I dont think this would be a problem. I tried digging up some positive info. for re-assurance.
: Amino Acids. 1998;15(1-2):13-25. Related Articles, Links
The effects of the beta 2-agonist drug clenbuterol on taurine levels in heart and other tissues in the rat.
Doheny MH, Waterfield CJ, Timbrell JA.
Department of Toxicology, School of Pharmacy, University of London, United Kingdom.
The administration of a single subcutaneous dose of clenbuterol to rats altered the level of taurine in certain tissues. Taurine levels in cardiac tissue were significantly decreased 3 h after the administration of 250 micrograms/kg of clenbuterol and remained significantly depressed at 12 h post-dose only returning to control values by 24 h. The level of taurine in the liver increased 3 h after clenbuterol administration but was lower than the control value at 24 h post dose. Lung taurine levels were significantly lower than the control value at 12 hr post dose and remained depressed until 24 h post dose. Clenbuterol caused a significant increase in taurine levels in serum and muscle at 3 and 6 hr postdosing respectively but not at other time points. Serum creatine kinase (CK), activity was slightly but significantly raised at the 12 and 24 h time point. The effects of clenbuterol on tissue taurine content were not dose-dependent over the range studied (63-500 micrograms/kg). However taurine levels in the lung were significantly reduced at all doses and in the heart were significantly lower in the treated groups at all except the lowest dose, 12 h post dosing. Liver taurine levels were significantly increased at the highest dose of 500 micrograms/kg. The reduction of taurine concentrations in the heart, caused by clenbuterol, is of concern as taurine has been shown to have protective properties in many tissues especially the heart.
Am J Physiol. 1999 Mar;276(3 Pt 1):G647-54. Related Articles, Links
beta2-adrenergic receptor-selective agonist clenbuterol prevents Fas-induced liver apoptosis and death in mice.
Andre C, Couton D, Gaston J, Erraji L, Renia L, Varlet P, Briand P, Guillet JG.
Institut National de la Sante et de la Recherche Medicale (INSERM) U380, Institut Cochin de Genetique Moleculaire, Universite Rene Descartes, 75014 Paris, France. email@example.com
Stimulation of the cAMP-signaling pathway modulates apoptosis in several cell types and inhibits Jo2-mediated apoptosis in cultured rat hepatocytes. No information is yet available as to whether the hepatic beta2-adrenergic receptor (AR) expression level, including beta2-AR-dependent adenylyl cyclase activation, modulates hepatocyte sensitivity to apoptosis in vivo or whether this sensitivity can be modified by beta2-AR ligands. We have examined this using C57BL/6 mice, in which hepatic beta2-AR densities are low, and transgenic F28 mice, which overexpress beta2-ARs and have elevated basal liver adenylyl cyclase activity. The F28 mice were resistant to Jo2-induced liver apoptosis and death. The beta-AR antagonist propranolol sensitized the F28 livers to Jo2. In normal mice clenbuterol, a beta2-AR-specific agonist, considerably reduced Jo2-induced liver apoptosis and death; salbutamol, another beta2-AR-selective agonist, also reduced Jo2-induced apoptosis and retarded death but with less efficacy than clenbuterol; and propranolol blocked the protective effect of clenbuterol. This indicates that the expression level of functional beta2-ARs modulates Fas-regulated liver apoptosis and that this apoptosis can be inhibited in vivo by giving beta2-AR agonists. This may well form the basis for a new therapeutic approach to diseases involving abnormal apoptosis.
Dont forget the milk thistle and sam-e as effective liver protectors. http://boards.elitefitness.com/forum...hreadid=254157