No effect of creatine supplementation on oxidative stress and cardiovascular parameters in spontaneously hypertensive rats

Lipid hydroperoxidation, one important oxidative stress marker, remained unchanged in the coronary artery (Cr: 12.6 ± 1.5 vs. Pl: 12.2 ± 1.7 nmol·mg-1; p = 0.87), heart (Cr: 11.5 ± 1.8 vs. Pl: 14.6 ± 1.1 nmol·mg-1; p = 0.15), plasma (Cr: 67.7 ± 9.1 vs. Pl: 56.0 ± 3.2 nmol·mg-1; p = 0.19), plantaris (Cr: 10.0 ± 0.8 vs. Pl: 9.0 ± 0.8 nmol·mg-1; p = 0.40), and EDL muscle (Cr: 14.9 ± 1.4 vs. Pl: 17.2 ± 1.5 nmol·mg-1; p = 0.30). Additionally, Cr supplementation affected neither arterial blood pressure nor heart structure in SHR (p > 0.05).Using a well-known experimental model of systemic arterial hypertension, this study did not confirm the possible therapeutic effects of Cr supplementation on oxidative stress and cardiovascular dysfunction associated with arterial hypertension.It has been suggested that exacerbated oxidative stress and its consequent oxidative damage may be mediators involved in cardiovascular diseases, such as systemic arterial hypertension [1]. Supporting this notion, a reduction in antioxidant bioavailability along with increased oxidative stress has been reported in both experimental and human hypertension [2].Creatine (Cr) supplementation has emerged as a promising adjunct therapy in several pathological conditions [3], including cardiovascular diseases [4,5]. Interestingly, a growing body of experimental and clinical literature has suggested that Cr may exert protective effect in diseases where exacerbated oxidative stress plays a detrimental role (e.g., Huntington's disease) [6-8]. In fact, in vitro experiments have revealed that Cr may possess antioxidant properties by acting as a scavenger of free radicals, such as superoxide anions and peroxynitrite [8,9]. For instance, Cr pre-loading was found to be cytoprotective in different cell cultures with oxidative stressors (i.e., H2O2, tBOOH and peroxynitrite) [10]. Moreover, Cr may also "indirectly" attenuate the formation of reactive oxygen species trough the coupling of Cr with ATP into the mitoch