand & Testing Technol, Urumqi 830091, Peoples R China

3.JiLin Agr Sci & Technol Univ, Digital Agr Key Discipline Jilin Prov, Jilin 132101, Peoples R China

关键词： Cadmium; Kidney injury; Mitochondrion; Energy metabolism; Apoptosis; Integrated biomarker response

期刊名称：AQUATIC TOXICOLOGY （ 影响因子：4.5； 五年影响因子：5.2 ）

ISSN： 0166-445X

年卷期： 2023 年 261 卷

页码：

收录情况： SCI

摘要： Toxic effect of heavy metal cadmium (Cd) on fish kidneys had been reported. Mitochondrion is an important organelle for maintaining kidney function, while its role in Cd-induced kidney injury in common carp remained unclarified. In this experiment, we established a poisoning model of common carp with Cd exposure (0.26 mg/L) for 15, 30, and 45 days. Serum biochemistry determination, histological observation, TUNEL assay, qRT-PCR, Western blot, and integrated biomarker response (IBR) were applied to assess the nephrotoxicity of Cd to common carp. Our results displayed that Cd exposure increased the levels of serum biochemical indexes (UREA, CRE, and UA), indicating kidney injury. We further revealed via histological observation that Cd damaged structural integrity of kidneys, as evidenced by renal glomerulus and renal tubular injury, hallmark phenotypes of apoptosis, and mitochondrial damage, suggesting that mitochondria damage and apoptosis were involved in Cd-induced kidney injury. Moreover, Cd exposure decreased ATPase (Na+/K+-ATPase, Ca2+-ATPase, Mg2+ATPase, and Ca2+Mg2+-ATPase) activities as well as PGC-1a and Mfn2 levels, while increased Drp1 and PINK1 levels as well as LC3-II/LC3-I ratio, which indicated that Cd-impaired renal energy metabolism was related to mitochondrial dysfunction. Additionally, we found that Cd induced oxidative stress (abnormal levels of SOD, CAT, GPX, MDA, and H2O2) in kidneys, which was involved in triggering mitochondrial dysfunction and further impairing mitochondrial energy metabolism. Moreover, the occurrence of mitochondria-dependent apoptosis was found after Cd-exposure in common carp kidneys, as indicated by enhanced levels of Bax, CytC, APAF1, Caspase-9, and Caspase-3, while declined level of Bcl-2. Subsequently, we confirmed a time-dependent nephrotoxicity of Cd to common carp via IBR assessment. In conclusion, Cd induced time-dependent nephrotoxicity in common carp via mitochondrial pathway. This mitochondria-oriented study shed light on underlying mechanisms of Cd-induced renal pathologies and provided a theoretical basis for evaluating Cd toxicity to aquatic organisms.

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