BACKGROUND Leishmaniasis is a parasitosis caused by several species of the genus
Leishmania
. These parasites present high
resistance against oxidative stress generated by inflammatory cells.
OBJECTIVES To investigate oxidative stress and molecular inflammatory markers in BALB/c mice infected with
L. amazonensis
and the effect of antioxidant treatment on these parameters.
METHODS Four months after infection, oxidative and inflammatory parameters of liver, kidneys, spleen, heart and lungs from
BALB/c mice were assessed.
FINDINGS In liver,
L. amazonensis caused thiol oxidation and nitrotyrosine formation; SOD activity and SOD2 protein content
were increased while SOD1 protein content decreased. The content of the cytokines IL
-1β, IL-6, TNF-α, and the receptor of
advanced glycation endproducts (RAGE) increased in liver. Treatment with the antioxidant
N-acetyl-cysteine (20 mg/kg b.w) for
five days inhibited oxidative stress parameters.
MAIN CONCLUSIONS L. amazonensis induces significant alterations in the redox status of liver but not in other organs. Acute
antioxidant treatment alleviates oxidative stress in liver, but it had no effect on pro-inflammatory markers. These results indicate
that the pathobiology of leishmaniasis is not restricted to the cutaneous manifestations and open perspectives for the development
of new therapeutic approaches to the disease, especially for liver function.
