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Long-term intake of aspartame at the acceptable daily dose causes oxidative stress in rodent brain mainly due to the dysregulation of glutathione (GSH) homeostasis. N-Acetylcysteine provides the cysteine that is required for the production of GSH, being effective in treating disorders associated with oxidative stress. We investigated the effects of N-acetylcysteine treatment (150 mg kg(-1), i.p.) on oxidative stress biomarkers in rat brain after chronic aspartame administration by gavage (40 mg kg(-1)). N-Acetylcysteine led to a reduction in the thiobarbituric acid reactive substances, lipid hydroperoxides, and carbonyl protein levels, which were increased due to aspartame administration. N-Acetylcysteine also resulted in an elevation of superoxide dismutase, glutathione peroxidase, glutathione reductase activities, as well as non-protein thiols, and total reactive antioxidant potential levels, which were decreased after aspartame exposure. However, N-acetylcysteine was unable to reduce serum glucose levels, which were increased as a result of aspartame administration. Furthermore, catalase and glutathione S-transferase, whose activities were reduced due to aspartame treatment, remained decreased even after N-acetylcysteine exposure. In conclusion, N-acetylcysteine treatment may exert a protective effect against the oxidative damage in the brain, which was caused by the long-term consumption of the acceptable daily dose of aspartame by rats.

Neuropathic pain is a very common dysfunction caused by several types of nerve injury. This condition leads to a variety of pathological changes in central nervous system regions related to pain transmission. It has been demonstrated that nociception is modulated by reactive oxidative species and treatments with antioxidant compounds produce antinociceptive effects. Thus, the aim of the present study was to investigate oxidative parameters in spinal and supraspinal regions following sciatic nerve transection (SNT). In behavioral assessments, animals showed mechanical allodynia and a significant functional impairment following SNT, measured by von Frey hairs test and sciatic functional index, respectively. Superoxide dismutase activity was increased 3 and 7 days following SNT in cerebral cortex and brainstem. Catalase activity was also increased in cerebral cortex 3 days after SNT. Ascorbic acid levels were decreased 7 days in the spinal cord only in SNT group. We also showed an increase in lipid peroxidation in cerebral cortex and brainstem 3 days after surgery in SNT and sham groups. These results showed that supraspinal regions also exhibit changes in antioxidant activity after SNT and demonstrate an intricate relationship among antioxidant defenses in different regions of the neuro axis related to pain transmission.