Abstract Introduction: Cigarette smoking is the main, modifiable risk factor for atherosclerosis. We have previously reported reversal of endothelial dysfunction in young, healthy smokers with taurine supplementation. A heterogeneous population of endothelial cells (shed circulating endothelial cells (CECs) and endothelial progenitor cells (EPCs)) is found in circulation. These correlate with the magnitude of injury and the reparative response respectively. We hypothesise, that taurine decreases structural endothelial injury and restores the reparative mobilisation of EPCs from the bone marrow in young smokers. Methods: We tested this hypothesis with a model of brief upper limb ischaemia, by characterising the response of CECs and EPCs to ischaemia in matched groups of non-smoking (n = 15) and healthy smoking young males (n = 15). Smokers were then treated for five days with Taurine, and the test repeated. Endothelial cell populations were determined by flow cytometry using CD45, CD133 and CD145. TABLE—ABSTRACT P82 Control (n = 15) Smokers (n = 15) Taurine Tx. (n = 8) CEC EPC CEC EPC CEC EPC Baseline 1.2 ± 0.34 1.2 ± 0.7 λ 3.1 ± 0.54 ∗ 0.53 ± 0.24 γ 1.25 ± 0.4 4.25 ± 0.65 Post IR injury 1.13 ± 0.4 1.7 ± 0.6 5.5 ± 1.0 ∗∧ 1.0 ± 0.44 1.13 ± 0.4 0.88 ± 0.36 ∗ P < 0.05 v control baseline. λ P < 0.001 v Taurine baseline ANOVA, LSD post-hoc. γ P < 0.001 v Taurine baseline ANOVA, LSD post-hoc. ∧ P < 0.001 v Taurine baseline ANOVA, LSD post-hoc. Results: Baseline CECs were increased in smokers who also demonstrated an exaggerated CEC response; both of these observations were restored to control levels with taurine. In addition, taurine increased baseline EPCs in smokers. Conclusion: This study clearly demonstrates increased endothelial injury in smokers, furthermore this injury is attenuated by taurine. These observations may have therapeutic implications given that the doses of the amino-acid used in these studies can be achieved with dietary modification.