Potent protective effect of apricot and beta-carotene on methotrexate-induced intestinal oxidative damage in rats.
Several studies have well confirmed the contribution of oxidative stress in the pathogenesis of methotrexate (MTX)-induced damage in the small intestine. Many agents have been tried experimentally to reduce or inhibit the oxidative stress. To our knowledge, there is no study about apricot consumption on the MTX-induced damage in the small intestine. The aim of this study was to determine the possible protective effects of apricot and beta-carotene on MTX-induced intestinal damage in rats. The rats were randomly divided into seven groups as follows; I-control group; II-apricot group; III-beta-carotene group; IV-MTX group; V-apricot+MTX group; VI-beta-carotene+MTX group and VII-apricot+beta-carotene+MTX group. In the MTX group; fusion and shortening in the villus, epithelial desquamation, crypt loss, inflammatory cell infiltration in the lamina propria, goblet cell depletion and microvillar damage were observed in the small intestine. Parallel to histological results, malondialdehyde (MDA) content and myeloperoxidase (MPO) activity were found to be increased, whereas superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GP-x) activities and glutathione (GSH) content were decreased in the MTX group. However, single or combined application of apricot and beta-carotene ameliorated all of these hazardous effects in antioxidant system in MTX-treated groups. In conclusion, our results demonstrate that apricot and/or beta-carotene treatment may protect the impairment of oxidative stress and ameliorate MTX-induced intestine damage at biochemical and histological levels.
Vardi
Nigar
N
Department of Embryology and Histology, Inonu University, 44280 Malatya, Turkey. nvardi@inonu.edu.tr
Parlakpinar
Hakan
H
Ozturk
Feral
F
Ates
Burhan
B
Gul
Mehmet
M
Cetin
Asli
A
Erdogan
Ali
A
Otlu
Ali
A
D000818:Animals; D001713:Biphenyl Compounds; D002374:Catalase / Q000378:metabolism; D005493:Folic Acid Antagonists / Q000633:toxicity*; D016166:Free Radical Scavengers / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007422:Intestines / Q000187:drug effects / Q000473:pathology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008727:Methotrexate / Q000633:toxicity*; D008854:Microscopy, Electron; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D010636:Phenols / Q000494:pharmacology; D010851:Picrates; D010936:Plant Extracts / Q000494:pharmacology; D020011:Protective Agents; D027861:Prunus / Q000737:chemistry*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D019207:beta Carotene / Q000494:pharmacology*
D001713:Biphenyl Compounds; D005493:Folic Acid Antagonists; D016166:Free Radical Scavengers; D010636:Phenols; D010851:Picrates; D010936:Plant Extracts; D020011:Protective Agents; D019207:beta Carotene; C004931:1,1-diphenyl-2-picrylhydrazyl; D002374:Catalase; D009195:Peroxidase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D008727:Methotrexate