Mercury Toxicity: Comparative Insights into Inorganic and Organic Forms with Emphasis on Minamata Disease

Abstract

Mercury toxicity manifests in two primary chemical forms: inorganic (elemental mercury and mercury salts) and organic (alkylated compounds, especially methylmercury). Each form exhibits distinct toxicological profiles and clinical manifestations. Inorganic mercury toxicity has been historically recognized, notably during the Industrial Revolution, affecting workers such as the “Mad Hatters,” with symptoms including neurological, psychological, and motor disturbances collectively known as erethism. Organic mercury toxicity, particularly from methylmercury exposure via contaminated seafood, gained prominence in the mid-20th century with devastating outbreaks like the Minamata disease in Japan and mass poisoning in Iraq. Methylmercury bioaccumulates and biomagnifies in the food chain, crossing critical biological barriers and causing irreversible neurological damage, especially in fetuses and children. Irreversible suppression of selenium enzymes is the main mechanism of mercury toxicity, resulting in oxidative stress and brain degeneration.Clinical presentations range from sensory disturbances and ataxia to cognitive decline and severe neurodevelopmental defects. Diagnosis relies on exposure history, clinical symptoms, and biomonitoring of mercury levels, with differing approaches for inorganic and organic mercury. The Minamata disaster underscores the environmental and public health challenges posed by industrial mercury pollution, emphasizing the need for vigilant regulation and preventive strategies.