Energy metabolism, thyroid calorigenesis, and oxidative stress: functional and cytotoxic consequences

Abstract

To cite this article: L.A. Videla (2000) Energy metabolism, thyroid calorigenesis, and oxidative stress: functional and cytotoxic consequences, Redox Report,5:5,[265][266][267][268][269][270][271][272][273][274][275] To link to this article: http://dx.

Oxidative Stress and Antioxidant Status in Hypo- and Hyperthyroidism

“…The great majority of the reactive oxygen species (ROS) are generated at mitochondrial level, via oxidative phosphorylation. Thyroid hormones act on mitochondria by regulating energy metabolism, and mitochondria are a major source of intracellular free radicals [82,83]. During thyroid hormone synthesis, there is a constant production of oxygenated water, which is absolutely indispensable for iodine intrafollicular oxidation in the presence of thyroid peroxidase.…”

The Relationship Between Thyroid States, Oxidative Stress and Cellular Damage

“…The first is a short-term signaling mechanism with the allosteric activation of cytochrome-C oxidase and the second is a long-term pathway producing nuclear and mitochondrial gene transcription through T 3 signaling, thus stimulating basal thermogenesis (Oppenheimer et al, 1994). This last mechanism causes the synthesis of the enzymes involved in energy metabolism and the components of the respiratory-chain apparatus, leading to a higher capacity of oxidative phosphorylation (Videla, 2000;Soboll, 1993). These short-and long-term pathways are mainly responsible for the increased cellular respiration caused by the hyperthyroid state.…”

“…These short-and long-term pathways are mainly responsible for the increased cellular respiration caused by the hyperthyroid state. Other processes may also play a role, namely 1) energy expenditure caused by a higher active cation transport, 2) loss of energy from futile cycles caused by increases in catabolic and anabolic pathways of intermediary metabolism, 3) higher activity of membrane-bound enzymes associated with electron transfer and metabolite carriers caused by changes in the lipid composition of mitochondrial membranes (Soboll, 1993), and 4) O 2 equivalents related to oxidative stress (Videla, 2000), a REDOX imbalance that leads to various pathological events in several organs as the liver (Jaeschke et al, 2002). In these pathologies, the cellular damage occurs when the balance between oxidant and antioxidants is disturbed and the antioxidant system does not balance the oxidants, thus altering the ROS steady-state level (Lushchak, 2011).…”

In vitro efficacy of some cattle drugs on bovine serum paraoxonase 1 (PON1) activity

“…Mitochondria are the important sites for production of reactive oxygen species (ROS) due to incomplete reduction of molecular oxygen to water as a consequence of electron leakage in the electron transport chain 7,8 . Increased oxygen consumption and oxidative phosphorylation result in increased production of ROS 9,10 . Ohara et al reported that higher levels of plasma lipids are associated with increased production of ROS 11 .…”