Issue 7, 2024

Exploration of glutaredoxin-1 oxidative modification in carbon nanomaterial-induced hepatotoxicity

Abstract

Herein, we present toxicological assessments of carbon nanomaterials in HL-7702 cells, and it was found that reactive oxygen species (ROS) levels were elevated. Mass spectrometry results indicated that cysteine sulfhydryl of glutaredoxin-1 (GLRX1) was oxidized to sulfenic acids and sulfonic acids by excessive ROS, which broke the binding of GLRX1 to apoptosis signal-regulating kinase 1, causing the activation of the JNK/p38 signaling pathway and ultimately hepatocyte apoptosis. However, a lower level of ROS upregulated GLRX1 instead of sulfonation modification of its active sites. Highly expressed GLRX1 in turn enabled the removal of intracellular ROS, thereby exerting inconspicuous toxic effects on cells. Taken together, these findings emphasized that CNM-induced hepatotoxicity is attributable to oxidative modifications of GLRX1 arising from redox imbalance.

Graphical abstract: Exploration of glutaredoxin-1 oxidative modification in carbon nanomaterial-induced hepatotoxicity

Supplementary files

Article information

Article type
Communication
Submitted
11 ม.ค. 2567
Accepted
21 ก.พ. 2567
First published
05 มี.ค. 2567

Analyst, 2024,149, 1971-1975

Exploration of glutaredoxin-1 oxidative modification in carbon nanomaterial-induced hepatotoxicity

W. Gao, Y. Wang, W. Cao, G. Li, X. Liu, X. Huang, L. Wang and B. Tang, Analyst, 2024, 149, 1971 DOI: 10.1039/D4AN00051J

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