Heavy metal exposure is a significant health concern due to its presence in soil and water, leading to various toxic effects. This review discusses the molecular pathways of heavy metal-induced cellular damage, its relationship with aging, and protective strategies. Heavy metals, such as lead, chromium, cadmium, mercury, and arsenic, damage cells through oxidative stress, mitochondrial dysfunction, apoptosis, and endoplasmic reticulum (ER) stress. These processes are interconnected and contribute to cellular senescence and aging. Recent studies have shown that heavy metal exposure can induce oxidative stress, leading to DNA damage, protein modifications, and lipid peroxidation. Antioxidants and other protective agents have been found to mitigate heavy metal-induced damage. Heavy metals disrupt the redox balance by impairing antioxidant systems and increasing reactive oxygen species (ROS). Ferroptosis, an iron-dependent form of cell death, is also induced by heavy metals, leading to cellular damage. Heavy metal exposure can also trigger ER stress, which activates autophagy or mitophagy. Additionally, heavy metals induce apoptosis, necrosis, and necroptosis, which are part of the molecular cascade of heavy metal toxicity. These processes are influenced by various signaling pathways and can lead to cellular dysfunction and organ damage. Chronic exposure to heavy metals can cause a range of clinical disorders, including neurological damage, cardiovascular issues, chronic kidney disease, hepatitis, and reproductive problems. Heavy metals also contribute to cancer development through oxidative stress and genomic instability. Protective strategies include chelation therapy, which removes heavy metals from the body, and antioxidants that reduce oxidative stress. Recent advances in molecular pathways have highlighted the potential of new compounds targeting oxidative stress to protect against heavy metal-induced damage. This review emphasizes the importance of understanding the molecular mechanisms of heavy metal toxicity and the need for effective protective strategies to mitigate its harmful effects on human health.Heavy metal exposure is a significant health concern due to its presence in soil and water, leading to various toxic effects. This review discusses the molecular pathways of heavy metal-induced cellular damage, its relationship with aging, and protective strategies. Heavy metals, such as lead, chromium, cadmium, mercury, and arsenic, damage cells through oxidative stress, mitochondrial dysfunction, apoptosis, and endoplasmic reticulum (ER) stress. These processes are interconnected and contribute to cellular senescence and aging. Recent studies have shown that heavy metal exposure can induce oxidative stress, leading to DNA damage, protein modifications, and lipid peroxidation. Antioxidants and other protective agents have been found to mitigate heavy metal-induced damage. Heavy metals disrupt the redox balance by impairing antioxidant systems and increasing reactive oxygen species (ROS). Ferroptosis, an iron-dependent form of cell death, is also induced by heavy metals, leading to cellular damage. Heavy metal exposure can also trigger ER stress, which activates autophagy or mitophagy. Additionally, heavy metals induce apoptosis, necrosis, and necroptosis, which are part of the molecular cascade of heavy metal toxicity. These processes are influenced by various signaling pathways and can lead to cellular dysfunction and organ damage. Chronic exposure to heavy metals can cause a range of clinical disorders, including neurological damage, cardiovascular issues, chronic kidney disease, hepatitis, and reproductive problems. Heavy metals also contribute to cancer development through oxidative stress and genomic instability. Protective strategies include chelation therapy, which removes heavy metals from the body, and antioxidants that reduce oxidative stress. Recent advances in molecular pathways have highlighted the potential of new compounds targeting oxidative stress to protect against heavy metal-induced damage. This review emphasizes the importance of understanding the molecular mechanisms of heavy metal toxicity and the need for effective protective strategies to mitigate its harmful effects on human health.