Cr(VI) is a heavy metal environmental pollutant and carcinogen. Excessive Cr(VI) exposure injures kidneys. This study aimed to investigate mitophagy induced by mitochondrial function damage in chicken kidney exposed to Cr(VI). To explore the mechanism involved, we randomly divided 40 one-day-old Hy-line Brown cockerels into four groups, with each group exposed to different concentrations of Cr(VI), i.e., 0, 10, 30 and 50 mg kg⁻¹, which were orally administered daily for 45 days. Excessive Cr(VI) increased tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and chemokine (C-X-C motif) ligand 1(CXCL1) expression and decreased Ca²⁺-adenosine triphosphatase (Ca²⁺-ATPase), Mg²⁺-ATPase and Na⁺/k⁺-ATPase activities in chicken kidney. Furthermore, Cr(VI) significantly increased reactive oxygen species (ROS) production and induced mitochondrial membrane potential (MMP) collapse and typical autophagosome formation. With the increase of Cr(VI) concentration, the Parkin translocation, value of LC3-II increased and decreased the content of p62/SQSTM1 and the translocase of outer mitochondrial membrane 20 (TOMM20). In summary, our findings explicated that mitochondrial function damage and mitophagy-related indicators were related to Cr(VI) concentration in chicken kidney.

六价铬是一种重金属环境污染物和致癌物。过量摄入六价铬会伤害肾脏。这项研究旨在调查线粒体功能损伤引起的暴露于六价铬的鸡肾脏中的线粒体。为了探索涉及的机制，我们将40只一天大的Hy-line Brown公鸡随机分为四组，每组暴露于不同浓度的Cr（VI），即0、10、30和50 mg kg ^-1，每天口服45天。Cr（VI）过多会增加肿瘤坏死因子-α（TNF-α），白介素6（IL-6）和趋化因子（CXC基序）配体1（CXCL1）的表达并降低Ca 2 ⁺ -腺苷三磷酸酶（Ca 2 ⁺ - ATPase），Mg ²⁺ -ATPase和Na ⁺ / k ⁺鸡肾脏中的ATPase活性。此外，Cr（VI）大大增加了活性氧（ROS）的产生，并诱导线粒体膜电位（MMP）崩溃和典型的自噬体形成。随着Cr（VI）浓度的增加，Parkin易位，LC3-II的值增加并降低p62 / SQSTM1和线粒体外膜20（TOMM20）的转位酶的含量。总之，我们的研究结果表明，线粒体功能损伤和线粒体相关指标与鸡肾脏中的Cr（VI）浓度有关。