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TOXICOLOGY
Arch. Toxieol. 42, 275-279 (1979)
9 Springer-Verlag 1979
Effeets of Sodium Selenite on Methylmereury Distribution in Miee of Late Gestational Period Hiroshi Satoh and Tsuguyoshi Suzuki Department of Public Health, School of Medicine, Tohoku University, Seiryo-Cho 2-1, Sendai 980, Japan
Abstract. Mercury distribution in pregnant mice, subcutaneously injected with 1.5 or 15.0 p,mol/kg of methylmercury chloride (MeHg) and 0, 1.5 or 15.0 p~mol/kg of sodium selenite, was investigated. Selenite increased the retention of mercury in maternal brain in every combination of doses. Selenite also increased mercury concentrations in maternal blood except one combination (MeHg 1.5; selenite 1.5 ~mol/kg), and the increased mercury was partitioned to red blood cells. The increased mercury retention by selenite was also found in fetal brain.
Key words: Methylmercury - Selenite - Interaction - Brain - Fetus.
Introduction The simultaneous injection of sodium selenite with methylmercury increased the uptake of mercury in the brain of rats (Magos and Webb, 1977) and mice (Iijima et al., 1978). However, the effect of selenite on the methylmercury retention in the fetal organs and tissues has not been studied. Thus, this paper describes the changes of mercury retention in the fetal and maternal organs depending on the ratio of the administered dose of methylmereury to that of selenite.
Materials and Methods Animals were IVCS pregnant mice. On day 16 of gestation, methylmercury chloride (CH3HgCI: MeHg, Wako Pure Chemical Industries Ltd., Osaka, Japan) was subcutaneously injected in gluteal region and sodium selenite (Na2SeO3 95 H20, Nakaral Chemicals, Ltd., Kyoto, Japan) in neck just after the injection of MeHg. The chemicals were dissolved in physiological saline. The doses administered were 0 (for the control, physiological saline alone), 1.5 or 15.0 ~mol/kg body weight, and the volume was appoximately 0.2 ml for each injection. In the combination of doses of MeHg and selenite, Send offprint requests to: T. Suzuki at the above address
0340-5761/1979/0042/0275/$ 01.00
c
Factor MeHg
n.s.
b
n.s.
c
10.60 _+ 2.03 11.03 -+ 3.29 16.28 _+ 2.62
14.98 + 3.37 17.06+2.34 14.93 _+ 0.93
Liver
n.s.
n.s.
c
0.237 _+ 0.070 0.234 _+ 0.083 0.251 _+ 0.059
0.296 + 0.061 0.422_+0.242 0.303 _+ 0.043
Spleen
c
n.s.
n.s.
3.00 + 0.69 3.11 _+ 0.54 3.73 + 0.95
4.03 + 0.62 3.34+0.32 2.50 + 0.34
Kidneys
n.s. c
n.s. n.s.
n.S,
n.s.
n.s. b
0.049 + 0.011 0.070 + 0.011 0.065 +_ 0.014 a
0.187 +_ 0.044 0.235 +_ 0.060 0.212 + 0.018
1.07 _+ 0.05 1.12 + 0.35 1.35 + 0.18
n.s.
0.072 + 0.010 0.052 + 0.010 0.055 _+ 0.005
Amniotic membrane
0.258 + 0.040 0.233 + 0.045 0.215 _+ 0.027
Placenta
1.26 + 0.20 1.48 + 0.16 1.08 _ 0.17
Uterus
a The number of samples was 3 b or c; significant Co < 0.05 or p < 0.01, by two-way analysis of variance) }* The difference between two means is significant by the least significant differences method (p < 0.05)
Interaction
c
0.319 _+ 0.067/*] 0.564 -+ 0.135/ ~* 0.728 _+ 0.160 J
15.0-- 0 15.0--1.5 15.0--15.0
Se
0.556 + 0.119] 0.710 + 0.111~* 0.835 _+ 0.076)
Brain
Maternal
1.5-- 0 1.5-- 1.5 1.5--15.0
MeHg-Se (~mol/k8)
Table 1. Mercury contents 24 h after subcutaneous injection (Percent of the dose; mean _+ SD)
e~
Effects of Selenite on Methylmercury Distribution in Pregnant Mice
277
two combinations: MeHg 0; selenite 1.5 and MeHg 0; selenite 15.0 ttmol/kg, were excluded. Each group consisted of four pregnant mice. Twenty-four hours after injection, they were anesthetized by ether and blood was collected from the juglar vein with heparin. Uterus was exposed and araniotic fluid was collected by puncture and then fetuses were killed by decapitation to obtain fetal brain, fiver and kidneys. Maternal brain, liver, spleen and kidneys were collected as well as uterus, placenta and amniotic membrane. These organs and tissues were stored in a freezer until mercury analyses. Total mercury was measured by Magos' method (1971). The data were subjected to the two-way analysis of variance and the means of different doses of selenite in each dose level of MeHg were compared by the least significant difference method. The size of fitter was similar among all groups. Resorption and maceration were few and omitted from mercury analyses. Two mother mice aborted before sacrifice in the group of MeHg 15.0; selenite 15.0 ~.mol/kg. Aborted fetuses and placenta were not damaged and fetal organs were identifiable, thus they were available for mercury measurement; although the amniotic membrane and amniotic fluid were not available.
Results
Table 1 shows mercury contents (as percent dose) in maternal organs, placenta and amniotic membrane. Amount of mercury detected in organs or tissues of control group was subtracted from the amount of mercury in corresponding organs or tissues of treated groups. Only for the brain, selenite increased the percent dose of MeHg, and the increase was parallel with the increasing dose of selenite. When not the percent dose but the concentration of mercury was compared among different doses of selenite, the same pattern of increase was observed due to selenite. As for mercury in maternal liver, the factors of MeHg and interaction, but not selenite, were significant, i.e., the increase was observed in the case of equimolar doses of both substances.
Table
2. Mercury concentration in maternal blood and amniotic fluid (nmol/ml; Mean _+ SD)
MeHg-Se (l~mol/kg)
Whole blood
1.5-- 0 1.5-- 1.5 1.5--15.0 15.0- 0 15.0- 1.5 15.0:15.0
Red blood cells
0.90 _ 0.15 0.75 +_0.10 1.18 _+0.08
1.71 _+0.32 1.33 _ 0.26 2.38 _+0.19
Plasma
Amniotic fluid
0.29 +_0.04 0.32 _+0.05 0.28 +- 0.01
0.06 + 0.03 0.04 _+0.02 0.03 _+ 0.01 0.28_+0.10 0.27 _+ 0.06 0.45 a
6.27_+ 1.04 ] 7.96 _+ 1.06/,[* 10.04 _+ 1.37J J
11.59_+2.34 ] 15.43 _+ 2.89 ]*/* 20.65 _+ 2.78 J
2.12+_0.44 2.42 _+0.37 2.18 _+0.42
b
b
b
b
b
n.s.
b
b
n.s.
Factor
MeHgb Se Interaction
The number of samples was 2 b Significant (p < 0.01, by two-way analysis of variance) }* The difference between means is significant by the least significant difference method (p < 0.05)
278
H. Satoh and T. Suzuki
Table 3. Mercury contents in fetal organs and fetus 24 h after injection (percent of the dose; mean + SD)
MeHg-Se (~mol/kg) 1.5- 0 1.5-1.5 1.5-15.0
Brain
Liver
Kidneys
Fetusb
0.068 + 0.010 0.064 + 0.016 0.071 _+0.017
( 1.05 _+0.14)a ( 0.82 + 0.19) ( 0.79 + 0.15)
0.139 + 0.037 0.160 + 0.020 0.144 _+0.015
0.0041+ 0.0016 0.0052 _+0.0013 0.0062 + 0.0021
1.33 + 0.16 1.30 + 0.05 1.18 + 0.17
0.045 + 0.012/, 0.088 + 0.024J 0.073+0.007
( 7.00 + 2.02)/, ] 0.147 + 0.054 (11.63+ 2.51)/ ~* 0.177 + 0.056 (11.21+2.56) / 0.176+0.024
0.0066 + 0.0037 0.0076 + 0.0022 0.0070+0.0011
1.32 _+0.36 1.31 + 0.46 1.37+0.15
MeHg
n.s.
a
n.s.
c
n.s.
Se
c
e
n.s.
n.s.
n.s.
c
e
n.s.
n.s.
n.s.
15.5-- 0 15.0-1.5 15.0-15.0 Factor
Interaction
"The numerals in parentheses were concentrations of mercury in fetal brain (nmol/g) b The numerals were average for individual fetus c or a; significant (p < 0.05 or p < 0.01, by two-way analysis of variance) }* The difference between means is significant by the least significant difference method (p < 0.05)
A m o n g other organs, kidneys, uterus and amniotic membranes were only significant for the factor of interaction, and the percent dose retained in spleen was significantly different by the dose of MeHg. Table 2 shows mercury concentrations in maternal whole blood, red blood cells, plasma, and amniotic fluid. In the high dose level of MeHg, selenite increased mercury concentrations in whole blood. The elevation was observed in red blood cells, but not plasma. Amniotic fluid had very low mercury concentrations, for which statistical examination was not applied, because the number of samples of the group: M e H g 15.0; selenite 15.0 p,mol/kg, was two. Table 3 shows mercury contents in fetal brain, liver, kidneys and fetus. Mercury content in fetus was calculated from the mercury contents in these three organs and carcass (remnant after removal o f these three organs). Mercury concentrations in fetal brain were included in Table 3. The factors of selenite and interaction were significant for both mercury content and concnentration in fetal brain, but the effect o f selenite was not seen in the low dose level of MeHg. Mercury contents in fetal liver and kidneys and fetus as a whole were almost similar among three groups of the same dose level of MeHg.
Discussions
Bodily distribution of mercury 24 h after injection of MeHg with or without selenite were demonstrated for pregnant mice. The most characteristic change of mercury distribution by simultaneous administration of selenite was observed in maternal and fetal brains. As mentioned in the introduction section, the increase of mercury in brain of adult rats (Magos and Webb, 1977) and mice (Iijima et al., 1978) was
Effects of Selenite on Methylmercury Distribution in Pregnant Mice
279
already observed. The increase of mercury in fetal brain by selenite was a new finding. The residual blood volume in the maternal brain of mice on day 17 of gestation, from which the brain was harvested as in the same manner in the present experiment, was 0.7% (v/w) (Satoh, 1979). By calculation using the above value, an apparent increase in the mercury content in maternal brain was estimated as about 1% at the maximum. We could not directly evaluate the effect of residual blood in the fetal brain of mice, but according to the results in rats by Wannag (1976), the apparent increase was calculated as 2.6% at the maximum, when the mercury concentration in fetal blood was assumed 1.3 times greater than that of maternal blood. Nevertheless, the increase of mercury contents and concentrations in maternal and fetal brains due to selenite was invariably significant after subtraction of apparent increase by residual blood volume. Behavioral deviations, such as a prolonged reaction time to open-field test (Spyker et al., 1972; Su and Okita, 1976) and an abnormal swimming behaviour (Spyker et al., 1972) were reported in the young mice which had been exposed to MeHg in utero. Electron microscopy revealed various changes in cerebellar cells of mice with behavioral deviations after in utero exposure to MeHg (Chang et al., 1977). Since selenite has modified the embryocidal and teratogenic effects of MeHg in a long-term feeding experiment of mice (Nobunaga et al., 1979), it may also modify these reported effects of MeHg exposure in utero by a single injection; although the elevated mercury concentration in brain of the weanling rats, which was fed MeHg and selenite concomitantly, was by no means correlated with the neurological manifestation of MeHg toxicity (Ohi et al., 1976).
References Chang, L. W., Reuhl, K. R., Spyker, J. M.: Ultrastructural study of latent effects of methylmercuryon nervous system after prenatal exposure. Environ. Res. 13, 171--185 (1977) Iijima, S., Tohyama, C., Lu, C-v, Matsumoto, N.: Placental transfer and body distribution of methylmercury and selenium in pregnant mice. Toxicol. Appl. Pharmacol. 44, 143-146 (1978) Magos, L.: Selective atomic-absorption determination of inorganic mercury and methylmercury in undigested biological samples. Analyst 96, 847-853 (1971) Magos, L., Webb, M.: The effect of selenium on the brain uptake of methylmercury.Arch. Toxicol. 38, 201-207 (1977) Nobunaga, T., Satoh, H., Suzuki, T.: Effects of sodium selenite on methylmercuryembryotoxicityand teratogenicity in mice. Toxicol. Appl. Pharmacol. 47, 79--88 (1979) Ohi, G., Nishigaki, S., Seki, H., Tamura, Y., Maki, T., Konno, H., Ochiai, S., Yamada, H., Shimamura, Y., Mizoguchi, I., Yagu, H.: Efficacyof selenium in tuna and selenite in modifyingmethylmercury intoxication. Environ. Res. 12, 49--58 (1976) Satoh, H.: Residual blood volumesin organs of pregnant mice and fetuses. Tohoku. J. Exp. Med. 128 (in press, 1979) Spyker, J. M., Sparber, S. B., Goldberg, A. M.: Subtle consequences of methylmercury exposure; behavioral deviations in offspring from treated mothers. Science 177, 621-623 (1972) Su, M-Q., Okita, G. T.: Behavioral effects on the progenyof micetreated with methylmercury.Toxicol. Appl. Pharmacol. 38, 195--205 (1976) Wannag, A.: The importance of organ blood mercury when comparing foetal and maternal organ distribution of mercury after methyl mercury exposure. Acta Pharmacol. Toxicol. 38, 289--298 (1976) Received March 13, 1979
TOXICOLOGY
Arch. Toxieol. 42, 275-279 (1979)
9 Springer-Verlag 1979
Effeets of Sodium Selenite on Methylmereury Distribution in Miee of Late Gestational Period Hiroshi Satoh and Tsuguyoshi Suzuki Department of Public Health, School of Medicine, Tohoku University, Seiryo-Cho 2-1, Sendai 980, Japan
Abstract. Mercury distribution in pregnant mice, subcutaneously injected with 1.5 or 15.0 p,mol/kg of methylmercury chloride (MeHg) and 0, 1.5 or 15.0 p~mol/kg of sodium selenite, was investigated. Selenite increased the retention of mercury in maternal brain in every combination of doses. Selenite also increased mercury concentrations in maternal blood except one combination (MeHg 1.5; selenite 1.5 ~mol/kg), and the increased mercury was partitioned to red blood cells. The increased mercury retention by selenite was also found in fetal brain.
Key words: Methylmercury - Selenite - Interaction - Brain - Fetus.
Introduction The simultaneous injection of sodium selenite with methylmercury increased the uptake of mercury in the brain of rats (Magos and Webb, 1977) and mice (Iijima et al., 1978). However, the effect of selenite on the methylmercury retention in the fetal organs and tissues has not been studied. Thus, this paper describes the changes of mercury retention in the fetal and maternal organs depending on the ratio of the administered dose of methylmereury to that of selenite.
Materials and Methods Animals were IVCS pregnant mice. On day 16 of gestation, methylmercury chloride (CH3HgCI: MeHg, Wako Pure Chemical Industries Ltd., Osaka, Japan) was subcutaneously injected in gluteal region and sodium selenite (Na2SeO3 95 H20, Nakaral Chemicals, Ltd., Kyoto, Japan) in neck just after the injection of MeHg. The chemicals were dissolved in physiological saline. The doses administered were 0 (for the control, physiological saline alone), 1.5 or 15.0 ~mol/kg body weight, and the volume was appoximately 0.2 ml for each injection. In the combination of doses of MeHg and selenite, Send offprint requests to: T. Suzuki at the above address
0340-5761/1979/0042/0275/$ 01.00
c
Factor MeHg
n.s.
b
n.s.
c
10.60 _+ 2.03 11.03 -+ 3.29 16.28 _+ 2.62
14.98 + 3.37 17.06+2.34 14.93 _+ 0.93
Liver
n.s.
n.s.
c
0.237 _+ 0.070 0.234 _+ 0.083 0.251 _+ 0.059
0.296 + 0.061 0.422_+0.242 0.303 _+ 0.043
Spleen
c
n.s.
n.s.
3.00 + 0.69 3.11 _+ 0.54 3.73 + 0.95
4.03 + 0.62 3.34+0.32 2.50 + 0.34
Kidneys
n.s. c
n.s. n.s.
n.S,
n.s.
n.s. b
0.049 + 0.011 0.070 + 0.011 0.065 +_ 0.014 a
0.187 +_ 0.044 0.235 +_ 0.060 0.212 + 0.018
1.07 _+ 0.05 1.12 + 0.35 1.35 + 0.18
n.s.
0.072 + 0.010 0.052 + 0.010 0.055 _+ 0.005
Amniotic membrane
0.258 + 0.040 0.233 + 0.045 0.215 _+ 0.027
Placenta
1.26 + 0.20 1.48 + 0.16 1.08 _ 0.17
Uterus
a The number of samples was 3 b or c; significant Co < 0.05 or p < 0.01, by two-way analysis of variance) }* The difference between two means is significant by the least significant differences method (p < 0.05)
Interaction
c
0.319 _+ 0.067/*] 0.564 -+ 0.135/ ~* 0.728 _+ 0.160 J
15.0-- 0 15.0--1.5 15.0--15.0
Se
0.556 + 0.119] 0.710 + 0.111~* 0.835 _+ 0.076)
Brain
Maternal
1.5-- 0 1.5-- 1.5 1.5--15.0
MeHg-Se (~mol/k8)
Table 1. Mercury contents 24 h after subcutaneous injection (Percent of the dose; mean _+ SD)
e~
Effects of Selenite on Methylmercury Distribution in Pregnant Mice
277
two combinations: MeHg 0; selenite 1.5 and MeHg 0; selenite 15.0 ttmol/kg, were excluded. Each group consisted of four pregnant mice. Twenty-four hours after injection, they were anesthetized by ether and blood was collected from the juglar vein with heparin. Uterus was exposed and araniotic fluid was collected by puncture and then fetuses were killed by decapitation to obtain fetal brain, fiver and kidneys. Maternal brain, liver, spleen and kidneys were collected as well as uterus, placenta and amniotic membrane. These organs and tissues were stored in a freezer until mercury analyses. Total mercury was measured by Magos' method (1971). The data were subjected to the two-way analysis of variance and the means of different doses of selenite in each dose level of MeHg were compared by the least significant difference method. The size of fitter was similar among all groups. Resorption and maceration were few and omitted from mercury analyses. Two mother mice aborted before sacrifice in the group of MeHg 15.0; selenite 15.0 ~.mol/kg. Aborted fetuses and placenta were not damaged and fetal organs were identifiable, thus they were available for mercury measurement; although the amniotic membrane and amniotic fluid were not available.
Results
Table 1 shows mercury contents (as percent dose) in maternal organs, placenta and amniotic membrane. Amount of mercury detected in organs or tissues of control group was subtracted from the amount of mercury in corresponding organs or tissues of treated groups. Only for the brain, selenite increased the percent dose of MeHg, and the increase was parallel with the increasing dose of selenite. When not the percent dose but the concentration of mercury was compared among different doses of selenite, the same pattern of increase was observed due to selenite. As for mercury in maternal liver, the factors of MeHg and interaction, but not selenite, were significant, i.e., the increase was observed in the case of equimolar doses of both substances.
Table
2. Mercury concentration in maternal blood and amniotic fluid (nmol/ml; Mean _+ SD)
MeHg-Se (l~mol/kg)
Whole blood
1.5-- 0 1.5-- 1.5 1.5--15.0 15.0- 0 15.0- 1.5 15.0:15.0
Red blood cells
0.90 _ 0.15 0.75 +_0.10 1.18 _+0.08
1.71 _+0.32 1.33 _ 0.26 2.38 _+0.19
Plasma
Amniotic fluid
0.29 +_0.04 0.32 _+0.05 0.28 +- 0.01
0.06 + 0.03 0.04 _+0.02 0.03 _+ 0.01 0.28_+0.10 0.27 _+ 0.06 0.45 a
6.27_+ 1.04 ] 7.96 _+ 1.06/,[* 10.04 _+ 1.37J J
11.59_+2.34 ] 15.43 _+ 2.89 ]*/* 20.65 _+ 2.78 J
2.12+_0.44 2.42 _+0.37 2.18 _+0.42
b
b
b
b
b
n.s.
b
b
n.s.
Factor
MeHgb Se Interaction
The number of samples was 2 b Significant (p < 0.01, by two-way analysis of variance) }* The difference between means is significant by the least significant difference method (p < 0.05)
278
H. Satoh and T. Suzuki
Table 3. Mercury contents in fetal organs and fetus 24 h after injection (percent of the dose; mean + SD)
MeHg-Se (~mol/kg) 1.5- 0 1.5-1.5 1.5-15.0
Brain
Liver
Kidneys
Fetusb
0.068 + 0.010 0.064 + 0.016 0.071 _+0.017
( 1.05 _+0.14)a ( 0.82 + 0.19) ( 0.79 + 0.15)
0.139 + 0.037 0.160 + 0.020 0.144 _+0.015
0.0041+ 0.0016 0.0052 _+0.0013 0.0062 + 0.0021
1.33 + 0.16 1.30 + 0.05 1.18 + 0.17
0.045 + 0.012/, 0.088 + 0.024J 0.073+0.007
( 7.00 + 2.02)/, ] 0.147 + 0.054 (11.63+ 2.51)/ ~* 0.177 + 0.056 (11.21+2.56) / 0.176+0.024
0.0066 + 0.0037 0.0076 + 0.0022 0.0070+0.0011
1.32 _+0.36 1.31 + 0.46 1.37+0.15
MeHg
n.s.
a
n.s.
c
n.s.
Se
c
e
n.s.
n.s.
n.s.
c
e
n.s.
n.s.
n.s.
15.5-- 0 15.0-1.5 15.0-15.0 Factor
Interaction
"The numerals in parentheses were concentrations of mercury in fetal brain (nmol/g) b The numerals were average for individual fetus c or a; significant (p < 0.05 or p < 0.01, by two-way analysis of variance) }* The difference between means is significant by the least significant difference method (p < 0.05)
A m o n g other organs, kidneys, uterus and amniotic membranes were only significant for the factor of interaction, and the percent dose retained in spleen was significantly different by the dose of MeHg. Table 2 shows mercury concentrations in maternal whole blood, red blood cells, plasma, and amniotic fluid. In the high dose level of MeHg, selenite increased mercury concentrations in whole blood. The elevation was observed in red blood cells, but not plasma. Amniotic fluid had very low mercury concentrations, for which statistical examination was not applied, because the number of samples of the group: M e H g 15.0; selenite 15.0 p,mol/kg, was two. Table 3 shows mercury contents in fetal brain, liver, kidneys and fetus. Mercury content in fetus was calculated from the mercury contents in these three organs and carcass (remnant after removal o f these three organs). Mercury concentrations in fetal brain were included in Table 3. The factors of selenite and interaction were significant for both mercury content and concnentration in fetal brain, but the effect o f selenite was not seen in the low dose level of MeHg. Mercury contents in fetal liver and kidneys and fetus as a whole were almost similar among three groups of the same dose level of MeHg.
Discussions
Bodily distribution of mercury 24 h after injection of MeHg with or without selenite were demonstrated for pregnant mice. The most characteristic change of mercury distribution by simultaneous administration of selenite was observed in maternal and fetal brains. As mentioned in the introduction section, the increase of mercury in brain of adult rats (Magos and Webb, 1977) and mice (Iijima et al., 1978) was
Effects of Selenite on Methylmercury Distribution in Pregnant Mice
279
already observed. The increase of mercury in fetal brain by selenite was a new finding. The residual blood volume in the maternal brain of mice on day 17 of gestation, from which the brain was harvested as in the same manner in the present experiment, was 0.7% (v/w) (Satoh, 1979). By calculation using the above value, an apparent increase in the mercury content in maternal brain was estimated as about 1% at the maximum. We could not directly evaluate the effect of residual blood in the fetal brain of mice, but according to the results in rats by Wannag (1976), the apparent increase was calculated as 2.6% at the maximum, when the mercury concentration in fetal blood was assumed 1.3 times greater than that of maternal blood. Nevertheless, the increase of mercury contents and concentrations in maternal and fetal brains due to selenite was invariably significant after subtraction of apparent increase by residual blood volume. Behavioral deviations, such as a prolonged reaction time to open-field test (Spyker et al., 1972; Su and Okita, 1976) and an abnormal swimming behaviour (Spyker et al., 1972) were reported in the young mice which had been exposed to MeHg in utero. Electron microscopy revealed various changes in cerebellar cells of mice with behavioral deviations after in utero exposure to MeHg (Chang et al., 1977). Since selenite has modified the embryocidal and teratogenic effects of MeHg in a long-term feeding experiment of mice (Nobunaga et al., 1979), it may also modify these reported effects of MeHg exposure in utero by a single injection; although the elevated mercury concentration in brain of the weanling rats, which was fed MeHg and selenite concomitantly, was by no means correlated with the neurological manifestation of MeHg toxicity (Ohi et al., 1976).
References Chang, L. W., Reuhl, K. R., Spyker, J. M.: Ultrastructural study of latent effects of methylmercuryon nervous system after prenatal exposure. Environ. Res. 13, 171--185 (1977) Iijima, S., Tohyama, C., Lu, C-v, Matsumoto, N.: Placental transfer and body distribution of methylmercury and selenium in pregnant mice. Toxicol. Appl. Pharmacol. 44, 143-146 (1978) Magos, L.: Selective atomic-absorption determination of inorganic mercury and methylmercury in undigested biological samples. Analyst 96, 847-853 (1971) Magos, L., Webb, M.: The effect of selenium on the brain uptake of methylmercury.Arch. Toxicol. 38, 201-207 (1977) Nobunaga, T., Satoh, H., Suzuki, T.: Effects of sodium selenite on methylmercuryembryotoxicityand teratogenicity in mice. Toxicol. Appl. Pharmacol. 47, 79--88 (1979) Ohi, G., Nishigaki, S., Seki, H., Tamura, Y., Maki, T., Konno, H., Ochiai, S., Yamada, H., Shimamura, Y., Mizoguchi, I., Yagu, H.: Efficacyof selenium in tuna and selenite in modifyingmethylmercury intoxication. Environ. Res. 12, 49--58 (1976) Satoh, H.: Residual blood volumesin organs of pregnant mice and fetuses. Tohoku. J. Exp. Med. 128 (in press, 1979) Spyker, J. M., Sparber, S. B., Goldberg, A. M.: Subtle consequences of methylmercury exposure; behavioral deviations in offspring from treated mothers. Science 177, 621-623 (1972) Su, M-Q., Okita, G. T.: Behavioral effects on the progenyof micetreated with methylmercury.Toxicol. Appl. Pharmacol. 38, 195--205 (1976) Wannag, A.: The importance of organ blood mercury when comparing foetal and maternal organ distribution of mercury after methyl mercury exposure. Acta Pharmacol. Toxicol. 38, 289--298 (1976) Received March 13, 1979
