Mitigation of cadmium-induced hepatotoxicity by orally administered Xylopia aethiopica synthesized silver nanoparticles in rats.

Cadmium is a major environmental pollutant that results in hepatic necrosis by mediating oxidative stress and inflammation. Xylopia aethiopica is a natural plant that has been reported to have a wide range of pharmacological properties. The study aimed at determining the ameliorative potential of Xylopia aethiopica synthesized silver nanoparticles (Xa-AgNPs) against hepatotoxicity induced by cadmium in rats. Thirty male Wistar rats were randomly grouped into six (n = 5). I: served as control, II: received 10 mg/kg of silymarin only, III, IV, V, and VI were given 20 mg/kg b.wt of cadmium chloride (CdCl) orally for seven consecutive days. After which, IV, V, and VI were treated with 10 mg/kg bwt of silymarin, 5 and 10 mg/kg Xa-AgNPs consecutively for 21 days. Synthesized silver nanoparticles were characterized. Biomarkers were determined as well as histological examination. X-ray diffraction revealed that the structure of silver nanoparticles is spherical and polydispersed. Scanning electron microscope confirmed the spherical nature, size and, the crystallinity of nanoparticles. The average size of nanoparticles, 2.13 nm, was recorded. Oral administration of CdCl caused significant (p < 0.05) increase of alanine transaminase (ALT) and aspartate aminotransferase (AST), arginase, serum albumin, and γ-glutamyl transferase (GGT) activities compared with normal control. Also, malondialdehyde (MDA) increased in Cd-induced only against treatment groups. Conversely, administration of 10 mg/kg of Xa-AgNPs and silymarin respectively reversed these changes with significant (p < 0.05) reduction of MDA, ALT and elevation of serum albumin, increase activities of superoxide dismutase (SOD), and catalase(CAT) in test groups against Cd-induced only. Similarly, arginase, and GGT activities increased in test groups compared with the Cd-induced only. Therefore, it can be ascertained that Xa-AgNPs ameliorate Cd-induced hepatotoxicity in rats.