Possible Ameliorative Effects of the Royal Jelly on Hepatotoxicity and Oxidative Stress Induced by Molybdenum Nanoparticles and/or Cadmium Chloride in Male Rats

SIMPLE SUMMARY: The aim of the present investigation is valuable due to the importance of possible contaminations and negative effects of these cadmium chloride and molybdenum nanoparticles. The physicochemical properties of molybdenum nanoparticles have been characterized, as well as their ultrastructural organization. A rat experimental model was then employed to assess the liver toxicity of molybdenum nanoparticles, even in combination with CdCl(2). The toxicity of molybdenum nanoparticles and cadmium chloride was estimated via liver damage by means of chemico-biological markers of liver injury, serum lipids, inflammation, oxidative status, and histological and immunohistochemistry patterns. Moreover, the possible effects of royal jelly were evaluated. The results clarified that both chemicals induced hepatic toxicity with the excessive triggering of reactive oxygen species that induced severe oxidative injury, histological alterations in the hepatic structure, and hepatic ultrastructure. These results are concurrent with obtaining normal biochemical levels in groups either treated with royal jelly or even a combination of royal jelly and two xenobiotics. The royal jelly is considered an essential potential source of natural antioxidants capable of frustrating the effects of oxidative injury, which is considered the main cause of many diseases. ABSTRACT: The present study aimed to investigate the effect of the royal jelly (RJ) on hepatotoxicity induced by molybdenum nanoparticles (MoO(3)-NPs), cadmium chloride (CdCl(2)), or their combination in male rats at biochemical, inflammation, immune response, histological, and ultrastructural levels. The physicochemical properties of MoO(3)-NPs have been characterized, as well as their ultrastructural organization. A rat experimental model was employed to assess the liver toxicity of MoO(3)-NPs, even in combination with CdCl(2). Different cellular studies indicate divergent mechanisms, from increased reactive oxygen species production to antioxidative damage and cytoprotective activity. Seventy male rats were allocated to groups: (i) control; (ii) MoO(3)-NPs (500 mg/kg); (iii) CdCl(2) (6.5 mg/kg); (iv) RJ (85 mg/kg diluted in saline); (v) MoO(3)-NPs followed by RJ (30 min after the MoO(3)-NPs dose); (vi) CdCl(2) followed by RJ; and (vii) a combination of MoO(3)-NPs and CdCl(2), followed by RJ, for a total of 30 successive days. Hepatic functions, lipid profile, inflammation marker (CRP), antioxidant biomarkers (SOD, CAT, GPx, and MDA), and genotoxicity were examined. Histological changes, an immunological marker for caspase-3, and transmission electron microscope variations in the liver were also investigated to indicate liver status. The results showed that RJ alleviated the hepatotoxicity of MoO(3)-NPs and/or CdCl(2) by improving all hepatic vitality markers. In conclusion, the RJ was more potent and effective as an antioxidant over the oxidative damage induced by the combination of MoO(3)-NPs and CdCl(2).