Oxidative stress in rats experimentally infected by Sporothrix schenckii Ver ^ onica S.P. Castro a , Aleksandro S. Da Silva b, c, * , Gustavo R. Thom  e d , Patrícia Wolkmer a , Jorge L.C. Castro a ,M  arcio M. Costa a , Dominguita L. Graça a , Daniele C. Oliveira e , Sydney H. Alves e , Maria R.C. Schetinger c , Sonia T.A. Lopes a , Lenita M. Stefani b , Maria I. Azevedo e , Matheus D. Baldissera e , Cinthia M. Andrade a a Department of Small Animals, Universidade Federal de Santa Maria, Brazil b Department of Animal Science and Graduate Program in Animal Science, Universidade Do Estado de Santa Catarina, Brazil c Department of Clinical and Toxicological Analysis, Universidade Federal de Santa Maria, Brazil d Department of Chemistry, Federal Technological Universityof Paran a (UTFPR), Pato Branco-PR, Brazil e Department of Microbiology and Parasitology, Universidade Federal de Santa Maria, Brazil article info Article history: Received 14 January 2017 Received in revised form 12 February 2017 Accepted 5 March 2017 Available online 7 March 2017 Keywords: Sporotrichosis TBARS CAT SOD Pathogenesis abstract The aim of this study was to evaluate whether oxidative stress occurs in rats experimentally infected by Sporothrix schenckii, and its possible effect on disease pathogenesis. Thirty rats were divided into two groups: the group A (uninfected, n ¼ 18) and the group B (infected by S. schenckii, n¼21). Blood samples were collected on days 15, 30 and 40 post-infection (PI). At each sampling time, six rats of the group A, and seven of the group B were bled. TBARS (thiobarbituric acid reactive substances) levels in serum samples were measured to evaluate lipid peroxidation. In addition, catalase (CAT) and superoxide dis- mutase (SOD) activities, known as biomarkers of antioxidants levels, were verified in whole blood. Seric pro-inflammatory cytokine levels were measured (IFN-g, TNF-a, and IL-6), which showed that these inflammatory mediators were at higher levels in the infected rats (P < 0.001). In comparison to unin- fected animals, rats with sporotrichosis showed significantly higher (p < 0.01) levels of TBARS on day 40 PI; CAT activity was significantly increased (p < 0.01) on days 30 and 40 PI; and SOD activity was increased (p < 0.01) on day 40 PI. Infected rats showed larger testicles and granulomas in the testicular capsule, as well as hepatic granulomas and splenic follicular hyperplasia. All tissues (testicle, spleen, and liver) showed inflammation associated with numerous fungal structures. These results demonstrated that the intense inflammatory response (seric and tissue) in sporotrichosis is a likely mechanism for redox imbalance, and consequently cause the oxidative stress in experimentally infected rats. © 2017 Elsevier Ltd. All rights reserved. 1. Introduction Sporothrix schenckii is the etiologic agent of a disease called sporotrichosis with worldwide distribution, and great impact on public health [1]. This disease affects the skin and lymphatic vessels near the infected tissue and it may spread to bones, joints, and muscles of humans and other mammals, such as cats, dogs, rats, and horses [2]. Skin lesions might be superficial with nodular ul- cers, compromising lymphatic vessels. The systemic form of the disease is characterized by visceral lesions [3], which leads to oxidative stress due to an imbalance in the oxidant and antioxidant status, causing further harm to the patient. Oxidative stress may cause cell and tissue damage [4], which induce or contribute to dermal pathologies [5], as observed in cases of sporotrichosis. The occurrence of oxidative stress appears to be a consequence of fungal diseases as reported by Beigh et al. [6] while studying the oxidant/antioxidant imbalance in dogs naturally infected by dermatophytosis caused by Microsporum sp. and Tri- chophyton sp. However, it should be noted that the oxidative stress occurs due to an imbalance between the generation of oxidizing compounds, and the performance of antioxidant defense systems, described as an undesirable mechanism in the pathogenesis of several diseases. Thus, the aim of this study was to evaluate whether oxidative stress occurs in rats experimentally infected by * Corresponding author. Departamento de Pequenos Animais, Universidade Federal de Santa Maria, Camobi e 9, Hospital Veterin ario, Sala 109, 97105900, Santa Maria, RS, Brazil. E-mail addresses: dasilva.aleksandro@gmail.com (A.S. Da Silva), cmelazzoandrade1@gmail.com (C.M. Andrade). Contents lists available at ScienceDirect Microbial Pathogenesis journal homepage: www.elsevier.com/locate/micpath http://dx.doi.org/10.1016/j.micpath.2017.03.001 0882-4010/© 2017 Elsevier Ltd. All rights reserved. Microbial Pathogenesis 107 (2017) 1e5