Application of Se-Met to CdTe QDs significantly reduces toxicity by modulating redox balance and inhibiting apoptosis

• Published in: Ecotoxicology and environmental safety Vol. 267; p. 115614
• Main Authors: Ni, Xinyu, Lu, Yudie, Li, Meiyu, Liu, Yue, Zhang, Miao, Sun, Fuqiang, Dong, Sijun, Zhao, Lining
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 15-11-2023; Elsevier
• Subjects: Antioxidant defense system; Apoptosis; CdTe QDs; Protein expression; Redox balance; Selenomethionine; Toxicity inhibition; CdTe QDs; Redox balance; Protein expression; Toxicity inhibition; Selenomethionine; Antioxidant defense system; Apoptosis
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2023.115614

Cadmium tellurium quantum dots (CdTe QDs) as one of the most widely used QDs have been reported the toxicity and biosafety in recent years, little work has been done to reduce their toxicity however. Based on the mechanisms of toxicity of CdTe QDs on liver target organs such as oxidative stress and apoptosis previously reported by other researchers, we investigated the mechanism of action of trace element selenium (Se) to mitigate the hepatotoxicity of CdTe QDs. The experimental results showed that Se-Met at 40–140 μg L−1 could enhance the function of intracellular antioxidant defense system and the molecular structure of related antioxidant enzymes by reduce the production of ROS by 45%, protecting the activity of antioxidants and up-regulating the expression of selenoproteins with antioxidant functions, Gpx1 increase 225% and Gpx4 upregulated 47%. In addition, Se-Met could alleviate CdTe QDs-induced apoptosis by regulating two apoptosis-inducing factors, as intracellular caspase 3/9 expression levels were reduced by 70% and 87%, decreased Ca2+ concentration, and increased mitochondrial membrane potential measurements. Overall, this study indicates that Se-Met has a significant protective effect on the hepatotoxicity of CdTe QDs. Se-Met can be applied to the preparation of CdTe QDs to inhibit its toxicity and break the application limitation.
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●Combining cellular and molecular levels to study the role and regulation mechanism of Se-Met in adverse effects induced by CdTe QDs.●Se-Met maintains redox balance and mitochondrial function by protecting the structural changes of SOD/CAT and enhancing the antioxidant function of selenoproteins, reduces the level of apoptosis induced by CdTe QDs, and attenuates the toxicity of CdTe QDs on hepatocytes.