Involvement of oxidative stress, cholinergic and adenosinergic systems on renal damage caused by Trypanosoma evansi infection: Relationship with lipid peroxidation

• Trypanosoma evansi alters the cholinergic and adenosinergic systems in renal tissue.
• T. evansi infection increases lipid peroxidation in renal tissue.
• AChE, BChE and ADA reduction probably played an effect on inflammatory response.
• These alterations are in attempt to reduce the oxidative damage caused by T. evansi.

The aim of this study was to evaluate the oxidative stress variables, and enzymes of cholinergic (acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)) and adenosinergic (adenosine deaminase (ADA)) systems in renal tissue, as well as the relationship between these systems and lipid peroxidation. The animals were divided into two groups with six animals each: uninfected (negative control) and infected (positive control). On day 4 post-infection (PI), animals were euthanized and the kidney was collected. Thiobarbituric acid reactive species (TBARS) and lipid peroxidation (FOX) levels increased, while the catalase (CAT), AChE, BChE and ADA activities decreased in kidney tissue on day 4 PI. A negative correlation between AChE and TBARS (r = −0.750), AChE and FOX (r = −0.650), as well as ADA and TBARS (r = −0.345) and ADA and FOX (r = −0.540) were observed (p < 0.05). In summary, the T. evansi infection cause lipid peroxidation in the renal tissue, altering the antioxidant-oxidant status, alterations compatible to oxidative stress and oxidative damage. Also, the T. evansi decrease the activities of AChE, BChE and ADA in order to reduce the oxidative damage increasing the levels of ACh, BCh and adenosine. These alterations in the kidney may be contribute on pathophysiology of T. evansi infection.