N-acetyl-cysteine inhibits liver oxidative stress markers in BALB/c mice infected with Leishmania amazonensis

Leishmaniasis is a parasitosis caused by several species of the genus Leishmania. These parasites present high resistance against oxidative stress generated by inflammatory cells. To investigate oxidative stress and molecular inflammatory markers in BALB/c mice infected with L. amazonensis and the e...

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Bibliographic Details
Published in:Memórias do Instituto Oswaldo Cruz Vol. 112; no. 2; pp. 146 - 154
Main Authors: Gasparotto, Juciano, Kunzler, Alice, Senger, Mario Roberto, Souza, Celeste da Silva Freitas de, Simone, Salvatore Giovanni de, Bortolin, Rafael Calixto, Somensi, Nauana, Dal-Pizzol, Felipe, Moreira, José Claudio Fonseca, Abreu-Silva, Ana Lúcia, Calabrese, Kátia da Silva, Silva, Jr, Floriano Paes, Gelain, Daniel Pens
Format: Journal Article
Language:English
Published: Brazil Instituto Oswaldo Cruz, Ministério da Saúde 01-02-2017
Fundação Oswaldo Cruz (FIOCRUZ)
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Summary:Leishmaniasis is a parasitosis caused by several species of the genus Leishmania. These parasites present high resistance against oxidative stress generated by inflammatory cells. 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. Four months after infection, oxidative and inflammatory parameters of liver, kidneys, spleen, heart and lungs from BALB/c mice were assessed. 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. 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.
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AUTHORS’ CONTRIBUTION
JG conducted the experiments, designed the study, analysed the data and drafted the manuscript; AK and FDP performed oxidative stress assays and western blots; MRS was responsible for design and submitting the project to the Committee of Ethics for the Use of Animals; SGS and FPS-Jr helped to design the study and provided the structure for parasite infection and animal care in FIOCRUZ laboratory; RCB and NS performed oxidative damage assays. Statistical analysis, and animal infection were carried out by CSFS, ALA-S and KSC. Data evaluation and manuscript revision were carried out by JCFM; DPG supervised and coordinated this work. All authors have read and approved the final manuscript.
ISSN:0074-0276
1678-8060
1678-8060
0074-0276
DOI:10.1590/0074-02760160403