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<p>Cadmium (Cd) is a heavy metal that adversely affects the environment, as well as the cellular and metabolic systems of organisms. Cadmium salts, such as cadmium chloride (CdCl<sub>2</sub>; CD), are one of the most common pollutants. As CD is not easily degradable, its risk to humans via food-chain contamination is constantly increasing. Crocin (CRO), a potent antioxidant, is isolated from saffron, an important spice rich in carotenoids, commonly consumed globally and used as a drug to treat numerous diseases. This study mainly examined the amelioration of hepatotoxicity and oxidative stress damage induced by CD in male rats by CRO administration. CRO was chemically characterised using Infrared (FT-IR), ultraviolet (UV–Vis), X-Ray diffraction (XRD), Scanning Electron microscope (SEM), and Transmission electron microscope (TEM); it was confirmed to contain hydroxyl, ketonic ester and glycoside groups. Twenty-four male albino rats were randomised into the following groups. Control, CD (5&#xa0;mg/kg), CRO (50&#xa0;mg/kg), CD plus CRO at the same dose. At the end, liver and blood samples were analysed for biochemical, molecular and histological variations, revealing that CD administration notably reduced hepatic superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) levels. Meanwhile, along with hyperlipidemia, Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Lactate dehydrogenase (LDH) and Alpha-Fetoprotein (AFP) activities, and malonyldialdehyde levels (MDA) were elevated. Histopathology of liver sections revealed inflammatory cell infiltration, hepatocellular necrosis and areas of haemorrhage. Furthermore, significant induction of mammalian target of rapamycin (mTOR) and ATK1 protein kinase, which is part of the AKT subfamily of serine/threonine kinases and is involved in many signalling pathways essential for normal cell function, was observed in comparison to the control group. Meanwhile, a marked decline in beclin, autophagy-related protein light chain 3 (LC3 II) a protein involved in autophagy and cell metabolism, and Phosphatase and Tensin homolog “PTEN”-induced kinase 1 levels was detected in the hepatocytes. Western blots revealed an enhanced release of cytochrome c from the CD group compared with the CRO-treated group. In contrast to CRO-based improvement, significant hepatic amelioration was observed, with a decline in hepatocellular congestion post-CRO administration; meanwhile, no hepatocellular haemorrhage or hepatic necrosis was observed. In summary, CRO alleviated CD-induced hepatic injury due to its potent antioxidant capacities and hepatoprotective activities.</p>

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Ameliorative effects of Crocin as a potent antioxidant with its spectral characterization against Cadmium chloride-induced hepatotoxicity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • Reham Z. Hamza,
  • Samy M. El-Megharbel,
  • Bander Albogami,
  • Eman H. Al-Thubaiti,
  • Seham S. AlZahrani,
  • Khadeejah Alsolami,
  • Najah M. Albaqami,
  • Dalal Sulaiman Alshaya,
  • Jawaher J. Albaqami,
  • Abd El-Aziz A. Diab,
  • Mai S. Attia

摘要

Cadmium (Cd) is a heavy metal that adversely affects the environment, as well as the cellular and metabolic systems of organisms. Cadmium salts, such as cadmium chloride (CdCl2; CD), are one of the most common pollutants. As CD is not easily degradable, its risk to humans via food-chain contamination is constantly increasing. Crocin (CRO), a potent antioxidant, is isolated from saffron, an important spice rich in carotenoids, commonly consumed globally and used as a drug to treat numerous diseases. This study mainly examined the amelioration of hepatotoxicity and oxidative stress damage induced by CD in male rats by CRO administration. CRO was chemically characterised using Infrared (FT-IR), ultraviolet (UV–Vis), X-Ray diffraction (XRD), Scanning Electron microscope (SEM), and Transmission electron microscope (TEM); it was confirmed to contain hydroxyl, ketonic ester and glycoside groups. Twenty-four male albino rats were randomised into the following groups. Control, CD (5 mg/kg), CRO (50 mg/kg), CD plus CRO at the same dose. At the end, liver and blood samples were analysed for biochemical, molecular and histological variations, revealing that CD administration notably reduced hepatic superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) levels. Meanwhile, along with hyperlipidemia, Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Lactate dehydrogenase (LDH) and Alpha-Fetoprotein (AFP) activities, and malonyldialdehyde levels (MDA) were elevated. Histopathology of liver sections revealed inflammatory cell infiltration, hepatocellular necrosis and areas of haemorrhage. Furthermore, significant induction of mammalian target of rapamycin (mTOR) and ATK1 protein kinase, which is part of the AKT subfamily of serine/threonine kinases and is involved in many signalling pathways essential for normal cell function, was observed in comparison to the control group. Meanwhile, a marked decline in beclin, autophagy-related protein light chain 3 (LC3 II) a protein involved in autophagy and cell metabolism, and Phosphatase and Tensin homolog “PTEN”-induced kinase 1 levels was detected in the hepatocytes. Western blots revealed an enhanced release of cytochrome c from the CD group compared with the CRO-treated group. In contrast to CRO-based improvement, significant hepatic amelioration was observed, with a decline in hepatocellular congestion post-CRO administration; meanwhile, no hepatocellular haemorrhage or hepatic necrosis was observed. In summary, CRO alleviated CD-induced hepatic injury due to its potent antioxidant capacities and hepatoprotective activities.