Abstract

Applications of medicinal uses of metals and their complexes have been gaining major clinical significance, especially during the COVID-19 pandemic. The ligation behavior of quercetin (Q), a flavonoid, and Zn metal, i.e., the Zn/Q complex, was fully characterized based on molar conductance, infrared (IR) spectra, elemental analysis, electronic spectra, thermogravimetric analysis, proton nuclear magnetic resonance (1H-NMR), and transmission electron microscopy (TEM) in our lab. Hepatotoxicity was induced by cadmium (CdCl2). A total of 40 male albino rats were randomly distributed into the following four groups: Control, hepatotoxic group (CdCl2), Zn/Q-treated group, and group treated with a combination of CdCl2 and Zn/Q. Serum hepatic enzymes (AST, ALT, and LDH), total protein, and enzymatic and nonenzymatic antioxidant levels were determined. Histology and TEM for hepatic tissues, in addition to the gene expression of SOD as an antioxidant enzyme in the hepatic tissues, were evaluated. The Q/Zn treatment demonstrated potent protective effects against CdCl2-induced sever oxidative stress and suppressed hepatic toxicity, genotoxicity, liver enzyme disturbances, and structural alterations. In conclusion, the Zn/Q complex produced a high potent antioxidant effect against the oxidative injury and genotoxicity induced by CdCl2 and could be considered to be a potent ameliorative hepatoprotective agent against CdCl2 hepatotoxicity, which could be beneficial during the COVID-19 pandemic.

Highlights

  • Cadmium (Cd) is a widespread heavy metal [1]

  • Several studies have demonstrated that exposure to CdCl2 results in large amounts of excessive free radical generation, eliciting high oxidative stress in almost all the body systems [4,5]

  • We investigated the impact of Cd exposure on the liver, as well as the potential ameliorative effect of a novel Zn/Q complex on Cd-induced hepatic toxicity

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Summary

Introduction

Cadmium (Cd) is a widespread heavy metal [1]. Cd has been listed among the toxic chemicals recognized by the WHO [1]. Mclellan et al [2] demonstrated that Cd absorption by humans occurs very slowly after oral exposure, generating cumulative hepatotoxicity. Studies have reported that Cd mainly accumulates in hepatic tissues [3]. Several studies have demonstrated that exposure to CdCl2 results in large amounts of excessive free radical generation, eliciting high oxidative stress in almost all the body systems [4,5]. Cadmium has the ability to elevate both p53 and Bax gene levels and decrease the gene expression of Bcl-2, elevating the cellular apoptosis [6]

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