| Autor: |
Baldissera MD; Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil. matheusd.biomed@yahoo.com.br., Gonçalves RA; Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil., Sagrillo MR; Laboratory of Cell Culture, Centro Universitário Franciscano, Santa Maria, RS, Brazil., Grando TH; Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil., Ritter CS; Laboratory of Cell Culture, Centro Universitário Franciscano, Santa Maria, RS, Brazil., Grotto FS; Laboratory of Cell Culture, Centro Universitário Franciscano, Santa Maria, RS, Brazil., Brum GF; Laboratory of Cell Culture, Centro Universitário Franciscano, Santa Maria, RS, Brazil., da Luz SC; Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil., Silveira SO; Department of Biochemistry, UFSM, Santa Maria, RS, Brazil., Fausto VP; Laboratory of Cell Culture, Centro Universitário Franciscano, Santa Maria, RS, Brazil., Boligon AA; Laboratory of Phytochemistry, UFSM, Santa Maria, RS, Brazil., Vaucher RA; Laboratory of Cell Culture, Centro Universitário Franciscano, Santa Maria, RS, Brazil., Stefani LM; Department of Animal Science, Universidade do Estado de Santa Catarina (UDESC), Chapecó, SC, Brazil., da Silva AS; Department of Animal Science, Universidade do Estado de Santa Catarina (UDESC), Chapecó, SC, Brazil., Souza CF; Department of Physiology and Pharmacology, UFSM, Santa Maria, RS, Brazil., Monteiro SG; Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (UFSM), Santa Maria, RS, Brazil. |
| Abstrakt: |
Diminazene aceturate (DA) is the active component of some trypanocidal drugs used for the treatment of animals infected with trypanosomosis and babesiosis. Residues of DA may cause hepatotoxic and nephrotoxic effects. Therefore, the purpose of this study was to investigate the occurrence of oxidative stress, i.e., changes in the antioxidant defense system of rats treated with a single dose of 3.5 mg kg(-1) of DA. All treatments were intramuscularly administered, and evaluations were performed on days 7 and 21 post-treatment (PT). Liver and kidney samples were collected and evaluated by histopathology and oxidative stress parameters (thiobarbituric acid-reactive species, catalase, superoxide dismutase, carbonyl, non-protein thiols, and reduced glutathione). Finally, blood was collected to determine seric DA concentration. Superoxide dismutase (SOD) and catalase (CAT) activities in liver and kidney of rats were dramatically inhibited (p < 0.05) compared to the control group on day 21 PT. This difference is related to the concomitant increase (p < 0.05) in malondialdehyde (MDA) content, which was identified by an increase in thiobarbituric acid-reactive species (TBARS) levels. The carbonyl levels did not differ between groups (p > 0.05). Both non-protein thiols (NPSH) and glutathione (GSH) levels in liver and kidney decreased (p < 0.05) on day 21 PT. Chromatographic analyses showed lower levels of DA on day 21 PT compared to day 7 PT. A negative correlation was observed between DA concentration in serum and lipid peroxidation in liver and kidney tissues on 21 days PT. Histopathology revealed vacuolar degeneration in liver and kidney samples on day 21 PT. Our findings indicate that DA could cause oxidative damage to liver and kidney of rats. |
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