Effects of combined parenteral vitamins C and E administration on the severity of anaemia, hepatic and renal damage in Trypanosoma brucei brucei infected rabbits
Autor: | Ikechukwu Onyebuchi Igbokwe, Ismaila A. Umar, A.U. Wuro-Chekke, Abubakar Gidado |
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Rok vydání: | 1999 |
Předmět: |
Male
Vitamin medicine.medical_treatment Trypanosoma brucei brucei Renal function Ascorbic Acid Trypanosoma brucei Pharmacology Kidney Parasitemia Pathogenesis chemistry.chemical_compound parasitic diseases medicine Animals Urea Vitamin E Aspartate Aminotransferases General Veterinary biology Alanine Transaminase Anemia General Medicine Creatine biology.organism_classification Ascorbic acid Trypanosomiasis African medicine.anatomical_structure Hematocrit Liver chemistry Immunology Parasitology Rabbits Liver function Injections Intraperitoneal |
Zdroj: | Veterinary Parasitology. 85:43-47 |
ISSN: | 0304-4017 |
DOI: | 10.1016/s0304-4017(99)00085-0 |
Popis: | Rabbits infected with Trypanosoma brucei brucei (Basa isolate) were intraperitoneally administered with vitamins C and E at 100 mg/kg and 10 mg/kg body weight, respectively, from day 7 before infection to day 12 post-infection (p.i.). Another group of rabbits were similarly infected, but received no vitamin treatment. The uninfected (control) rabbits were either untreated or treated with vitamins like the infected group. Treatment of the infected animals did not affect the onset and level of parasitaemia. On day 12 p.i., the anaemia tended to be ameliorated, but insignificantly, by the treatment. The infection increased (p0.05) serum urea and creatinine concentrations to similar levels in treated and untreated groups. However, the increase (p0.05) in alanine and aspartate transaminases in the untreated infected animals was prevented in the treated infected ones. Therefore, it seemed that the treatment with antioxidant vitamins boosted their storage in hepatic cells, but not in erythrocytes and glomeruli, to annul any cellular injury due to infection. It is concluded that this may be an indirect evidence that the hepatic damage may be principally due to oxidative injury. |
Databáze: | OpenAIRE |
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