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Glutathione peroxidase activity was not affected by drug treatment or by training in saline-treated rats but was increased with training in PDTC and PROP groups (P Akt inhibitor changed in response to drug treatment or endurance training. Endurance training is known to promote skeletal muscle mitochondrial biogenesis and the gene expression of proteins controlling energy metabolism and intracellular redox status (Wu et al. 1999; Lin et al. 2005; Lira et al. 2010). While PGC-1�� and other PGC-1 family transcriptional cofactors (such as PGC-1�� and PRC) play a key role in these training adaptations, several other signal transduction pathways, such as calcium flux, AMP:ATP ratio, NF��B and the ��-adrenergic system, could exert strong influences on the PGC-1��-induced gene products by influencing its upstream enzymes and transcriptional factors or by direct physical interaction with the PGC-1�� promoter or EPZ-6438 molecular weight protein (Delerive et al. 1999; Coll et al. 2006; Handschin & Spiegelman, 2008; Alvarez-Guardia et al. 2010). In the present study, we investigated the effects of two pharmacological agents that could potentially interfere with PGC-1�� signalling, namely PDTC, a well-known antioxidant and NF��B inhibitor (Moellering et al. 1999), and propranolol, a commonly used ��-adrenergic blocker, in both sedentary rats and rats subjected to 8 weeks of endurance training. Female rats were used in the study and therefore the results obtained may be gender specific owing to the potential antioxidant property of estrogen in this animal species. Our study reveals that the effect of PDTC on the signal transduction of mitochondrial biogenesis is different depending on the metabolic status of the animals. In the trained rats, mitochondrial adaptation was attenuated by PDTC, whereas in the sedentary rats PDTC administration markedly increased muscle PGC-1�� expression. Pyrolidine dithiocarbamate is a strong antioxidant and is known to inhibit NF��B signalling due to reduction of ROS and oxidative stress, possibly due to its inhibition of protein kinase C or by acting directly on I��B-activated Montelukast Sodium kinase. It may also inhibit 26S proteasome activity, thus causing accumulation of p-I��B and feedback inhibition on I��B-activated kinase (L?vborg et al. 2006). Thus, training-induced ROS as signal for stimulating PGC-1�� expression could be muted by two injections of PDTC prior to each exercise session. It is intriguing that PDTC treatment increased the PGC-1�� level in the sedentary rats. Alvarez-Guardia et al. (2010) recently reported that the p65 subunit of NF��B is constitutively bound to PGC-1�� in mouse heart and that NF��B activation by tumour necrosis factor-�� exposure increases this binding.
