Anatomical mercury speciation in bay scallops by thio-bearing chelating resin concentration and GC-electron capture detector determination.

The highly toxic methyl-, ethyl- and phenylmercury species that may exist in the three main anatomical parts - the adductor muscle, the mantle and the visceral mass - of bay scallops (Argopecten irradias) were quantitatively released by cupric chloride, zinc acetate, sodium chloride and hydrochloric acid (HCl) under ultrasonic extraction. After centrifugation, the mercury species in the supernatant were concentrated by thio (SH)-bearing chelating resins, eluted with HClO4 and HCl and extracted with toluene. Separation was achieved by capillary GC equipped with programmed temperatures, a constant nitrogen flow and detected by a micro-electron capture detector (µECD). Under optimised conditions, the LODs for methyl-, ethyl- and phenylmercury in bay scallop samples were 1.1, 0.65 and 0.80 ng g(-1), respectively. The maximum RSD for three replicate determinations of methyl-, ethyl- and phenylmercury in bay scallop samples were 13.7%, 14.0% and 11.2%, respectively. In the concentration range of 4-200 ng g(-1) in bay scallop samples, the calibration graphs were linear with correlation coefficients not less than 0.997. Recoveries for spiked samples were in the range of 92.7-103.5% (methylmercury), 87.5-108.3% (ethylmercury) and 91.6-106.0% (phenylmercury), respectively. The method was verified by the determination of methylmercury in a CRM GBW10029 (Total Mercury and Methyl Mercury in Fish Tissue), with results in good agreement with the certified values. Methylmercury - the only existing species in bay scallops - was successfully determined by the method.

Metal-induced impairment of the cellular immunity of newborn harbor seals (Phoca vitulina).

The cellular immunity of newborn harbor seals and the influence of pollutants are rarely investigated. This study evaluated the lymphocyte proliferation using a lymphocyte proliferation test (LTT) to understand the dynamics of immune response in seal pups of varying ages from the moment they arrived in a seal center after active beaching until their release into wildlife 3 months later after rehabilitation. Moreover, the effect of various metals (Ag, Al, Au, Be, Cd, Co, Cr, Cu, different Hg compounds, Mo, Ni, Pb, Pd, Pt, Sn, Ti) on lymphocyte proliferation in terms of immunosuppression and hypersensitivity was investigated. First, a strong lymphocyte proliferation in newborns as a reflection of relative immunocompetence was found. Second, different metal-induced influences on lymphocyte proliferation such as specific inhibition by Be, Cd, Hg, and Sn as well as stimulation induced by Mo and Ni were determined. For seals tested repeatedly, the suppressive effect was detected in newborns but not found in the same animals when they were older and had become immunologically competent. Summarizing, the lymphocyte proliferation used as a marker in this investigation provided useful immunological information on these developing animals, and its application for toxicological studies on pollutants can be recommended.

Diagnostic value of urine mercury measurements.

A review of referrals to a regional heavy metals centre for possible mercury poisoning was made. Samples were received either from subjects who were well but were known to have some contact with mercury or from patients with an illness under investigation but undiagnosed. The problems associated with diagnosis of mercury toxicity in the absence of known exposure are illustrated by two case reports.

The transplacental toxicity of methyl mercury to fetal rat liver mitochondria. Morphometric and biochemical studies.

Ultrastructural morphometric and biochemical changes in liver mitochondria of fetal rats whose mothers were exposed to methyl mercury hydroxide in their drinking water at concentrations of 0, 3, 5, or 10 p.p.m. for 4 weeks prior to mating and through day 19 of pregnancy are described. A dose-related decrease in the volume density of mitochondria was observed in fetal hepatocytes of dams given the 5- and 10-p.p.m. dose levels. This finding was associated with decreased mitochondrial protein synthesis, which appeared to result primarily from decreased synthesis of mitochondrial structural proteins. Loss of respiratory control was observed in mitochondria from animals in the 3-p.p.m. dose group whereas state 3 respiration was abolished in animals exposed to the 5- and 10-p.p.m. dose levels. The specific activities of monoamine oxidase and cytochrome oxidase, outer and inner mitochondrial membrane marker enzymes respectively, showed dose-related decreases of up to 62 and 78 per cent of control, respectively. delta-Aminolevulinic acid synthetase, which is loosely bound to the inner mitochondrial membrane, also showed dose-related decreases of up to 68 per cent of control. Malate dehydrogenase, a mitochondrial matrix marker enzyme, showed no change in activity at any dose level tested. These observations were correlated with dose-related tissue concentrations of methyl and inormpaired mitochondrial biogenesis and functional development is one basis for explaining the sensitivity of fetal animals to methyl mercury toxicity.