Schistosoma mansoni infection causes oxidative stress and alters receptor for advanced glycation endproduct (RAGE) and tau levels in multiple organs in mice.
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.
Universidade Federal do Rio Grande do Sul, Departamento de Bioquímica, Centro de Estudos em Estresse Oxidativo, Porto Alegre, RS, Brazil.
Ramatis Birnfeld
RB
de Oliveira
Mario Roberto
MR
Senger
Laura Milan
LM
Vasques
Juciano
J
Gasparotto
João Paulo Almeida
JP
dos Santos
Matheus Augusto de Bittencourt
MA
Pasquali
José Claudio Fonseca
JC
Moreira
Floriano Paes
FP
Silva
Daniel Pens
DP
Gelain
D000818:Animals; D002374:Catalase / Q000378:metabolism; D002540:Cerebral Cortex / Q000469:parasitology / Q000473:pathology; D005786:Gene Expression Regulation / Q000502:physiology; D008168:Lung / Q000469:parasitology / Q000473:pathology; D051379:Mice; D009206:Myocardium / Q000473:pathology; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000276:immunology*; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000235:genetics / Q000378:metabolism*; D012550:Schistosoma mansoni / Q000502:physiology*; D012555:Schistosomiasis mansoni / Q000276:immunology* / Q000378:metabolism / Q000469:parasitology; D013482:Superoxide Dismutase; D016875:tau Proteins / Q000235:genetics / Q000378:metabolism*
C558298:Mapt protein, mouse; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D016875:tau Proteins; D002374:Catalase; D013482:Superoxide Dismutase