Journal
FRONTIERS IN ENDOCRINOLOGY
Volume 10, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fendo.2019.00216
Keywords
mitochondria; liver; mtDNA; oxidative damage; iodothyronines
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Funding
- FAR grant from the University of Sannio
- VALERE project from the University of Campania Luigi Vanvitelli
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This study evaluated the effect of 3,5-diiodo-L-thyronine (T2) and 3,5,3'-triiodo-L-thyronine (T3) on rat liver mitochondrial DNA (mtDNA) oxidative damage and repair and to investigate their ability to induce protective effects against oxidative stress. Control rats, rats receiving a daily injection of T2 (N+T2) for 1 week and rats receiving a daily injection of T3 (N+T3) for 1 week, were used throughout the study. In the liver, mtDNA oxidative damage [by measuring mtDNA lesion frequency and expression of DNA polymerase gamma (POLG)], mtDNA copy number, mitochondrial biogenesis [by measuring amplification of mtDNA/nDNA and expression of peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1 alpha)], and oxidative stress [by measuring serum levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG)] were detected. T2 reduces mtDNA lesion frequency and increases the expression of POLG, and it does not change the mtDNA copy number, the expression of PGC-1 alpha, or the serum levels of 8-OHdG. Therefore, T2, by stimulating the major mtDNA repair enzyme, maintains genomic integrity. Similar to T2, T3 decreases mtDNA lesion frequency but increases the serum levels of 8-OHdG, and it decreases the expression of POLG. Moreover, as expected, T3 increases the mtDNA copy number and the expression of PGC-1 alpha. Thus, in T3-treated rats, the increase of 8-OHdG and the decrease of POLG indicate that there is increased oxidative damage and that the decreased mtDNA lesion frequency might be a consequence of increased mitochondrial biogenesis. These data demonstrate that both T2 and T3 are able to decrease in the liver mtDNA oxidative damage, but they act via different mechanisms.
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