109Cd2+ was applied in the olfactory chambers of pikes (Esox lucius) and the dynamics of the axoplasmic flow of the metal was determined in the olfactory nerves by gamma spectrometry and autoradiography. The results showed that the 109Cd2+ is transported at a constant rate along the olfactory nerves. The profile of the 109Cd2+ in the nerves showed a wave front of transported metal followed by a saddle region. When the nasal chambers were washed 2 hr after application of the 109Cd2+ well-defined transport peaks for the metal were seen in the olfactory axons. The maximal velocity for the transport of 109Cd2+, which corresponds to the movement of the wave front, was 2.38 +/- 0.10 mm/hr (mean +/- S.E.) at the experimental temperature (10 degrees C). The average velocity for the transport of the 109Cd2+, which corresponds to the peak apex movement of the wave, was 2.18 +/- 0.05 mm/hr (mean +/- S.E.) at 10 degrees C. The transported 109Cd2+ was strongly accumulated in the anterior parts of the olfactory bulbs, whereas in other brain areas the levels of the metal remained low. Autoradiography of a pike exposed to 109Cd2+ via the water showed a strong labelling in the receptor-cell-containing olfactory rosettes, whereas other structures in the olfactory chambers were only weakly labelled. The accumulation and axonal transport in the olfactory neurons may be noxious and constitute an important component in the toxicology of cadmium in fish, and this may apply also to some other heavy metals.

We used whole-body autoradiography to study the distribution of 203Hg(II) in the central nervous system of brown (Salmo trutta) and rainbow (Oncorhynchus mykiss) trout. Fish were either exposed to waterborne Hg(II) for 7 and 21 d or they received an intravenous injection of the metal and were sacrificed 1 and 21 d later. Mercury did not accumulate in the brain after intravenous injection, indicating that the blood−brain barrier is impervious to Hg in plasma. In contrast, Hg was accumulated in specific areas of the brain (olfactory system, eminentia granulares and medulla of cerebellum, optic nerve and tectum, and rhombencephalon) and spinal cord (ventral horn ganglia) following water exposure. The specificity of the accumulation sites strongly suggests that waterborne Hg was taken up by water-exposed receptor cells of sensory nerves and subsequently transferred toward the brain by axonal transport, a normal physiological process for the transport of organelles and dissolved neuronal constituents along nerve axons. Accumulation of Hg in ventral horn ganglia is probably the result of leaching of metal from blood into muscle followed by uptake in motor plates. Axonal transport allows waterborne inorganic Hg, and possibly other xenobiotics, to circumvent the blood−brain barrier. Considering the importance of complex behavior in the life of fish, and the well-known deleterious effects of mercury on the nervous system, the toxicological significance of this uptake route needs to be assessed.

Brown trout (Salmo frutfa) were exposed to water containing 0.1 pg.L-' (1.8 nmo1.L-I) of s4Mn(Il) for 1, 3, or 6 weeks. Additional trout were exposed for 3 weeks and allowed to depurate for 1 or 3 weeks. Both the uptake and the organ distribution of manganese (Mn) were determined by gamma counting and whole-body autoradiography. Steady-state concentration, C,,, and biological half-life, f,,,, were calculated. The whole-body Mn concentration (1.78 pg.kg-l) reached after 6 weeks o f exposure was close to C,, (1.88 pg.kg-') and f,,, was 9.6 d. Manganese concentration in tissues followed the decreasing order liver > viscera without liver and kidney > gills > skin, fins, bones, and head excluding gills, brain, and eyes > kidney = epidermal mucus > brain > eyes > muscle. Autoradiograms indicated high Mn concentrations in the pancreatic tissue, skeleton, gastrointestinal mucosa, and olfactory system. Gills, viscera, and eyes (tl,2 = 3.7 to 8.8 d) were near steady state after 6 weeks of exposure, while the other tissues were not ( t l I 2 = 14.6 to 26.4 d). The depuration rate of total radioactivity was relatively rapid initially as 22% of Mn content was lost during the first week, and became slower in the following 2 weeks. Participation of Mn in enzymatic activities of liver, pancreas, and gastrointestinal mucosa may explain its high uptake in these tissues, whereas accumulation in the skeleton seems to be related to bone formation. The uptake of Mn by way of olfactory system favoured its accumulation in the brain of trout. As Mn is known to be neurotoxic, we suggest this route of uptake could be of toxicological significance for fish.

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Brown trout (Salmo trutta) were exposed to water containing 0.1 μg·L−1 (1.8 nmol·L−1) of 54Mn(II) for 1, 3, or 6 weeks. Additional trout were exposed for 3 weeks and allowed to depurate for 1 or 3 weeks. Both the uptake and the organ distribution of manganese (Mn) were determined by gamma counting and whole‐body autoradiography. Steady‐state concentration, Css, and biological half‐life, t1/2, were calculated. The whole‐body Mn concentration (1.78 μg·kg−1) reached after 6 weeks of exposure was close to Css (1.88 μg·kg−1) and t1/2 was 9.6 d. Manganese concentration in tissues followed the decreasing order liver > viscera without liver and kidney > gills > skin, fins, bones, and head excluding gills, brain, and eyes > kidney ≈ epidermal mucus > brain > eyes > muscle. Autoradiograms indicated high Mn concentrations in the pancreatic tissue, skeleton, gastrointestinal mucosa, and olfactory system. Gills, viscera, and eyes (t1/2 = 3.7 to 8.8 d) were near steady state after 6 weeks of exposure, while the other tissues were not (t1/2 = 14.6 to 26.4 d). The depuration rate of total radioactivity was relatively rapid initially as 22% of Mn content was lost during the first week, and became slower in the following 2 weeks. Participation of Mn in enzymatic activities of liver, pancreas, and gastrointestinal mucosa may explain its high uptake in these tissues, whereas accumulation in the skeleton seems to be related to bone formation. The uptake of Mn by way of olfactory system favoured its accumulation in the brain of trout. As Mn is known to be neurotoxic, we suggest this route of uptake could be of toxicological significance for fish.

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Brown trout, Salmo trutta, were exposed to water containing 0.1 microgram/l 203Hg2+, alone or with potassium ethylxanthate (PEX), sodium isopropylxanthate (SIX), sodium diethyldithiophosphate (SEP), sodium diisopropyldithiophosphate (SIP), sodium dimethyldithiocarbamate (SMC), sodium diethyldithiocarbamate (SEC) or sodium pyridinethione (SPyr), respectively. After 1 week the uptake and distribution of the 203Hg2+ in the fish were examined by gamma spectrometry. SIX, SIP, SMC, SEC and SPyr induced 2-3 times higher 203Hg2+ concentrations in most tissues in comparison with trout exposed to 203Hg2+ only. In the trout exposed to PEX slightly enhanced 203Hg2+ levels were found only in some tissues, and after exposure to SEP a few tissues showed decreased 203Hg2+ concentrations. Determinations of chloroform/water partition coefficients showed that lipophilic chelates are formed between all the examined substances and the 203Hg2+. However, SIX, SIP, SMC, SEC and SPyr, which induced markedly increased tissue levels of the metal, formed 203Hg2+ complexes with higher lipophilicities than SEX and SEP. A facilitated penetration of the lipophilic 203Hg2+ complexes over the gill membranes may underly the increment in the tissue levels of the metal, and the relative lipophilicity of the complexes may be of importance for this effect. In some instances, as with SEP, the 203Hg2+ chelated in complexes with low lipophilicity may even be less able to acumulate in some tissues than the non-complexed metal.