Dietary Supplementation of Calendula officinalis Counteracts the Oxidative Stress and Liver Damage Resulted from Aflatoxin

This study was conducted to evaluate the total phenolic compounds, the antioxidant properties, and the hepatorenoprotective potential of Calendula officinalis extract against aflatoxins (AFs-) induced liver damage. Six groups of male Sprague-Dawley rats were treated for 6 weeks included the control; the group fed AFs-contaminated diet (2.5？mg/kg diet); the groups treated orally with Calendula extract at low (CA1) and high (CA2) doses (500 and 1000？mg/kg？b.w); the groups treated orally with CA1 and CA2 one week before and during AFs treatment for other five weeks. The results showed that the ethanol extract contained higher phenolic compounds and posses higher 1,1-diphenyl 1-2-picryl hydrazyl (DPPH) radical scavenging activity than the aqueous extract. Animals fed AFs-contaminated diet showed significant disturbances in serum biochemical parameters, inflammatory cytokines, and the histological and histochemical pictures of the liver accompanied by a significant increase in malondialdehyde (MDA) and a significant decrease in superoxide dismutase (SOD) and glutathione peroxidase (GPx) in liver. Calendula extract succeeded to improve the biochemical parameters, inflammatory cytokines, decreased the oxidative stress, and improved the histological pictures in the liver of rats fed AFs-contaminated diet in a dose-dependent manner. It could be concluded that Calendula extract has potential hepatoprotective effects against AFs due to its antioxidant properties and radical scavenging activity. 1. Introduction Mycotoxins are fungal metabolites toxic to humans and animals, commonly found as contaminants of food or feed [1]. Aflatoxins (AFs) are principally produced by Aspergillus flavus and Aspergillus parasiticus. Among these, aflatoxin B1 (AFB1) is the predominant form as cereal and oilseed contaminants and presents the highest toxic potential [1], being hepatotoxic and carcinogenic in human and animals [2]. The biotransformation of AFB1 by liver microsomal enzymes resulted in toxic metabolites AFB1-8, 9-epoxide. The toxic effects of AFs mostly arise from the binding of this particular epoxide derivative to cellular macromolecules such as DNA and proteins [3]. AFB1 is classified by the International Agency of Research on Cancer (IARC) as Group 1 carcinogen [4]. This mycotoxin is also mutagenic, teratogenic, and immunosuppressive in farm and laboratory animals [5] and mainly affects the cell-mediated immunity [6]. Reactive oxygen species such as the hydroxyl radical, superoxide anion, and hydrogen peroxide, which are generated as a result of this metabolism, are