We evaluated the effects of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) protocols on the alterations in oxidative stress parameters caused by a high-fat diet (HFD), in the blood and liver of rats. The HFD enhanced thiobarbituric acid reactive substances (TBA-RS) and protein carbonyl content, while reducing total sulfhydryl content and catalase (CAT) and glutathione peroxidase (GSH-Px) activities in the blood. Both training protocols prevented an increase in TBA-RS and protein carbonyl content, and prevented a reduction in CAT. HIIT protocol enhanced SOD activity. In the liver, HFD didn't alter TBA-RS, total sulfhydryl content or SOD, but increased protein carbonyl content and CAT and decreased GSH-Px. The exercise protocols prevented the increase in protein carbonyl content and the MICT protocol prevented an alteration in CAT. In conclusion, HFD elicits oxidative stress in the blood and liver and both protocols prevented most of the alterations in the oxidative stress parameters.

Hyperargininemia is a metabolic disorder biochemically characterized by tissue accumulating of arginine and other guanidino compounds. Convulsions, lethargy and psychomotor delay or cognitive deterioration are predominant clinical features of this disease. Although neurologic symptoms predominate in this disorder, their pathophysiology is still unknown. In the present study we initially investigated the in vitro effect of arginine, homoarginine, N-acetylarginine and argininic acid on acetylcholinesterase and butyrylcholinesterase in hippocampus and serum of 15-, 30- and 60-day-old rats. Results showed that arginine in vitro significantly decreased acetylcholinesterase activity in hippocampus of 15-day-old rats and increased this enzyme activity in hippocampus of 60-day-old rats, homoarginine and N-acetylarginine significantly increased acetylcholinesterase activity both in hippocampus of 15- and 30-day-old rats. On the other hand, butyrylcholinesterase was inhibited by homoarginine in serum of 15-day-old rats. The influence of the antioxidants trolox and ascorbic acid on the effects elicited by arginine, homoarginine and N-acetylarginine was also studied. Results showed that these antioxidants were able to prevent the alteration on acetylcholinesterase and butyrylcholinesterase activities caused by guanidine compounds studied, suggesting that alterations on these cholinesterases were probably mediated by free radicals. It is presumed that these results might be associated, at least in part, with the neuronal dysfunction of patients affected by hyperargininemia.

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