Schistosoma mansoni infection causes oxidative stress and alters receptor for advanced glycation endproduct (RAGE) and tau levels in multiple organs in mice

• Published in: International journal for parasitology Vol. 43; no. 5; pp. 371 - 379
• Main Authors: de Oliveira, Ramatis Birnfeld, Senger, Mario Roberto, Vasques, Laura Milan, Gasparotto, Juciano, dos Santos, João Paulo Almeida, de Bittencourt Pasquali, Matheus Augusto, Moreira, José Claudio Fonseca, Silva, Floriano Paes, Gelain, Daniel Pens
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-04-2013
• Subjects: Animals; Antioxidant enzymes; Catalase - metabolism; Cerebral Cortex - parasitology; Cerebral Cortex - pathology; Gene Expression Regulation - physiology; Lung - parasitology; Lung - pathology; Mice; Myocardium - pathology; Oxidation-Reduction; Oxidative stress; Oxidative Stress - immunology; RAGE; Receptor for Advanced Glycation End Products; Receptors, Immunologic - genetics; Receptors, Immunologic - metabolism; Schistosoma; Schistosoma mansoni; Schistosoma mansoni - physiology; Schistosomiasis mansoni - immunology; Schistosomiasis mansoni - metabolism; Schistosomiasis mansoni - parasitology; Superoxide Dismutase; Tau; tau Proteins - genetics; tau Proteins - metabolism; Oxidative stress; Tau; Schistosoma; RAGE; Antioxidant enzymes
• ISSN: 0020-7519; 1879-0135
• DOI: 10.1016/j.ijpara.2012.12.006

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► Schistosoma mansoni infection causes oxidative damage to different organs. ► Schistosoma mansoni changes SOD and CAT activities and protein content in liver, kidney and heart. ► Receptor for advanced glycation endproduct (RAGE) protein content is downregulated in lungs of S. mansoni-infected animals. ► Schistosoma mansoni affects tau expression and phosphorylation in the brain.
Schistosomiasis is a parasitic disease caused by trematode worms from the Schistosoma genus and is characterized by high rates of morbidity. The main organs affected in this pathology, such as liver, kidneys and spleen, are shifted to a pro-oxidant state in the course of the infection. Here, we compared oxidative stress parameters of liver, kidney and spleen with other organs affected by schistosomiasis – heart, brain cortex and lungs. The results demonstrated that mice infected with Schistosoma mansoni had altered non-enzymatic antioxidant status in lungs and brain, increased carbonyl levels in lungs, and a moderate level of oxidative stress in heart. A severe redox imbalance in liver and kidneys and decreased non-enzymatic antioxidant capacity in spleen were also observed. Superoxide dismutase and catalase activities were differently modulated in liver, kidney and heart, and we found that differences in Superoxide dismutase 2 and catalase protein content may be responsible for these differences. Lungs had decreased receptor for advanced glycation endproduct expression and the brain cortex presented altered tau expression and phosphorylation levels, suggesting important molecular changes in these tissues, as homeostasis of these proteins is widely associated with the normal function of their respective organs. We believe that these results demonstrate for the first time that changes in the redox profile and expression of tissue-specific proteins of organs such as heart, lungs and brain are observed in early stages of S. mansoni infection.