in bt4cn cells, 3-thiatetradecanoic acid could activate all ppar subtypes dose-dependently. in cell culture experiments, the pparγ-selective ligand brl49653 moderately inhibited growth of bt4cn cells, while administration of 3-thiatetradecanoic acid led to a marked growth inhibition. moreover, the administration of the pparγ-selective antagonist gw9662 abolished brl49653-induced growth inhibition, but only marginally reduced the effect of 3-thiatetradecanoic acid [1].
administration of 3-thiatetradecanoic acid increased mitochondrial and peroxisomal beta-oxidative capacity and carnitine palmitoyltransferase activity, but reduced free fatty acid and triacylglycerol levels in plasma compared to palmitic acid-treated rats and controls. 3-thiatetradecanoic acid administration was able to affect the fatty acid composition in plasma and liver by increasing the amount of monoenes [2].
1. berge k, tronstad kj, flindt en, rasmussen th, madsen l, kristiansen k, berge rk. tetradecylthioacetic acid inhibits growth of rat glioma cells ex vivo and in vivo via ppar-dependent and ppar-independent pathways. carcinogenesis. 2001 nov;22(11):1747-55.2. asiedu, d.k.,froyland, l.,vaagenes, h., et al. long-term effect of tetradecylthioacetic acid: a study on plasma lipid profile and fatty acid composition and oxidation in different rat organs. biochimica et biophysica acta 1300, 86-96 (1996).3. pettersen rj, salem m, skorve j, ulvik rj, berge rk, nordrehaug je. pharmacology and safety of tetradecylthioacetic acid (tta): phase-1 study. j cardiovasc pharmacol. 2008 apr;51(4):410-7.
