Rahimi, R. Creatine supplementation decreases oxidative DNA damage and lipid 
peroxidation induced by a single bout of resistance exercise. J Strength Cond 
Res 25(12): 3448-3455, 2011-Creatine (Cr), or methyl guanidine-acetic acid, can 
be either ingested from exogenous sources, such as fish or meat, or produced 
endogenously by the body, primarily in the liver. It is used as an ergogenic aid 
to improve muscle mass, strength, and endurance. Heretofore, Cr's positive 
therapeutic benefits in various oxidative stress-associated diseases have been 
reported in the literature and, recently, Cr has also been shown to exert direct 
antioxidant effects. Therefore, the purpose of this study was to investigate the 
effects of an acute bout of resistance exercise (RE) on oxidative stress 
response and oxidative DNA damage in male athletes and whether supplementation 
with Cr could negate any observed differences. Twenty-seven resistance-trained 
men were randomly divided into a Cr supplementation group (the Cr group [21.6 ± 
3.6 years], taking 4 × 5 g Cr monohydrate per day) or a placebo (PL) 
supplementation group (the PL group [21.2 ± 3.2 years], taking 4 × 5 g 
maltodextrin per day). A double-blind research design was employed for a 7-day 
supplementation period. Before and after the seventh day of supplementation, the 
subjects performed an RE protocol (7 sets of 4 exercises using 60-90 1 
repetition maximum) in the flat pyramid loading pattern. Blood and urine samples 
taken before, immediately, and 24-hour postexercise were analyzed for plasma 
malondialdehyde (MDA) and urinary 8-hydroxy-2-deoxyguanosine (8-OHdG) excretion. 
Before the supplementation period, a significant increase in the urinary 8-OHdG 
excretion and plasma MDA levels was observed after RE. The Cr supplementation 
induces a significant increase in athletics performance, and it attenuated the 
changes observed in the urinary 8-OHdG excretion and plasma MDA. These results 
indicate that Cr supplementation reduced oxidative DNA damage and lipid 
peroxidation induced by a single bout of RE.