Atsuhiro Nakano

Declining risk of methylmercury exposure to infants during lactation.

Methylmercury (MeHg) can be transferred to infants through milk, in addition to passage through the placenta during intrauterine life. The higher MeHg accumulation and susceptibility to toxicity in the fetus than in the mother during the gestation period is well known. However, the contribution of Hg exposure through breast milk to the MeHg concentration in infants is not clear. Our objective in this study was to examine the changes in MeHg levels in infants who were reared on breast milk to evaluate the risks between fetal and breast-feeding periods based on Hg concentrations in red blood cells (RBCs-Hg). RBCs-Hg and plasma-Hg concentrations (Plasma-Hg) in seven pairs of maternal and infant blood samples were compared at birth and 3 months after parturition. RBCs to Plasma-Hg ratio was approximately 8:1 for mothers at parturition and after 3 months, suggesting that their Hg source is MeHg from consumed fish as is general in Japanese. In all seven cases, RBCs-Hg in the umbilical cords were higher than those in the mothers at parturition. The geometric mean of RBCs-Hg in umbilical cords (10.6ng/g) was about 1.4 times higher than that in the mothers (7.1ng/g). There was a strong correlation in RBCs-Hg in mothers and umbilical cords. However, all the infants showed declines in Hg concentrations throughout the breast-feeding period. The geometric mean RBCs-Hg at 3 months of age was 5.8ng/g, accounting for 54% of that in the umbilical cords. Consequently, maternal RBCs-Hg surpassed that of infants at 3 months, opposite to the situation at parturition. The decline in infant RBCs-Hg during the breast-feeding period can be explained by the low Hg transfer through breast milk and the rapid growth of infants after birth. The geometric mean Milk-Hg was low (0.21ng/g), around 20% of that in maternal Plasma-Hg. The average body weight of infants at 3 months increased to about 1.9 times of that at birth. Thus, offspring are subjected to MeHg exposure through both the gestation and the breast-feeding periods; the risk is especially high during gestation but may decrease during breast-feeding.

Widespread neuronal degeneration in rats following oral administration of methylmercury during the postnatal developing phase: a model of fetal-type Minamata disease

The neurotoxicity of methylmercury (MeHg) treatment during the postnatal developing phase in rats was studied. Rats on postnatal day 1 were orally administered 5 mg/kg/day methylmercury chloride (MMC) for more than 30 consecutive days. Body weight loss began 26 days after MMC was administered, and severe paralysis of the hind-limbs and unsteadiness appeared subsequently. Histopathologically, the widespread neuronal degeneration was observed in the cerebral neocortex, neostriatum, red nucleus, brainstem, cerebellum and spinal dorsal root ganglia on day 32. The widespread distribution of the lesions was quite similar to that in fetal cases of MeHg intoxication in Minamata, Japan. These findings suggest that MMC treatment during the postnatal development phase in rats produce a good model of fetal-type Minamata disease.

Bioaccumulation of mercury in a vestimentiferan worm living in Kagoshima Bay, Japan

The present study reports on the mercury concentrations of the vestimentiferan worm, Lamellibrachia satsuma, (Annelida: Pogonophora) found near hydrothermal vents at a depth of 80-100 m in the northern parts of Kagoshima Bay. The vestimentiferan worms had total mercury concentrations of 238 ng/g in the anterior muscle of the body and 164 ng/g in the posterior trophosome. Methylmercury constituted only 7.6% of total mercury detected anteriorly and 16.3% posteriorly. The mean total mercury concentration in filtrated ambient seawater of the worm habitat was 1.1 ng/l. The worm should accumulate mercury in seawater by a one-step into the anterior and posterior parts as 2.2 x 10(%) and 1.5 x 10(5) times those of the filtered ambient seawater, respectively. The bioaccumulation factor of mercury by the worms with only their respiration would be actually larger than that by other marine animals through food webs. The high bioaccumulation factor of mercury in the worms suggest the following two possibilities: (i) the biological half-life of organomercury in the worm could be exceptionally long; or (ii) the lifetime of vestimentiferan worms examined in the present study could be extremely long. Various metals in one specimen of the worm were analyzed by using ICP-MS, and then gold as well as silver were detected in the worm. Gold was detected for the first time from marine animals.

Stimulation of elemental mercury oxidation by SH compounds

Anthropogenic mercury pollution has been a serious environmental problem. The presence of mercury in the environment has received a great deal of attention due to its highly toxic nature and translocation through the food chain. Elemental mercury released into the Amazon River basin due to gold mining activities is roughly estimated at 130 tons per year. In fact, high levels of total mercury, mostly in the form of methylmercury, in fish collected from around the gold mining areas and high levels of methylmercury in the hair of humans living in fishing villages downstream of these areas have recently been documented. These results suggest that the reaction which converts the discharged elemental mercury into mercuric mercury is present in nature before the methylation of the generated mercuric mercury. Methylation and reduction of mercuric mercury and decomposition of organomercury have been extensively studied. However, little information is available concerning the conversion of elemental mercury in aquatic ecosystems. The purpose of this study was to clarify the mechanism of oxidation of elemental mercury to mercuric mercury in the aquatic environment. 11 refs., 4 figs.

Effects of methylmercury on the lipid components in rats.

The effects of methyl mercury chloride on the variation of both the content and fatty acid composition of lipads in the liver, kidney and brain of rats is retorted. Methyl mercury is identified as an extremely toxici substance for man and his environment. Though the toxic effects of mercury have been widely studied from biochemical, physiological, and pathological points of view, there are very few reports which give clear elucidation of the mechanism for the occurrence of neuroinclear elucidation of the mechnism for the occurrence of neuroin-toxication.

Simple analysis of total mercury and methylmercury in seafood using heating vaporization atomic absorption spectrometry.

This study aimed to develop a simpler method for determining total mercury (T-Hg) and methylmercury (MeHg) in biological samples by using methyl isobutyl ketone (MIBK) in the degreasing step. The fat in the samples was extracted by MIBK to the upper phase. T-Hg transferred into the water phase. This was followed by the extraction of MeHg from the water phase using HBr, CuCl2 and toluene. The MeHg fraction was reverse-extracted into L-cysteine-sodium acetate solution from toluene. The concentrations of T-Hg and MeHg were determined by heating vaporization atomic absorption spectrometry. Certified reference materials for T-Hg and MeHg in hair and fish were accurately measured using this method. This method was then applied to determine T-Hg and MeHg concentrations in the muscle, liver and gonads of seafood for the risk assessment of MeHg exposure. The mean T-Hg and MeHg concentrations in squid eggs were 0.023 and 0.022 µg/g, and in squid nidamental glands 0.052 and 0.049 µg/g, respectively. The MeHg/T-Hg ratios in the eggs and nidamental glands of squid were 94.4% and 96.5%, respectively. The mean T-Hg and MeHg concentrations in the gonads of sea urchins were 0.043 and 0.001 µg/g, respectively, with a MeHg/T-Hg ratio of 3.5%. We developed an efficient analytical method for T-Hg and MeHg using MIBK in the degreasing step. The new information on MeHg concentration and MeHg/T-Hg ratios in the egg or nidamental glands of squid and gonads of sea urchin will also be useful for risk assessment of mercury in seafood.

Effects of Methyl Mercury in Postnatal Developing Rats1

Rats on Postnatal Days 1 (PD 1), 14 (PD 14), and 35 (PD 35) were orally administered 0, 2.60, 3.64, 5.10, 7.14, and 10 mg/kg/day of methyl mercury chloride (MMC) for 10 consecutive days. Mercury (Hg) accumulation in the brain of the rats treated with 10 mg/kg/day of MMC for 10 consecutive days was highest in PD-14 rats, followed by PD-35 and PD-1 rats. Hg accumulations in the liver and kidney were lowest in PD-1 rats and increased markedly with development in postnatal phase. The effect of MMC treatment on body weight change was most severe in PD-35 rats. The body weight loss began on Day 5 in PD-35 rats and on Day 10 in PD-14 rats treated with 10 mg/kg/day of MMC, but not in PD-1 rates under the same treatment. The phenomenon of hindlimb-crossing was induced on Day 11 in PD-14 rats and on Day 14 in PD-35 rats treated with 10 mg/kg/day of MMC, but was not observed in PD-1 rats. The deficit of rotarod performance was apparent only at the dose of 7.14 mg/kg/ day of MMC in PD-35 rats, whereas rotarod performance was dose-dependently inhibited by MMC treatment in PD-14 rats, and lowered even at the dose of 2.6 mg/kg/day of MMC. However, the performance was gradually restored to the control level by 1 month except in rats given 7.14 mg/kg/day of MMC. These findings indicated that the Hg distribution and the effects of MMC treatment on body weight gain and motor coordination were different among the rat postnatal developing phases.