Journal of advanced research · 2026
miR-7480-5p/SIRT3/GSH axis mediates selenium Deficiency-Exacerbated trimethyltin chloride-induced ferroptosis in chicken thymus.
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Gao Hongxin, Gao Meichen, Liu Yanwei, Nie Tong, Wang Jingqiu, Xu Tong, Lin Hongjin
Аннотация
INTRODUCTION: Trimethyltin chloride (TMT) is a widespread environmental contaminant with significant biotoxicity. Selenium is an essential trace element, and its deficiency can exacerbate pollutant toxicity, with ferroptosis and mitochondrial stress as key events.
OBJECTIVES: This research aimed to explore the influence of combined selenium deficiency (SeD) and TMT exposure on poultry thymus toxicity and the underlying molecular mechanisms.
METHODS: Broiler chicken and MDCC-MSB-1 cell models were established with individual or combined SeD and TMT treatment. Mechanisms of thymic injury were explored using transcriptomics, immunofluorescence, Western blot, and other methods.
RESULTS: The study demonstrated that both individual and combined SeD and TMT exposure induced thymic structural abnormalities, mitochondrial oxidative stress, disruption of mitochondrial homeostasis and function, mitophagy, and ferroptosis. Further investigations revealed that mitochondrial oxidative stress and mitophagy regulate ferroptosis, with combined exposure causing more severe damage. Mechanistically, TMT and SeD regulated mitochondrial quality control (MQC) system and ferroptosis through the miR-7480-5p/SIRT3/GSH axis.
CONCLUSION: This study reveals that SeD and TMT induce thymic injury by triggering mitochondrial dysfunction and ferroptosis via the miR-7480-5p/SIRT3/GSH axis, providing novel mechanistic insights and potential intervention targets and potential interventions for TMT pollution in selenium-deficient regions.
OBJECTIVES: This research aimed to explore the influence of combined selenium deficiency (SeD) and TMT exposure on poultry thymus toxicity and the underlying molecular mechanisms.
METHODS: Broiler chicken and MDCC-MSB-1 cell models were established with individual or combined SeD and TMT treatment. Mechanisms of thymic injury were explored using transcriptomics, immunofluorescence, Western blot, and other methods.
RESULTS: The study demonstrated that both individual and combined SeD and TMT exposure induced thymic structural abnormalities, mitochondrial oxidative stress, disruption of mitochondrial homeostasis and function, mitophagy, and ferroptosis. Further investigations revealed that mitochondrial oxidative stress and mitophagy regulate ferroptosis, with combined exposure causing more severe damage. Mechanistically, TMT and SeD regulated mitochondrial quality control (MQC) system and ferroptosis through the miR-7480-5p/SIRT3/GSH axis.
CONCLUSION: This study reveals that SeD and TMT induce thymic injury by triggering mitochondrial dysfunction and ferroptosis via the miR-7480-5p/SIRT3/GSH axis, providing novel mechanistic insights and potential intervention targets and potential interventions for TMT pollution in selenium-deficient regions.