Abstract
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.
Original language | English (US) |
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Title of host publication | Diet and Nutrition in Neurological Disorders |
Publisher | Elsevier |
Pages | 387-410 |
Number of pages | 24 |
ISBN (Electronic) | 9780323898348 |
ISBN (Print) | 9780323915717 |
DOIs | |
State | Published - Jan 1 2023 |
Keywords
- Calcium gradients
- Crypts
- Developmental lead exposure
- Gastrointestinal system
- Hyaluronic acid
- Lead absorption
- Lead neurotoxicity
- Lead poisoning
- Perinatal lead exposure
- Villi
ASJC Scopus subject areas
- General Medicine
- General Neuroscience