Toxoplasma gondii: Effects of diphenyl diselenide in experimental toxoplasmosis on biomarkers of cardiac function.
This study aimed to investigate the effects of diphenyl diselenide (PhSe)2 to treat mice experimentally infected by Toxoplasma gondii on seric biomarkers of cardiac function (creatine kinase, creatine kinase MB, troponin, and myoglobin), and lactate dehydrogenase, as well as to evaluate the enzymatic activity of creatine kinase (CK) and adenylate kinase (AK) in heart tissue. For the study, 40 female mice were divided into four groups of 10 animals each: the group A (uninfected and untreated), the group B (uninfected and treated), the group C (infected and untreated) and the group D (infected and treated). The inoculation was performed with 50 cysts of T. gondii (ME-49 strain). Mice from groups B and D were treated at days 1 and 20 post-infection (PI) with 5 μmol kg(-1) of (PhSe)2 subcutaneously. On day 30 PI, the mice were anesthetized and euthanized for blood and heart collection. As a result, it was observed a decrease in AK activity (P < 0.01) in the heart samples of groups C and D compared to the group A. Cardiac CK increased in the group C compared to the group A (P < 0.01). CK levels increased in infected mice (the group C) compared to other groups (A and D). Regarding CK-MB level, there was a decrease in the group D compared to the group B, without statistical difference compared to control groups (A and C). It was observed an increase on myoglobin in groups C and D, differently of troponin, which did not show statistical difference (P < 0.05) between groups. Mice from the group C showed an increase in lactate dehydrogenase (LDH) levels compared to other groups (A, B, and D). Histopathological evaluation of heart samples revealed necrosis, hemorrhagic regions and inflammatory infiltrates in mice from the Group C, differently from the group D where animals showed only inflammatory infiltrates. Based on these results we conclude that the (PhSe)2 had a protective effect on the heart in experimental toxoplasmosis by modulating tissue and seric CK activity, and avoiding an increase on seric LDH levels, probably due to the antioxidant effect of this compound.
Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil; Graduate Program on Biology: Toxicological Biochemistry, UFSM, Santa Maria, RS, Brazil.
Vanessa S
VS
Machado
Graduate Program on Biology: Toxicological Biochemistry, UFSM, Santa Maria, RS, Brazil.
Nathieli B
NB
Bottari
Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil.
Matheus D
MD
Baldissera
Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil.
Maria
M
Isabel de Azevedo
Graduate Program in Nanoscience, Centro Universitário Franciscano, Santa Maria, RS, Brazil.
Virginia C
VC
Rech
Graduate Program in Nanoscience, Centro Universitário Franciscano, Santa Maria, RS, Brazil.
Francine R
FR
Ianiski
Laboratory of Molecular Biology, Centro Universitário Franciscano, Santa Maria, RS, Brazil.
Rodrigo A
RA
Vaucher
Section of Veterinary Pathology, Instituto Federal Catarinense, Concórdia, SC, Brazil.
Ricardo E
RE
Mendes
Department of Preventive Veterinary Medicine, UFSM, Santa Maria, RS, Brazil.
Giovana
G
Camillo
Department of Preventive Veterinary Medicine, UFSM, Santa Maria, RS, Brazil.
Fernanda F
FF
Vogel
Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil.
Mario L
ML
de la Rue
Graduate Program on Biology: Toxicological Biochemistry, UFSM, Santa Maria, RS, Brazil.
Guilherme M
GM
Carmo
Department of Veterinary Medicine, Universidade do Oeste de Santa Catarina (UNOESC), Xanxerê, SC, Brazil.
Alexandre A
AA
Tonin
Graduate Program on Biology: Toxicological Biochemistry, UFSM, Santa Maria, RS, Brazil; Department of Animal Science, Universidade do Estado de Santa Catarina (UDESC), Chapecó, SC, Brazil. Electronic address: aleksandro_ss@yahoo.com.br.
Aleksandro S
AS
Da Silva
D000263:Adenylate Kinase / Q000378:metabolism; D000818:Animals; D001555:Benzene Derivatives / Q000494:pharmacology* / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D003402:Creatine Kinase / Q000097:blood* / Q000378:metabolism; D052279:Creatine Kinase, MB Form / Q000097:blood; D016054:DNA, Protozoan / Q000302:isolation & purification; D005260:Female; D007770:L-Lactate Dehydrogenase / Q000097:blood; D051379:Mice; D009211:Myoglobin / Q000097:blood*; D016566:Organoselenium Compounds / Q000494:pharmacology* / Q000627:therapeutic use; D016133:Polymerase Chain Reaction; D014122:Toxoplasma / Q000235:genetics; D014124:Toxoplasmosis, Animal / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D014336:Troponin / Q000097:blood*
D001555:Benzene Derivatives; D015415:Biomarkers; D016054:DNA, Protozoan; D009211:Myoglobin; D016566:Organoselenium Compounds; D014336:Troponin; C061132:diphenyldiselenide; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D000263:Adenylate Kinase
Adenylate kinase; Creatine kinase; Creatine kinase-MB; Lactate dehydrogenase; Myoglobin; Toxoplasma gondii; Troponin