Abstract

Trimethylstannyl chloride (TMT) exhibits multiorgan toxicity and is widely used as a plastic heat stabilizer. Selenium is an essential trace element for humans, and its deficiency can cause renal tissue damage in both humans and animals. This study reveals a geographic co-occurrence between selenium deficiency and TMT exposure. Transcriptomic analysis indicates that selenium deficiency is closely associated with ribosomal damage, inflammation, and aging processes following TMT exposure. Pathological analysis of broiler kidneys revealed tubular injury and inflammatory cell infiltration. Downregulation of AMPK/SIRT3 expression, coupled with ROS production disrupting the antioxidant system, activated ribosomal stress responses. This triggered significant inflammation and accelerated the aging processes. In vitro experiments demonstrated that adding ROS inhibitors (NAC) and SIRT3 activators (2-APQC) significantly downregulated the expression levels of inflammation- and aging-related genes. In summary, −SE and TMT induce renal aging through multiple mechanisms involving the AMPK/SIRT3 signaling pathway and ribosomal stress.