Protective Strategies Against Cadmium Chloride-Induced Hepatic Injury: Role of Antioxidants and Experimental Evidence

Cadmium chloride (CdCl) is among the most toxic heavy metals in the environment and is extremely harmful even in very small concentrations due to prolonged biological half-life and cumulative characteristics. Something important in cadmium contamination of environment has been rapid industrialization and mining, metal coating (electroplating), production of batteries, pigment synthesis, phosphate fertilizers and use of tobacco as these have been the major ways of introducing cadmium into the air land water, agricultural products, etc. Cadmium exposure leads to deposition mostly in liver and kidney tissues from where it slowly moves out and affects other target organs too. Since the liver has been described as one of the major organs of processing foreign compounds (xenobiotics), neutralizing the foreign body's toxins (detoxification), metabolizing nutrients and managing bodily metabolism, it is most targeted organ in cadmium toxicity. Oxygen free radicals are key in liver cell death (hepatocytelysis) by CdCl via mechanisms such as depletion of antioxidant reserves, generation of intracellular ROS (reactive oxygen species) inflammation DNA damage, peroxidaion in lipids, and apoptosis at the cell level. Experimental studies have been reporting high levels of hepatic enzymes in blood, extensive changes at the tissue level (histopathology), mitochondrial damage and liver fibrosis due to cadmium exposure. These changes are the result of an overall weakening of liver function by the cadmium and may lead ultimately to liver-related illnesses or even liver cancer. This paper reviews the present literature on the use of antioxidants to counteract cadmium-induced damage to the liver. Focus areas included the measurement of oxidative stress, the role of endogenous anti-oxidant defenses, the microscopic appearance of liver tissues before and after cadmium exposure, the molecular basis of hepatic protection, and the newest treatment possibilities of liver injury due to cadmium. The review also outlines the shortcomings of present research, translational barriers, and the future directions which will hopefully lead to new prevention and therapies for liver damage caused by cadmium.

Authors

Publication Details

Journal
Zenodo (CERN European Organization for Nuclear Research)
Published
2026-07-28
DOI
https://doi.org/10.5281/zenodo.21643304
Primary Topic
Heavy Metal Exposure and Toxicity
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Protective Strategies Against Cadmium Chloride-Induced Hepatic Injury: Role of Antioxidants and Experimental Evidence

A. K. Patra, Dr. Yeduru Krishnan Reddy
Zenodo (CERN European Organization for Nuclear Research)
Heavy Metal Exposure and Toxicity
article

Protective Strategies Against Cadmium Chloride-Induced Hepatic Injury: Role of Antioxidants and Experimental Evidence

A. K. Patra, Dr. Yeduru Krishnan Reddy
article en

Abstract

Cadmium chloride (CdCl) is among the most toxic heavy metals in the environment and is extremely harmful even in very small concentrations due to prolonged biological half-life and cumulative characteristics. Something important in cadmium contamination of environment has been rapid industrialization and mining, metal coating (electroplating), production of batteries, pigment synthesis, phosphate fertilizers and use of tobacco as these have been the major ways of introducing cadmium into the air land water, agricultural products, etc. Cadmium exposure leads to deposition mostly in liver and kidney tissues from where it slowly moves out and affects other target organs too. Since the liver has been described as one of the major organs of processing foreign compounds (xenobiotics), neutralizing the foreign body's toxins (detoxification), metabolizing nutrients and managing bodily metabolism, it is most targeted organ in cadmium toxicity. Oxygen free radicals are key in liver cell death (hepatocytelysis) by CdCl via mechanisms such as depletion of antioxidant reserves, generation of intracellular ROS (reactive oxygen species) inflammation DNA damage, peroxidaion in lipids, and apoptosis at the cell level. Experimental studies have been reporting high levels of hepatic enzymes in blood, extensive changes at the tissue level (histopathology), mitochondrial damage and liver fibrosis due to cadmium exposure. These changes are the result of an overall weakening of liver function by the cadmium and may lead ultimately to liver-related illnesses or even liver cancer. This paper reviews the present literature on the use of antioxidants to counteract cadmium-induced damage to the liver. Focus areas included the measurement of oxidative stress, the role of endogenous anti-oxidant defenses, the microscopic appearance of liver tissues before and after cadmium exposure, the molecular basis of hepatic protection, and the newest treatment possibilities of liver injury due to cadmium. The review also outlines the shortcomings of present research, translational barriers, and the future directions which will hopefully lead to new prevention and therapies for liver damage caused by cadmium.

Zenodo (CERN European Organization for Nuclear Research)
Openalex Percentile: Top 9%
Heavy Metal Exposure and Toxicity
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.