Be careful - just because this paper reports positive effects of N-acetylcysteine in specific circumstances in rats does NOT imply that we can or should take N-acetylcysteine.
Nonetheless, some greater understanding on Nonthyroidal Illness Syndrome is desperately needed. It is all too easy to point a finger at low T3 levels and assume that use of liothyronine would be the answer. However, that is absolutely obvious, has been tried, and does not appear to be "the answer".
J Endocrinol
. 2020 Jun 1;JOE-19-0574.R3.
doi: 10.1530/JOE-19-0574. Online ahead of print.
Oxidative Remote Induction of Type 3 Deiodinase Impacts Nonthyroidal Illness Syndrome
Tatiana Ederich Lehnen 1 , Rafael Marschner 2 , Fernanda Dias 3 , Ana Luiza Maia 4 , Simone Magagnin Wajner 5
Affiliations
• PMID: 32590340
• DOI: 10.1530/JOE-19-0574
Abstract
Imbalances in redox status modulate type 3 deiodinase induction in nonthyroidal illness syndrome. However, the underlying mechanisms that lead to D3 dysfunction under redox imbalance are still poorly understood. Here we evaluated D3 induction, redox homeostasis, and their interrelationships in the liver, muscle, and brain in an animal model of NTIS. Male Wistar rats were subjected to left anterior coronary artery occlusion and randomly separated into two groups and treated or not (placebo) with the antioxidant N-acetylcysteine. Sham animals were used as controls. Animals were sacrificed 10- or 28-days post-MI induction, and tissues were immediately frozen for biochemical analysis. D3 activity, protein oxidation and antioxidant defenses were measured in liver, muscle, and brain. Compared to those of the sham group, the levels of D3 expression and activity were increased in the liver (P=0.002), muscle (P=0.03) and brain (P=0.01) in the placebo group. All tissues from the placebo animals showed increased carbonyl groups (P<0.001) and diminished sulfhydryl levels (P<0.001). Glutathione levels were decreased, and glutathione disulfide levels were augmented in all examined tissues. The liver and muscle showed augmented levels of glutathione peroxidase, glutathione reductase and thioredoxin reductase activity (P=0.001). NAC prevented all the alterations described above. D3 dysfunction in all tissues correlates with post-MI-induced protein oxidative damage and altered antioxidant defenses. NAC treatment prevents D3 dysfunction, indicating that reversible redox related- remote D3 activation explains, at least in part, the thyroid hormone derangements of NTIS.
Full paper is, as so often, behind a paywall:
