Vitamin E (α tocopherol) attenuates toxicity and oxidative stress induced by aflatoxin in rats

Adv Clin Exp Med. 2017 Sep;26(6):907-917. doi: 10.17219/acem/66347.

Abstract

Background: Aflatoxins are toxic metabolites produced by Aspergillus flavus and Aspergillus parasiticus and are classified as group I carcinogens by the International Agency for Research on Cancer (IARC).

Objectives: The purpose of this study was to investigate the possible preventive role of vitamin E (Vit E) on aflatoxin (AF) induced toxicity by using biochemical and histopathological approaches.

Material and methods: Wistar-Albino rats were divided into 4 groups as follows: control group, Vit E group (Vit E was administered), AFB1 group (a single dose of AFB1 was administered), AF + Vit E group (AF and Vit E were administered). The effects of Vit E on AFB1 induced tissue toxicity were evaluated by using malondialdehyde (MDA), reduced glutathione (GSH) levels, antioxidant enzyme activities, and histopathological examination in tissues.

Results: AF caused the oxidative stress by the increased MDA level and the reduced GSH level, glutathioneS-transferase (GST), catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and glucose-6-phosphate dehydrogenase (G6PD) activities in tissues. Plasma aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) activities, creatinine, and urea concentrations significantly increased; whereas, chloride, phosphorus, and magnesium concentrations were insignificantly affected. Plasma glucose, protein and sodium concentrations significantly decreased. Administration of AF caused hepatotoxicity, cardiotoxicity, and nephrotoxicity. As far as histopathological changes are concerned, a statistically significant difference was found in AFB1 group compared to the control group. Vit E considerably reduced plasma AST, ALT, ALP, LDH activities, and urea concentration and ameliorated the deleterious effects of AF on oxidative stress markers and pathological changes.

Conclusions: This data indicated that the natural antioxidant Vit E might have a protective effect against AF-induced toxicity and oxidative stress.

Keywords: aflatoxin; antioxidant; oxidative stress; vitamin E.

MeSH terms

  • Aflatoxin B1*
  • Animals
  • Antioxidants / pharmacology*
  • Biomarkers / blood
  • Cardiotoxicity
  • Chemical and Drug Induced Liver Injury / blood
  • Chemical and Drug Induced Liver Injury / enzymology
  • Chemical and Drug Induced Liver Injury / etiology
  • Chemical and Drug Induced Liver Injury / prevention & control*
  • Disease Models, Animal
  • Heart Diseases / blood
  • Heart Diseases / chemically induced
  • Heart Diseases / enzymology
  • Heart Diseases / prevention & control*
  • Kidney / drug effects*
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney Diseases / blood
  • Kidney Diseases / chemically induced
  • Kidney Diseases / enzymology
  • Kidney Diseases / prevention & control*
  • Liver / drug effects*
  • Liver / enzymology
  • Liver / pathology
  • Male
  • Myocytes, Cardiac / drug effects*
  • Myocytes, Cardiac / enzymology
  • Myocytes, Cardiac / pathology
  • Oxidative Stress / drug effects*
  • Rats, Wistar
  • Vitamin E / pharmacology*

Substances

  • Antioxidants
  • Biomarkers
  • Vitamin E
  • Aflatoxin B1