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The effect of taurine supplementation on taurine transporter content and ROS-induced lipid peroxidation during fatiguing contractions in rat skeletal muscle

C.A. Goodman,1,2,4 D. Horvath,3,4 C.G. Stathis,3,4 K. Croft5 and A. Hayes,3,4 1School of Human Movement, Recreation and Performance, Victoria University, Melbourne, VIC 8001, Australia., 2Department of Physiology, The University of Melbourne, Parkville, VIC 3010, Australia, 3School of Biomedical and Health Sciences, Victoria University, Melbourne, VIC 8001, Australia, 4Centre for Ageing, Rehabilitation, Exercise and Sport, Victoria University, Melbourne, VIC 8001, Australia and 5School of Medicine and Pharmacology, University of Western Australia, Crawley, WA 6009, Australia.

Taurine (Tau; 2-aminoethane sulfonic acid), a non-toxic beta amino acid found in most mammalian cells, is reported to function as an osmotic regulator, a cell membrane stabilizer, a modulator of inflammation, an intracellular ion regulator (esp. calcium) and a direct or indirect antioxidant (for review see Huxtable, 1992). Studies in liver have shown that Tau may attenuate non-enzymatic reactive oxygen species (ROS)-induced lipid peroxidation (e.g. Yildirim et al., 2007). It has also been shown in various cell lines and tissues that increased Tau levels down-regulates Tau transporter mRNA and protein expression (Tappaz, 2004). The aim of this study was to investigate: 1) whether Tau supplementation would increase muscle Tau content and lead to a decrease in Tau transporter protein; 2) whether continuous or repeated fatiguing tetanic contractions would lead to an increase in non-enzymatic ROS-induced lipid peroxidation as indicated by F2-isoprostane production; and 3) whether increased muscle Tau can reduce any non-enzymatic ROS-induced lipid peroxidation during fatiguing repeated tetanic contractions.

Male Sprague Dawlay rats (8 wks) were supplemented with Tau in drinking water (2.5% w/v) for 2 weeks. Fast twitch extensor digitorum longus (EDL) muscles were dissected out under anaesthesia (Nembutal; 85mg/kg) in accordance with Victoria University AEEC procedures and subjected to one of two different stimulation protocols: 1) 10s continuous stimulation at a frequency of 100Hz (0.2ms pulse duration); 2) 3 min intermittent stimulation (1s stimulation at 100Hz followed by 4s recovery). Fatigued muscles and their non-fatigued contra-lateral controls were blotted, weighed, frozen in liquid N2 and F2-isoprostanes analysed by GC/MS (Mori et al., 1999). Non-fatigued control muscles were also analysed for Tau content by HPLC and Tau transporter protein by western blotting.

Tau supplementation increased muscle Tau content by 39.5% (p = 0.0002, n=8) with no change in Tau transporter protein (p = 0.41, n=8). Ten seconds of continuous fatiguing tetanic stimulation, which reduced tetanic force by 60-66% of initial force, did not result in a change in the level of F2-isoprostanes in either non-supplemented (n=8) or Tau supplemented muscles (n = 8) compared to their non-stimulated contra-lateral controls. After 3 min of intermittent stimulation, however, in which tetanic force was reduced by 90-92%, there was a significant main effect (p=0.0003; 2-way ANOVA with Bonferoni post-test) for contractions to increase F2-isoprostane levels by 46.7% (1.47 ± 0.09 vs 2.16 ± 0.13 pg F2-isoprostanes/μg arachidonic acid; n = 8) and by 13.0 % (1.85 ± 0.13 vs 2.09 ± 0.09 pg F2-isoprostanes/μg arachidonic acid; n = 8) compared to non-stimulated contra-lateral control muscles (n = 8). There was also a strong trend (p = 0.06) for Tau to attenuate F2-isoprostane production than stimulated control muscles.

In conclusion, 2 wks of Tau supplementation significantly increased muscle Tau content but did not cause a down-regulation of Tau transporter protein expression. In addition, repeated tetanic contractions led to a significant increase in non-enzymatic ROS-induced lipid peroxidation, as indicated by raised F2-isoprostane content. There was a strong trend for Tau to attenuate lipid peroxidation.

Huxtable RJ (1992) Physiolgical Reviews, 72, 101-163.

Mori TA, Croft KD, Puddey IB, Beilin LJ. (1999) Analytical Biochemistry, 268, 117-127.

Tappaz ML (2004) Neurochemistry Research, 29, 83-96.

Yildirim Z, Kiliç N, Ozer C, Babul A, Take G, Erdogan D. (2007) Annals of the New York Academy of Science, 1100, 553-561.