Effects of thioredoxin 2 on the mitochondrial structure and function in selenium deficiency rat hearts.

Objective To study the dynamic changes of thioredoxin 2 (Trx2) protein expression in the cardiac mitochondria of selenium deficiency rats and its effect on cardiac mitochondria damage. Methods Thrity-six rats were randomized into normal control group (n = 18) and selenium deficiency model group (n = 18) . When rats were fed for 20 weeks, 30 weeks and 40 weeks, respectively, their cardiac function was determined by carotid artery intubation. At the corresponding time points, damage of cardiac mitochondria was observed under electron microscope; the mitochondrial stereological parameters including surface density (Sv), volume density (Vv) and specífic surface (Rsv, surface-to-volume ratio) were further studied. The cardiac mitochondria were extracted from the rats at the corresponding time points to assess the enzyme activities of succinate dehydrogenase (SDH) and cytochrome C oxidase (COX), and to detect the protein expression of Trx2 with Wettern blot. Results ① Rats in the model group had notably decreased cardiac function, and electron microscopy showed mitochondrial swelling with fractured or dissolved crsitae. Further study showed notable decreases in Sv, Rsv, SDH and COX, but remarkable increase in Vv in the selenium deficiency rat hearts compared with that in the corresponding control group (P<0.05) . With the time extension of low-selenium feeding, Sv, Rsv, SDH and COX all decreased, and Vv significantly increased (P<0. 05). ② The protein expression of Trx2 in the cardiac mitochondria of selenium deficiency rats significantly decreased compared with that in the corresponding control group, and the decrease was greater as the time of seienmm deficiency prolonged (P<0.05). ③ Pearson linear correlation analysis showed that the protein expression of mitochondrial Trx2 had a positive correlation with Sv, Rsv, SDH and COX, but a negative correlation with Vv (P <0 .01). Conclusion Selenium deficiency down-regulates the protein expression of mitochondrial Trx2 in the rat heart, which results in cardiac mitochondrial injury and the uiimate progress of heart failure. [ABSTRACT FROM AUTHOR]