In the olfactory epithelium the primary olfactory neurones are in contact with the environment and via the axonal projections they are also connected to the olfactory bulbs of the brain. Therefore, the primary olfactory neurones provide a pathway by which foreign materials may gain access to the brain. In the present study we used autoradiography and gamma spectrometry to show that intranasal instillation of manganese (54Mn2+) in rats results in initial uptake of the metal in the olfactory bulbs. The metal was then seen to migrate via secondary and tertiary olfactory pathways and via further connections into most parts of the brain and also to the spinal cord. Intranasal instillation of cadmium (109Cd2+) resulted in uptake of the metal in the anterior parts of the olfactory bulbs but not in other areas of the brain. This indicates that this metal is unable to pass the synapses between the primary and secondary olfactory neurones in the bulbs. Intraperitoneal administration of 54Mn2+ or 109Cd2+ showed low uptake of the metals in the olfactory bulbs, an uptake not different from the rest of the brain. Manganese is a neurotoxic metal which in man can induce an extrapyramidal motor system dysfunction associated with occupational inhalation of manganese-containing dusts or fumes. We propose that the neurotoxicity of inhaled manganese is related to an uptake of the metal into the brain via the olfactory pathways. In this way manganese can circumvent the blood-brain barrier and gain direct access to the central nervous system.
We fed immature 1+ arctic charr with a single dose of
methyl[203Hg]mercury (MeHg) and quantified distribution
kinetics with a new and simple three-compartment caternary
model having well-perfused viscera and blood as the
central compartment (VB), whereas gut (G) and the rest
of body (R) constituted the peripheral compartments. The
model accurately described distribution kinetics of
MeHg in the fish, using either data of MeHg content in
compartments or blood concentration data. Despite the
known fast translocation of MeHg between binding sites
at the molecular level, its translocation rate between
compartments was surprisingly slow, 27 days being needed
to complete 95% of the transfer from gut to blood and
48 days for the subsequent transfer to compartment R. This
probably results from a limitation of the stepwise transfer
rate of MeHg from red blood cells, which contain most
of blood MeHg, to plasma and then to tissues due to low
plasmatic concentration of small mobile sulfhydryl
ligands. The model presented is a convenient tool that
could be used to compare the fate of MeHg and other
organometals, such as butyltins and alkylleads, in various
aquatic and terrestrial animal species.
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