Inhibition of Autophagy Alleviates Cadmium-Induced Mouse Spleen and Human B Cells Apoptosis

Jie Gu, Yanwei Wang, Yanmin Liu, Meilin Shi, Liangdong Yin, Yongzhong Hou, Yang Zhou, Chris K C WONG, Dongfeng Chen, Zhigang Guo, Haifeng Shi*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

30 Citations (Scopus)


Cadmium (Cd) is a toxic heavy metal that can accumulate and cause severe damage to many organs, such as liver, kidney, lung, etc. Cd also significantly suppresses immunity, however, the underlying mechanism involved in Cd-induced immunnotoxicity is still unclear. The present study indicated that semichronic Cd exposure (7 days) induced apoptotic damage of mouse spleen. In human Ramos B cells, Cd exposure also induced apoptosis, which was dependent on Cd-induced vacuole membrane protein 1 (VMP1) expression and autophagy. Cd-induced autophagy and apoptosis were abated when VMP1 expression was knockdown. In addition, Cd-induced VMP1 expression, autophagy, and apoptosis were dependent on the elevation of Ca 2+ and reactive oxygen species (ROS). More important, Cd exposure also induced VMP1 expression and autophagy in mouse spleen tissue, and the intraperitoneal injection of the autophagy inhibitor chloroquine (CQ) into mice effectively reduced Cd-induced spleen apoptotic damage. Taken together, these results indicate Cd-induced autophagy, promotes apoptosis in immune cells, and inhibition of autophagy can alleviate Cd-induced spleen and immune cell apoptosis. This study might provide the groundwork for future studies on Cd-induced immunomodulatory effects and immune diseases.

Original languageEnglish
Pages (from-to)109-122
Number of pages14
JournalToxicological Sciences
Issue number1
Publication statusPublished - 1 Jul 2019

Scopus Subject Areas

  • Toxicology

User-Defined Keywords

  • Apoptosis
  • Autophagy
  • Cadmium
  • Immunotoxicity
  • VMP1


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