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Published June 27, 2017 | Version v1
Journal article Open

Lead-induced Oxidative Stress and Chemoprotective Role of Dietary Supplements on Wistar Albino Rats

  • 1. Environmental Biochemistry and Toxicology Unit, Department of Biochemistry, Federal University of Technology, Owerri, Nigeria & Nutritional and Medical Biochemistry Unit, Department of Biochemistry, Federal University of Technology, Owerri, Nigeria.
  • 2. Nutritional and Medical Biochemistry Unit, Department of Biochemistry, Federal University of Technology, Owerri, Nigeria.
  • 3. Environmental Biochemistry and Toxicology Unit, Department of Biochemistry, Federal University of Technology, Owerri, Nigeria.

Description

The heavy metal lead (Pb) is a common environmental pollutant with widespread distribution, and oxidative stress has been implicated in the pathogenesis of its toxicity. The ameliorative effect of nutritional contents of palm oil and cod liver oil (dietary supplements) following exposure to sublethal concentration of Pb on adult Wistar albino rats was studied. Toxicity was induced by administering intraperitoneally, 30 mg/kg body weight of lead acetate at alternate days for 21 days. Groups treated with supplements received daily oral dose of 2.5 ml palm oil or cod liver oil or 1.25 ml palm oil and 1.25 ml cod liver oil (synergy). Increased activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, decreased activities of superoxide dismutase, catalase, glutathione peroxidase and increased concentrations of total bilirubin and lipid peroxidation product were observed in Pb exposed rats without nutritional supplement treatment. However, these negative oxidative states were ameliorated in rats by the concomitant administration of nutritional supplements, singly and in combination. Furthermore, non-significant changes were observed in the haematological parameters determined. These observations indicate potential therapeutic benefits in the use of palm oil and cod liver oil in the management of lead-induced toxicity.

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