Chromium Affects Mitochondrial Function, Leading to Apoptosis and Autophagy in Turtle Primary Hepatocytes.

in Animals : an open access journal from MDPI by Shuqin Lin, Yunjuan Xiao, Jing Lin, Yue Yuan, Haitao Shi, Meiling Hong, Li Ding

TLDR

  • This study looked at how hexavalent chromium (Cr(VI)) affects the primary hepatocytes of Reeves' turtles. They found that Cr(VI) caused oxidative stress and disrupted mitochondrial function, which led to cell apoptosis and autophagy. This highlights the serious health risks posed by Cr(VI) pollution and emphasizes the need to protect wild turtle populations.

Abstract

Hexavalent chromium (Cr(VI)), a pervasive industrial contaminant, is highly toxic to both humans and animals. However, its effects on turtles are largely unexplored. Our study aimed to investigate the toxic effects of Cr(VI) on the Reeves' turtles () primary hepatocytes. We exposed hepatocytes to two concentrations (25 μM and 50 μM) of Cr(VI) for 24 h. The results showed that compared to controls, Cr(VI)-treated cells showed elevated antioxidant enzyme activity (catalase (CAT) and superoxide dismutase (SOD)) and increased reactive oxygen species (ROS) levels. Adenosine triphosphatae (ATP) levels decreased, indicating mitochondrial dysfunction. Additionally, we found significant changes in mitochondrial dynamics related genes, with downregulation of mitofusin 2 (Mfn2) and silent information regulator 1 (SIRT1) and a decrease in sirtuin 3 (SIRT3) and tumor protein 53 (p53) mRNA levels. Annexin V-FITC fluorescence staining-positive cells increased with higher Cr(VI) concentrations, marked by elevated bcl-2-associated X protein (Bax) and cysteinyl aspartate specific proteinase (Caspase3) mRNA levels and reduced B-cell lymphoma-2 (Bcl2) expression. Autophagy-related genes were also affected, with increased microtubule-associated protein 1 light chain 3 (LC3-I), microtubule-associated protein light chain 3II (LC3-II), unc-51-like autophagy-activating kinase 1 (ULK1), and sequestosome 1 (p62/SQSTM1) mRNA levels and decreased mammalian target of rapamycin (mTOR) and Beclin1 expression. Taken together, Cr(VI) promotes cell apoptosis and autophagy in turtle hepatocytes by inducing oxidative stress and disrupting mitochondrial function. These findings highlight the serious health risks posed by Cr(VI) pollution and emphasize the need for protecting wild turtle populations.

Overview

  • The study investigates the toxic effects of hexavalent chromium (Cr(VI)) on Reeves' turtle primary hepatocytes
  • Two concentrations of Cr(VI) (25 μM and 50 μM) were used for 24-hour exposure
  • The study aims to answer the question: How does Cr(VI) affect the Reeves' turtle primary hepatocytes?

Comparative Analysis & Findings

  • Cr(VI)-treated cells showed elevated antioxidant enzyme activity (CAT and SOD) and increased ROS levels
  • ATP levels decreased, indicating mitochondrial dysfunction
  • Significant changes in mitochondrial dynamics related genes, with downregulation of Mfn2, Sirt1, Sirt3, and p53 mRNA levels
  • Annexin V-FITC fluorescence staining-positive cells increased with higher Cr(VI) concentrations, marked by elevated Bax and Caspase3 mRNA levels and reduced Bcl2 expression
  • Autophagy-related genes were also affected, with increased LC3-I, LC3-II, ULK1, and p62/SQSTM1 mRNA levels and decreased mTOR and Beclin1 expression

Implications and Future Directions

  • Cr(VI) promotes cell apoptosis and autophagy in turtle hepatocytes by inducing oxidative stress and disrupting mitochondrial function
  • The study highlights the serious health risks posed by Cr(VI) pollution and emphasizes the need for protecting wild turtle populations
  • Future research should focus on developing effective strategies to mitigate the toxic effects of Cr(VI) on turtles and other aquatic organisms
Read Full Article