Beneficial effects of Androctonus australis hector venom and its non-toxic fraction in the restoration of early hepatocyte-carcinogenesis induced by FB1 mycotoxin: Involvement of oxidative biomarkers

Some venom components are known to present potential biological activities that are useful as tools in therapeutics. In this study anti-tumoral activity of Androctonus australis hector (Aah) venom and its purified fraction on early step of hepato-carcinogenesis initiated by Fumonisin (FB1), was tested. Initiated hepatic tumor was assessed in mice by decreased doses of Fumonisin B1 associated to phenobarbital. Scorpion venom was used to investigate its activity on initiated tumor by FB1. Evaluation of oxidative unbalance, enzymatic activities and DNA quantification in the liver were correlated with tissue analysis. Obtained results showed that the initiated pathogenesis by FB1 at seven months was characterized by tissue alterations and biomarker variations. These alterations were characterized by atypical lesions such as muffled nucleus, karyo- and cyto-megaly; up normal and large number of nuclei into hepatocytes. These alterations were confirmed by DNA alteration. An unbalance of oxidative status was also observed, characterized by an increased levels of respectively oxidant (NO and MDA) and antioxidant (GSH and catalase activity) mediators. Aah venom and its non-toxic fraction used at low doses seemed to be able to restore partially the hepatic altered tissue induced by FB1. Decreased levels of oxidative and anti-oxidative mediators were also observed. DNA in hepatocytes returned also to the physiological values. Structure of hepatic tissue showed restoration of some alterations such as karyo- and cyto-megaly; decrease of polyploidy hepatocytes induced by FB1. Aah venom and its non-toxic fraction seem to contain some bioactive components with anti-tumoral activity. Purification of this activity from non-toxic fraction F1 could be of interest to identify the components with anti-tumoral activities. (C) 2015 Elsevier Inc. All rights reserved.