title: Vitamin E supplementation ameliorates aflatoxin B1-induced nephrotoxicity in rats.
abstract: Fungal toxins in nutrition can cause organ dysfunction or even failure. Aflatoxin B1 (AFB1)-induced renal impairment is not sufficiently studied regarding its extent and prevention. The aim of this experiment was to study the effect of AFB1 on renal cortical tissue and whether its possible harmful effect could be prevented by the conventional economical antioxidant, vitamin E. Forty rats were divided into four groups; I-IV. Group I represented the control while the others received vitamin E (Vit E), AFB1 and AFB1+Vit E, respectively. Renal cortex specimens were taken from each group after 25 days. Then, specimens were prepared for histological study by hematoxlyin and eosin (H&E), Masson's trichrome, caspase-3 as well as for ultrastructural examination and oxidative stress parameters evaluation. Data were morphometrically and statistically analyzed. In AFB1-treated group, focal tubulo-interstitial affection in the form of tubular cytoplasmic vacuolation, mitochondrial disruption, numerous lysosomes, marked increase in collagen deposition and in caspase-3 expression were observed. Glomerular impairment in the form of fusion of podocytes enlarged foot processes and thickening of the glomerular basement membrane (GBM) with loss of its trilaminar appearance were detected. In the group treated by AFB1+Vit E, there were minimal affection of the histological structure of the renal cortex as well as significant increase in the anti-oxidative parameters which were significantly decreased in the AFB1-treated group. Therefore, Vit E could be considered in wide experimental studies to be a first choice antioxidant of high cost-effectiveness in prevention of fungal toxins pro-oxidant-induced renal impairment.
authors: Department of Histology and Cell Biology, Faculty of Medicine, Mansoura University, PO 35516, Mansoura, Egypt. Electronic address: drahmadabdelhamid@gmail.com.
authors: Ahmed A M
authors: AA
authors: Abdel-Hamid
authors: Department of Histology and Cell Biology, Faculty of Medicine, Mansoura University, PO 35516, Mansoura, Egypt.
authors: Alaa El-Din L
authors: Ael-D
authors: Firgany
mesh_terms: D016604:Aflatoxin B1; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D053148:Caspase 3 / Q000378:metabolism; D019587:Dietary Supplements; D004353:Drug Evaluation, Preclinical; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D007672:Kidney Cortex / Q000187:drug effects / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress; D017207:Rats, Sprague-Dawley; D051437:Renal Insufficiency / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D014810:Vitamin E / Q000008:administration & dosage*
chemical_list: D000975:Antioxidants; D014810:Vitamin E; D008315:Malondialdehyde; D016604:Aflatoxin B1; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; C505410:Casp3 protein, rat; D053148:Caspase 3
keywords: Aflatoxin B(1); Caspase-3; Nephrotoxicity; Ultrastructure; Vitamin E