Cadmium Toxicity: Mechanisms of Oxidative Stress, Inflammation, and Organ Damage
Farahat, Y., El-Sayed, N., Hazem, R., Mehanna, E., Radwan, A. (2025). Cadmium Toxicity: Mechanisms of Oxidative Stress, Inflammation, and Organ Damage. EKB Journal Management System, 9(3), 40-49. doi: 10.21608/rpbs.2025.374101.1367
Yomna A. Farahat; Norhan Mohamed El-Sayed; Reem Hazem; Eman T. Mehanna; Asmaa Radwan. "Cadmium Toxicity: Mechanisms of Oxidative Stress, Inflammation, and Organ Damage". EKB Journal Management System, 9, 3, 2025, 40-49. doi: 10.21608/rpbs.2025.374101.1367
Farahat, Y., El-Sayed, N., Hazem, R., Mehanna, E., Radwan, A. (2025). 'Cadmium Toxicity: Mechanisms of Oxidative Stress, Inflammation, and Organ Damage', EKB Journal Management System, 9(3), pp. 40-49. doi: 10.21608/rpbs.2025.374101.1367
Farahat, Y., El-Sayed, N., Hazem, R., Mehanna, E., Radwan, A. Cadmium Toxicity: Mechanisms of Oxidative Stress, Inflammation, and Organ Damage. EKB Journal Management System, 2025; 9(3): 40-49. doi: 10.21608/rpbs.2025.374101.1367

Cadmium Toxicity: Mechanisms of Oxidative Stress, Inflammation, and Organ Damage

Records of Pharmaceutical and Biomedical Sciences
Volume 9, Issue 3, March 2025, Page 40-49  XML PDF (614.24 K)
Document Type: Mini-reviews
DOI: 10.21608/rpbs.2025.374101.1367
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Authors
Yomna A. Farahat email 1; Norhan Mohamed El-Sayedorcid 2; Reem Hazemorcid 3; Eman T. Mehannaorcid 4; Asmaa Radwanorcid 5
1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia, Egypt
2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia 41522, Egypt
3Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia, 41522, Egypt.
4Department of Biochemistry, Faculty of Pharmacy, Suez Canal University, Ismailia, 41522, Egypt
5Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University
Abstract
Cadmium (Cd) is present in the environment in substantial quantities as a consequence of human activities, including the incineration of metal ores, the use of fossil fuels, and the burning of waste. Cd is a persistent heavy metal that does not degrade into less toxic forms and is excreted inefficiently from the body, leading to its bioaccumulation. Exposure to Cd can cause itai-itai disease and multiple organ dysfunction, including the lungs, testes, prostate, cardiovascular system, skeletal system, nervous system, and immune system. However, the primary sites of Cd accumulation are the liver, lungs, kidneys, and bones. At the cellular level, Cd induces toxicity through several mechanisms. One of the major pathways is the induction of oxidative stress, characterized by the excessive generation of reactive oxygen species (ROS) that overwhelm the cell’s antioxidant defense systems. This oxidative imbalance damages vital cellular components such as lipids, proteins, and DNA, leading to functional impairment and structural instability. In addition, Cd triggers inflammatory responses by activating pro-inflammatory signaling pathways and promoting cytokine production, contributing to chronic tissue inflammation and further exacerbating cellular injury. These disturbances disrupt cellular homeostasis and shift the balance toward cell death over survival, ultimately resulting in tissue and organ damage. This review aims to discuss the complex cellular events underlying Cd toxicity and their implications for human health.
Keywords
Toxicity; Oxidative stress; Inflammation; Apoptosis
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