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Background <p>The unique properties of carbon blacks (CBs) make them feasible for new applications and raise concerns about embryonic toxicity, whereas little is known about the underlying mechanism.</p> Objective <p>Here, we used human embryonic stem cells (hESCs) to evaluate human embryonic toxicity induced by CBs. We assessed cytotoxicity and reactive oxygen species (ROS) production in CBs-treated hESCs.</p> Results <p>Results showed that CBs significantly induced cytotoxicity and ROS levels. We also detected mitochondrial membrane potential (MMP) by immunofluorescence of CBs-treated hESCs, and found that CBs treatment induced mitochondrial damage. Moreover, CBs could raise the protein expression levels of caspase-3 and caspase-9. Co-treated with N-acetylcysteine (NAC) could scavenge ROS and attenuate the expressions of apoptosis related proteins.</p> Conclusion <p>These findings suggested that CBs induced hESCs apoptosis through the ROS/mitochondrial pathway, and pharmacological inhibition of ROS might have therapeutic potential in preventing CBs-associated embryonic toxicity.</p>

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Carbon blacks induce human embryonic stem cells apoptosis through reactive oxygen species/mitochondrial pathway

  • 期刊论文

  • 发表日期：

    2025年1月31日

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  • He Jiang,
  • Qianqian Zhao,
  • Junyan Yan

摘要

Background

The unique properties of carbon blacks (CBs) make them feasible for new applications and raise concerns about embryonic toxicity, whereas little is known about the underlying mechanism.

Objective

Here, we used human embryonic stem cells (hESCs) to evaluate human embryonic toxicity induced by CBs. We assessed cytotoxicity and reactive oxygen species (ROS) production in CBs-treated hESCs.

Results

Results showed that CBs significantly induced cytotoxicity and ROS levels. We also detected mitochondrial membrane potential (MMP) by immunofluorescence of CBs-treated hESCs, and found that CBs treatment induced mitochondrial damage. Moreover, CBs could raise the protein expression levels of caspase-3 and caspase-9. Co-treated with N-acetylcysteine (NAC) could scavenge ROS and attenuate the expressions of apoptosis related proteins.

Conclusion

These findings suggested that CBs induced hESCs apoptosis through the ROS/mitochondrial pathway, and pharmacological inhibition of ROS might have therapeutic potential in preventing CBs-associated embryonic toxicity.