Effects of Methylmercury on the Microvasculature of the Developing Brain

• Published in: Neurotoxicology (Park Forest South) 2004-09, Vol.25 (5), p.849-857
• Main Authors: Bertossi, M, Girolamo, F, Errede, M, Virgintino, D, Elia, G, Ambrosi, L, Roncali, L
• Format: Article
• Language: English
• Subjects: Animals; Astrocytes; Biological and medical sciences; Blood-Brain Barrier - physiology; Blood–brain barrier; Brain - growth & development; Brain - pathology; Capillaries - pathology; Cerebellum; Cerebellum - blood supply; Cerebellum - growth & development; Cerebellum - pathology; Cerebrovascular Circulation - drug effects; Chemical and industrial products toxicology. Toxic occupational diseases; Chick Embryo; Development; Horseradish Peroxidase - metabolism; Image Processing, Computer-Assisted; Medical sciences; Mercury - analysis; Mercury - pharmacokinetics; Mercury Poisoning - pathology; Metals and various inorganic compounds; Methylmercury; Methylmercury Compounds - toxicity; Microscopy, Electron; Neurotoxicity; Purkinje Cells - metabolism; Purkinje Cells - pathology; Spectrophotometry, Atomic; Toxicology
• ISSN: 0161-813X; 1872-9711
• DOI: 10.1016/j.neuro.2004.01.005

The study, undertaken with the aim of further investigating the effects of methylmercury (MeHg) exposure on the developing brain, was performed in the cerebellum of chick embryos, chronically treated with a MeHgCl solution dropped onto the chorioallantoic membrane, and in control embryo cerebella. Quantitative evaluations, performed by cold vapour atomic absorption spectrophotometry, demonstrated a high mercury content in the chorioallantoic membrane, encephalon, liver and kidney of the treated embryos. The morphological observations showed severe neuronal damage consisting of degenerative changes of the granules and Purkinje neurons. The effects on astrocytes were even more severe, since they were extremely rare both in the neuropil and around the vessel wall. Compared with the controls, the cerebellar vessels of MeHg-treated embryos showed immature morphology, poor differentiation of endothelial barrier devices, and high permeability to the exogenous protein horseradish peroxidase. These findings support the hypothesis that MeHg-related neuronal sufferance may be secondary to astrocytic damage and suggest that the developmental neurotoxicity of this compound could also be related to astrocyte loss-dependent impairment of blood–brain barrier (BBB) differentiation.