Veterinary Physiology Biochemistry & Pharmacology

Permanent URI for this communityhttps://repository.ui.edu.ng/handle/123456789/578

Browse

Filter results by typing the first few letters
Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    Changes in serum cytokine levels, hepatic and intestinal morphology in aflatoxin B1 induced injury: modulatory roles of melatonin and flavonoid-rich fractions from Chromolena odorata
    (Springer-Verlag, 2016) Akinrinmade, F. J.; Akinrinde, S. A.; Amid, A.
    Aflatoxins are known to produce chronic carcinogenic, mutagenic, and teratogenic effects, as well as acute inflammatory effects, especially in the gastrointestinal tract. The potentials of the flavonoid-rich extract from Chromolena odorata (FCO) and melatonin (a standard anti-oxidant and anti-inflammatory agent) against aflatoxin B1 (AFB1)-induced alterations in pro-inflammatory cytokine levels and morphology of liver and small intestines were evaluated in this study.We utilizedWistar albino rats (200–230 g) randomly divided into five groups made up of group A, control rats; group B, rats given AFB1 (2.5 mg/kg, intraperitoneal) twice on days 5 and 7; rats in groups C, D, and E were treated with melatonin (10 mg/kg, intraperitoneal) or oral doses of FCO1 (50 mg/kg) and FCO2 (100 mg/kg) for 7 days, respectively, along with AFB1 injection on days 5 and 7. Serum levels of interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) were determined using commercial ELISA kits and histopathological evaluation of the liver, duodenum, and ileum were also carried out.We observed significant elevation (p < 0.05) in serum IL-1β correlating with hemorrhages and leucocytic and lymphocytic infiltration in the liver and intestines as evidences of an acute inflammatory response to AFB1 administration. All treatments yielded significant reduction (p <0.05) in IL-1β levels, although TNF-α levels were not significantly altered in all rats that received AFB1, irrespective of the treatments. Melatonin and FCO2 produced considerable protection of hepatic tissues, although melatonin was not quite effective in protecting the intestinal lesions. Our findings suggest a modulation of cytokine expression that may, in part, be responsible for the abilities of C. odorata or melatonin in amelioration of hepatic and intestinal lesions associated with aflatoxin B1 injury.
  • Thumbnail Image
    Item
    Chemoprevention of aflatoxin B1-induced genotoxicity and hepatic oxidative damage in rats by kolaviron, a natural biflavonoid of garcinia kola seeds
    (Lippincott Williams & Wilkins, 2005) Farombi, E. O.; Adepoju, B. F.; Ola-Davies, O. E.; Emerole, G. O.
    The chemopreventive effects of kolaviron, a natural antioxidant biflavonoid from the seeds of Garcinia kola, on aflatoxin B1 (AFB1)-induced genotoxicity and hepatic oxidative damage was investigated in rats. Kolavironmadministered orally at a dose of 200 mg/kg once a day for the first 2 weeks and then 100 mg/kg twice a day for the last 4 weeks of AFB1 (2 mg/kg, single dose, intraperitoneal) treatment reduced the AFB1-increased activities of aspartate amino transferase (AST), alanine amino transferase (ALT) and gamma glutamyltransferase (c-GT) by 62%, 56% and 72% respectively. Malondialdehyde (MDA) formation and lipid hydroperoxide (LHP) accumulation were observed in the livers of AFB1-treated rats. Kolaviron significantly reduced the AFB1-induced MDA and LHP formation. Vitamins C and E were protective in reducing the increase in the activities of AST, ALT and c-GT as well as lipid peroxidation caused by AFB1 (P < 0.01). Administration of rats with kolaviron alone resulted in significant elevation in the activities of glutathione S-transferase, uridyl glucuronosyl transferase and NADH:quinone oxidoreductase by 2.45-, 1.62- and 1.38-folds respectively. In addition, kolaviron attenuated the AFB1-mediated decrease in the activities of these enzymes (P < 0.01). Pretreatment of rats with kolaviron, vitamins C and E alone did not exert genotoxicity assessed by the formation of micronucleated polychromatic erythrocytes (MNPCEs) (P> 0.05). Co-treatment of rats intraperitoneally with kolaviron (500 mg/kg) 30 min before and 30 min after AFB1 (1 mg/kg) administration inhibited the induction of MNPCEs by AFB1 (P < 0.001) after 72 h. While vitamin C was effective in reducing AFB1- induced MNPCEs formation, vitamin E did not elicit any antigenotoxic response. These results indicate kolaviron as effective chemopreventive agent against AFB1-induced genotoxicity and hepatic oxidative stress. Thus kolaviron may qualify for clinical trial in combating the menace of aflatoxicosis in endemic areas of aflatoxin contamination of foods.