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

Journal article
Authors J. Gu
Y. W. Wang
Y. M. Liu
M. L. Shi
L. D. Yin
Y. Z. Hou
Y. Zhou
C. K. C. Wong
Dongfeng Chen
Z. G. Guo
H. F. Shi
Published in Toxicological Sciences
Volume 170
Issue 1
Pages 109-122
ISSN 1096-6080
Publication year 2019
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 109-122
Language en
Keywords cadmium, immunotoxicity, apoptosis, VMP1, autophagy, oxidative stress, immune-response, cross-talk, death, calcium, homeostasis, disruption, activation, induction, pathways, Toxicology
Subject categories Pharmacology and Toxicology


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 (7days) 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 Ca2+ 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.

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