Dietary effects of lead as a neurotoxicant

The neurotoxicant lead (Pb²⁺) disrupts neural development with lasting impacts across the life span. Chronic low-level Pb2+ exposures remain a concern in the United States, especially for minority and economically disadvantaged communities. Ingestion is the major route of Pb²⁺ entry into an organism. Gastrointestinal (GI) Pb²⁺ absorption occurs, in part, through calcium (Ca²⁺) transcellular and paracellular pathways. Transcellular absorption means that Pb²⁺ is present intracellularly, at least transiently, where it can attach to Ca²⁺-binding and other proteins, potentially altering many physiological functions. Previously, Pb²⁺-induced pathophysiological changes in the structure of the villi and crypts have been observed, altering the surface area that might influence nutrient absorption, gut microbiota regulation, infection prevention, and gut-brain toxicokinetics. Currently, the molecular pathways for the effects of Pb²⁺ at low levels of exposure remain to be elucidated. The present study provides histological evidence of low-level perinatal Pb2+ exposure dysregulating the GI tract in both sex- and dose-dependent manners in a rat model of childhood low-level Pb2+ poisoning.