in vitro
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].
in vivo
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].
References
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.
