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

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.