Ameliorative effects of quercetin against hepatic toxicity of oral sub-chronic co-exposure to aluminum oxide nanoparticles and lead-acetate in male rats

• Published in: Naunyn-Schmiedeberg's archives of pharmacology Vol. 396; no. 4; pp. 737 - 747
• Main Authors: Abo-EL-Sooud, Khaled, Abd-Elhakim, Yasmina M., Hashem, Mohamed M. M., El-Metwally, Abeer E., Hassan, Bayan A., El-Nour, Hayat H. M.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.04.2023; Springer Nature B.V
• Subjects: Acetates - pharmacology; Alanine transaminase; Alkaline phosphatase; Aluminum oxide; Aluminum Oxide - metabolism; Aluminum Oxide - toxicity; Animals; Antioxidants - metabolism; Antioxidants - pharmacology; Aspartate aminotransferase; Bilirubin; Biomedical and Life Sciences; Biomedicine; Chemical and Drug Induced Liver Injury - drug therapy; Chemical and Drug Induced Liver Injury - etiology; Chemical and Drug Induced Liver Injury - prevention & control; Cholesterol; Glutathione peroxidase; Hepatitis - metabolism; Hepatotoxicity; High density lipoprotein; Lead; Lead - metabolism; Lead - pharmacology; Lipid peroxidation; Lipoproteins (very low density); Liver; Low density lipoprotein; Male; Nanoparticles; Neurosciences; Oxidative Stress; Pharmacology/Toxicology; Quercetin; Quercetin - pharmacology; Rats; Rats, Sprague-Dawley; Serum levels; Toxicants; Triglycerides; Oxidative stress; Lead acetate; Liver; Aluminum oxide nanoparticles; Quercetin
• ISSN: 0028-1298; 1432-1912
• DOI: 10.1007/s00210-022-02351-y

The present study was designed to evaluate the probable ameliorative role of quercetin (QCN) against oxidative hepatotoxicity induced by aluminum oxide nanoparticles (Al 2 O 3 NPs) with a diameter < 30 nm and lead acetate (Pb) co-exposure in adult male Sprague–Dawley rats. Rats were weighed and allocated to seven groups ( n  = 10 each) and were treated orally via orogastric gavage for 60 successive days: rats of the 1st group were kept as control given distilled water (1 ml/kg), rats of the 2nd group received 2 ml/kg BW/day corn oil; rats of the 3rd group were administered 20 mg/kg BW QCN/day; rats of the 4th group received 100 mg/kg BW Al 2 O 3 NPs; rats of the 5th group received 50 mg/kg BW Pb; rats of the 6th group co-received Al 2 O 3 NPs and Pb at the same previous doses; and rats of the 7th group were co-administered Al 2 O 3 NPs, Pb, and QCN at the same previous doses. At the end of the experiment, serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total, direct, indirect bilirubin, triglycerides, total cholesterol, HDL, VLDL, and LDL were estimated. The hepatic oxidative stress biomarkers as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPx), were also evaluated. Finally, the histopathological and histomorphometric evaluations and the residues of Al and Pb in hepatic tissues were assessed. Al 2 O 3 NPs and/or Pb exposure significantly elevated lipid peroxidation levels and considerably altered the hepatic biochemical parameters; nevertheless, QCN significantly reduced hepatic enzymes compared to toxicant exposed groups. Additionally, QCN significantly improved Al 2 O 3 NPs-afforded liver tissue damage, as established in microscopic findings on the liver in the group treated with Al 2 O 3 NPs + Pb. Conclusively, QCN could be a candidate natural agent to safeguard the liver versus the co-harmful impacts of Al 2 O 3 NPs and Pb toxicity.