{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T10:49:17Z","timestamp":1790419757011,"version":"4.1.0"},"reference-count":48,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2022,1,5]],"date-time":"2022-01-05T00:00:00Z","timestamp":1641340800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2022,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Humans and animals may be exposed to increasing contaminant lithium (Li) concentrations in the environment with the use and disposal of Li\u2010containing products. Meanwhile, Li plays a key role in the treatment of human mental disorders, while the excessive accumulation of Li salts in the body can cause renal damage and nephrotic syndrome. In this study, the mechanism of renal inflammatory reaction induced by Li excessive intake was studied by establishing mice models in vitro and in vivo. The results of histopathology staining and TdT\u2010mediated dUTP nick\u2010end labeling assay showed that high Li condition (Lithium carbonate, 20\u2009mg\/kg\/twice a day, i.e., for 30 consecutive days) caused inflammatory damage and apoptosis in kidney tissue cells. Western blot, qPCR, and immunohistochemical analysis were used to further study. In the vivo experiments, we found that Li reduced antioxidant enzyme capacity (glutathione peroxidase, total superoxide dismutase, total antioxidant capacity, and catalase) and induced the production of reactive oxygen species (ROS). Moreover, excessive Li activated nuclear factor kappa\u2010B (NF\u2010\u03baB) signaling pathway and nucleotide\u2010binding oligomerization domain\u2010like receptors domains\u2013containing protein 3 (NLRP3) inflammasome, resulting in activation of inflammatory factors tumor necrosis factor\u2010\u03b1 and IL\u20101\u03b2 in the kidney of mice. In the vitro study, ROS as an upstream signal phosphorylated I\u03baB\u03b1 and NF\u2010\u03baB, up\u2010regulated the NLRP3 inflammasome, increased caspase3, 6, 7, and 9 to exaggerate inflammation response, finally inducing pyroptosis in renal cells.<\/jats:p>","DOI":"10.1002\/tox.23446","type":"journal-article","created":{"date-parts":[[2022,1,5]],"date-time":"2022-01-05T04:45:45Z","timestamp":1641357945000},"page":"825-835","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":48,"title":["Lithium intoxication induced pyroptosis via\n                    <scp>ROS<\/scp>\n                    \/\n                    <scp>NF\u2010\u03baB<\/scp>\n                    \/\n                    <scp>NLRP3<\/scp>\n                    inflammasome regulatory networks in kidney of mice"],"prefix":"10.1002","volume":"37","author":[{"given":"Hongyuan","family":"Jing","sequence":"first","affiliation":[{"name":"College of Veterinary Medicine 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