Treatment with N‑acetylcysteine does not alter blood glucose levels and the oxidative stress status in diabetic rats

Abstract

Objectives: To verify the contribution of N‑acetylcysteine (NAC) as an antioxidant
drug in the therapy of diabetes, helping to reduce the deleterious effects resulting from
oxidative stress associated with the hyperglycemic state. Materials and Methods: The
animals were divided into normal (saline, 25 mg/kg NAC, and 75 mg/kg NAC) and
diabetic rats (saline, 25 mg/kg NAC, and 75 mg/kg NAC) with five rats per group,
and were treated for four weeks. Diabetes induction was performed by intraperitoneal
injection of alloxan after fasting for 12 hours. Subsequently, glucose solution was
used to promote wear of the pancreatic beta cells. Blood parameters such as glucose,
glycated hemoglobin, hepatic and renal biomarkers, and butyrylcholinesterase
activity were determined by commercial kits. Catalase, glutathione peroxidase, and
superoxide dismutase activities were measured using spectrophotometric techniques,
while glutathione and malondialdehyde levels were determined by chromatographic
techniques. Results: NAC had no significant differences on glycemic, hepatic, renal,
and oxidative stress biomarkers. Superoxide dismutase activity was significantly
higher(P < 0.05) in diabetic rats treated with NAC compared to the diabetic saline group,
while butyrylcholinesterase activity was significantly lower(P < 0.05) in the same groups.
There was a negative correlation between superoxide dismutase and butyrylcholinesterase
activities. Conclusion: NAC supplementation did not re‑establish the antioxidant system
and consequently the deleterious effects of diabetes did not decrease. Diabetic groups that
received NAC demonstrated that superoxide dismutase activity was indirectly linked to
the levels of butyrylcholinesterase. More studies are necessary to investigate the action of
NAC on superoxide dismutase and butyrylcholinesterase activities in the diabetic state.