Mercury Concentrations In Tissues Research Articles

Neurotoxic response of infant monkeys to methylmercury

Four infant monkeys were dosed orally with 500 μg Hg/kg body wt./day (as methylmercury (MeHg) chloride dissolved sodium carbonate) beginning at 1 day of age. Neurological and behavioral signs of MeHg toxicity and blood Hg levels were monitored weekly. At first sign of MeHg intoxication, dosing with MeHg was terminated and the infants were monitored to assess reversal of the signs of MeHg toxicity. The first signs of MeHg toxicity, exhibited as a loss in dexterity and locomotor ability, were observed after 28–29 days of treatment; the blood Hg levels were 8.0–9.4 μg Hg/g blood. Dosing was terminated at 28–29 days of treatment but the signs of MeHg toxicity continued to develop. The infants became ataxic, blind, comatose and were necropsied at 35–43 days after initiating treatment with MgHg. The mercury concentrations in tissues analyzed after necropsy were highest in liver (55.8 ± 3.2 μg Hg/g) followed by occipital cortex (35.6 ± 4.8 μg Hg/g) and renal cortex (32.8 ± 1.6 μg Hg/g). The frontal and temporal cortices had 27.0 ± 3.4 and 29.6 ± 4.9 μg Hg/g respectively while the cerebellar Hg concentration averaged 13.0 ± 1.5 μg Hg/g. The mean blood/brain ratio was 0.21 ± 0.4. Histopathologic lesions were marked in the cerebrum with less severe lesions in the cerebellar nuclei. The Purkinje and granular cells of the cerebellar vermis appeared histologically normal. Lesions were not observed in the peripheral nervous system. The signs of MeHg intoxication, the tissue distribution of MeHg and histopathologic lesions observed in the infant monkeys were similar to those reported for adult monkeys.

Synthesis and pharmacological study of a polymer which selectively binds mercury

A polymeric chelating agent (MBP) prepared by condensation of a mercaptoethyl sulfide with a terephthaldicarboxaldehyde exhibited a high degree of specificity for mercury (II) as judged by its ability to reduce rapidly the free metal ion concentration in an aqueous solution. The polymer exhibited a low degree of toxicity (LD50 > 5 g/kg) when administered orally to mice, and it was capable of antagonizing acute methyl mercury-induced lethality. MBP at a level of 1% in food promoted a rapid clearance of mercury from the body after acute administration of methyl mercury. The biological half-life of the metal was reduced from 10.0 days to 4.5 days. The concentration of mercury in various tissues including the brain was reduced 40 to 70% after administration of MBP when compared to contents obtained in animals not treated with MBP.

Pharmacodynamics of methyl mercury in the murine maternal/embryo: Fetal unit

To investigate fetal uptake of methyl mercury (MeHg) during organogenesis, a single dose of MeHg (5 mg of Hg/kg), 100 μCi 203 Hg/kg in 0.13 m NaCl, 0.01 m Na 2HPO 4, pH 7.4) was administered sc to pregnant Swiss-Webster CFW mice on Days 7 through 13 of gestation. Fetal accumulation of mercury increased with fetal age at time of administration at least up to Day 13 of gestation. MeHg administered on Days 10 through 13 of gestation produced fetal mercury concentrations higher than maternal blood concentrations by 7 (injected on Day 10 or 11) or 5 (injected on Day 12 or 13) days post administration. Peak fetal mercury concentrations were reached 3 days post administration, averaging 4.8 mg/kg in animals injected on Day 13 of gestation. Placental mercury concentrations were always equal to or higher than maternal blood mercury concentrations. An increase in maternal liver net elimination rate (1.3 μg of Hg/day when MeHg was administered on Day 7; 3.4 μg of Hg/day when administered on Day 13) was associated with the increased fetal sequestration of MeHg during later gestational stages. Maternal blood elimination rates increased slightly throughout the same period. To determine the uptake of mercury via suckling, offspring of dams given MeHg on Day 12 of gestation and control dams were cross-fostered. All tissue mercury concentrations of MeHg × MeHg offspring were nearly identical to those of the dams at 10 and 21 days postpartum. Tissue mercury concentrations in MeHg × Sal offspring ( in utero mercury exposure) were 15 to 30 times greater than in Sal × MeHg offspring (suckling mercury exposure), indicating far greater mercury transfer in utero.

Replacement of meat and bone meal with whale meal or whale solubles in pig diets and the accumulation of mercury in the carcase

The effects of replacing all or part of the protein supplied by meat and bone meal with whale meal or whale solubles were studied in four experiments with growing pigs fed diets based on wheat and barley. The growth rate and feed conversion efficiency of pigs receiving whale meal were equal to those fed meat and bone meal, whereas the performance of pigs fed whale solubles was inferior. Both whale meal and whale solubles contained mercury which accumulated in the tissues of growing pigs. The level of mercury accumulated was related to the dietary concentration and type of whale product, the period of time during which it was fed, and the type of carcase tissue. Whale meal contained more mercury than whale solubles and produced higher concentrations of mercury in the tissues. The levels of mercury in the tissues of pigs at 45 kg liveweight were lower than those of pigs at 80-85 kg liveweight. When the diets included more than 1 per cent whalemeal or 3 per cent whale solubles, the carcases contained more mercury than is tolerated by the health standards.

Preliminary Study of the Effects of Feeding Ethyl Mercury Chloride on Four Breeds of Chickens

Different breeds of chickens namely Single Comb White Leghorn (S.C.W.L.), New Hampshire (N.H.), Iraqi (IRQ.) and a cross (CRS.) S.C.W.L. × N.H. × IRQ. were housed in small pens (20 females and 2 males each) and given, in the diet, 40% wheat treated with ethyl mercury chloride, for 88 days.Throughout the whole experiment all birds remained active and showed no symptoms of toxicity.The Iraqi breed was significantly higher than the other breeds with respect to egg production. The results also indicated that mercury in egg white is almost three times as much as that in the yolk, although there was no significant difference between the breeds. The liver and kidney of the four breeds tended to accumulate the highest amount of mercury. Significant differences appeared between sexes according to liver and kidney. White Leghorn and local breeds behaved the same, but N.H. had the highest concentration of mercury in most tissues.

MERCURY POISONING IN A WILD MINK

Mercury poisoning was diagnosed in a clinically-ill wild mink (Mustela vison) on the basis of clinical signs, histopathologic lesions and tissue mercury concentrations. The probable source of mercury was through ingestion of fish from the nearby South Saskatchewan River which is known to be contaminated with mercury. This is believed to be the first documented case of mercury intoxication of a wild animal in North America.

The Uptake of Mercury from Water by the Grass Shrimp, Palaemonetes vulgaris (Say)

AbstractIn order to assess the toxicity of mercury to the grass shrimp (Palaemonetes vulgaris [Say]), the lethal concentration for 50% (LC50) of the tested population in a 24‐hour period for HgCl2 and MeHgCl were determined. The LC50 values were approximately 400 parts per billion (ppb) Hg for HgCl2 and 125 ppb Hg for MeHgCl. When shrimp were held in mercury solutions at sublethal concentrations (1.5 ppb Hg as HgCl2) for 15 days, a maximum of 500 ppb Hg was accumulated in the animal's tissues after 3 days. The average tissue concentration of mercury for the remaining 12 days was 450 ppb Hg. The actual tissue distribution of mercury was determined by exposure of shrimp to radioactively labeled HgCl2 and MeHgCl. No difference could be found in the tissue distribution of the two compounds. A significant difference is tissue mercury distribution occurred between the 24‐hour and 72‐hour exposures.

INCREASED METHYL MERCURY RETENTION IN MICE CONSUMED WITH JAPANESE ENCEPHALITIS VIRUS INFECTION

When the Japanese encephalitis (JE) virus infected mice were given methyl mercuric chloride (MMC) intraperitoneally, the mercury retention was increased in the blood and tissues of the JE mice compared to the control mice. However, the rate of mercury excretion was nearly the same in the both. In spite of the increased mercury concentrations in the liver of the JE mice, the total amount of mercury in the liver was about the same as the control mice, because of the reduced organ weight. Mercury content was actually increased only in the brain of the JE mice. In mice surviving after the JE virus infection, the rate of increase of mercury concentration in tissues was nearly proportional to the rate of maximum body weight loss. The consumption, due to the JE virus infection was presumed to be the major cause for the increased mercury retention.

Tissue concentrations of mercury after chronic dosing of squirrel monkeys with thiomersal

Squirrel monkeys were dosed intranasally with saline or thiomersal (sodium ethylmercurithiosalicylate, 0.002% w/v) daily for six months. The total amounts of thiomersal given during the six months period were 418 μg (low dose group) and 2280 μg (high dose group). This was equivalent to 207 and 1125 μg mercury. The dose differential was achieved by more frequent administration to the high dose group. Mercury concentrations were significantly raised over control values in brain (high dose group only), liver, muscle and kidney, but not in blood. Concentrations were highest in the kidney, moderate in liver and lowest in brain and muscle. Much of the mercury was present in the inorganic form (37–91%). No evidence of toxicity due to thiomersal was seen in any animal. Nevertheless accumulation of mercury from chronic use of thiomersal-preserved medicines is viewed as a potential health hazard for man.

Accumulation, tissue distribution and elimination of 203HgCl2 and CH3 203HgCl in the tissues of the American oyster Crassostrea virginica

Oysters (Crassostrea virginica) were exposed for 3 days to mercury-203 labeled HgCl2 or CH3HgCl added directly to artificial seawater or added preconcentrated on the marine diatom Phaeodactylum tricornutum. The concentration of mercury in 5 tissues was measured for 45 days after mercury was removed from the ambient water. At the beginning of the depuration period, the highest concentrations of mercury in tissues were attained in: gill>digestive system>mantle>gonad>muscle in oysters exposed to water containing mercury; and in digestive system>gill>mantle> gonad>muscle in oysters fed labeled algae. This same distribution pattern is seen for both chemical forms of mercury. Although the initial pattern of accumulation was identical for both mercury compounds within each exposure group, the fate of the accumulated mercury was very different after 45-days depuration. In oysters accumulating mercury directly from seawater, inorganic mercury residues rapidly declined in gill and digestive tissue, but were slowly reduced in mantle, gonadal, and muscle tissue. This pattern was duplicated by oysters exposed to methyl mercuric chloride in seawater except that gonadal and muscle residues greatly increased during depuration. In oysters ingesting labeled P. tricornutum cells, mercuric chloride and methyl mercuric chloride residues rapidly declined in gill and digestive tissue, remained constant in the mantle, but sharply increased in gonadal and muscle tissue during depuration.

Factors affecting the accumulation and removal of mercury from tissues of the American oyster Crassostrea virginica

Adult oysters, Crassostrea virginica (Gmelin) were held in seawater containing 10 or 100 ppb mercury in the form of mercuric acetate for 45 days. Mercury concentration in tissues was determined by analysis of individually homogenized oyster meats using wet digestion and flameless absorption spectrophotometry. After 45 days, average mercury tissue concentration was 91,600 and 12,100 ppb in the 100 and 10 ppb mercury groups, respectively. A slight decline in mercury residues in the 100 ppb group during the accumulation period was attributed to spawning. Clearance of mercury from tissues was studied in a constant temperature regime (25°C±2Co) for 25 days and in a declining temperature regime (25° to 5°C) for 80 days by exposing treated adults to estuarine water with no mercury added. The biological half-life of mercuric acetate was 16.8 and 9.3 days in the 25°C temperature regime, and 35.4 and 19.9 days in the declining temperature regime, for the 10 and 100 ppb groups, respectively. Smaller oysters (0 to 7 g) consistently accumulated more mercury per gram wet weight than larger oysters (7 to 20 g) in populations exposed to 10 and 100 ppb mercury.

Mercury and selenium in marine mammals and birds

Information is provided concerning the concentrations of mercury and selenium in tissues of marine animals. In marine mammals a 1:1 Hg/Se molecular increment ratio was found and an almost perfect linear correlation between mercury and selenium. It is suggested that marine mammals are able to detoxify methylmercury by a specific chemical mechanism in which selenium is involved. The results also indicate that the fate of methylmercury in fish-eating marine birds differs fundamentally from that in marine mammals.

Effects on Chickens of Chronic Exposure to Mercury at Low Levels Through Dietary Fish Meal

The effects of ingestion of low levels (0.014 and 0.018 p.p.m.) of mercury over prolonged periods by male and female birds of one broiler strain and three White Leghorn strains were studied. The sources of mercury were herring meals manufacutured from fish caught off the Pacific and Atlantic coasts of Canada and containing 0.22 and 0.17 p.p.m. respectively of mercury.The difference in concentrations of mercury in the two meals was reflected in differences in tissue concentrations of mercury of the birds fed the respective meals. Genetic differences in tissue accumulation of mercury were evident both in tissues which accumulated higher concentrations of mercury (feather, claw, kidney) as well as in muscle which accumulated relatively little. There was no apparent relationship between the incidence of mortality and tissue accumulation of mercury. Egg production and egg quality were unaffected by the source of herring meal in the diet. Most of the mercury in the eggs was present in the albumen and the overall average concentrations of 47 and 40 p.p.b. in the albumen and 16 and 15 p.p.b. in the yolks of the eggs from the hens fed the respective meals reflected the difference in the mercury concentration in the meals. The concentration of mercury in the eggs did not increase with the length of time during which the herring meals were fed. Fertility and hatchability of eggs were not affected by the source of herring meal fed.

Mercury concentrations in fish from the great smoky mountains national park

Excessive mercury concentrations ostensibly due to pollution have been widely reported in fish tissue. The concentrations of mercury occurring naturally in fish tissue have not been well defined. A collection for mercury analysis of 198 fish of five species was made in 1972 in three high altitude streams in the Great Smoky Mountains, 20–25 km from the nearest pollution source. Mercury concentrations were (means, p.p.m.): rainbow trout Salmo gairdneri, 0.036; brook trout Salvelinus fontinalis, 0.018 ; banded sculpin Cottus carolinae, 0.025; rosyside ace Clinostomus funduloides, 0.044; stoneroller Campostoma anomalum, 0.039. There was no significant difference in mercury concentration among fish analyzed whole, with gastrointestinal tract removed, or a strip of axial musculature. There was a significant (P0.05) difference in mercury concentration among species in one stream and in three species from different streams. A second collection of fish of the same species in 1973 verified the 1972 results. Methylmercury constituted 93 ±2.6% of total mercury. These results indicate that all fish acquire about the same tissue concentrations of mercury at chronic exposure to very low levels.

Effects of dietary mercury on mink.

A study was conducted to ascertain the effects of dietary mercury on mink. Five parts per million of dietary methylmercury was lethal to adult mink in about one month. Ten parts per million of mercuric chloride in the diet for five months did not produce adverse effects. Clinical signs of methyl mercurialism were anorexia, loss of weight, incoordination, tremors, and paroxysmal convulsions. The latency period was about 24 days; survival time averaged 33 days. Pathological changes were evident in the tissues of the mink that died of mercury poisoning. Tissue mercury residue analyses showed the highest concentration of mercury in tissues from mink fed methylmercury.

Accumulation and tissue distribution of mercury in the guinea pig during subacute administration of methyl mercury

Female guinea pigs were dosed po daily for 71 days with 0.4, 4, 40, or 400 μg Hg/kg given as radiolabeled methyl mercuric chloride. The accumulation of total mercury was followed in 10 tissues at 6 time intervals. After dosing ceased, the decay profiles of mercury were followed for an additional 35 days. The accumulation pattern for mercury was similar for each dose level, and the tissue mercury concentration on day 71 increased in the following order: blood < cerebellum < hypothalamus < calcarine cortex < frontal lobe < occipital lobe < caudate nucleus < muscle < liver < kidney. Mercury accumulation in all tissues, except kidney at the 4-, 40-, and 400-μg/kg dose levels, approached steady-state values in the 35–71 -day dosing period. The accumulation curves could be fitted by an exponential equation incorporating the mercury half-life obtained from the decay profiles. As the dose level increased, tissue mercury concentrations increased to a greater extent than anticipated. Although doses increased 1000-fold from 0.4 to 400 μg Hg/kg, kidney concentrations increased 3300-fold after 71 days of dosing. At this time, inorganic mercury (Hg 2+) comprised 42% of the total kidney mercury and 5% of the total liver mercury at the 400 μg/kg dose. Clinical signs of methyl mercury intoxication were induced in guinea pigs after dosing daily for 9 days at 5 mg Hg/kg. The activities of 6 enzymes were monitored and cholinesterase (serum), choline acetylase (caudate nucleus) and carboxylesterase (liver) were significantly lower than control values. The total mercury concentration in whole brain was 28 μg/g (wet weight). Animals dosed at 400 μg Hg/kg for 71 days showed no decrease in the activities of the selected enzymes, there was no change in weight gain when compared to the control and there were no signs of methyl mercury toxicity. The highest brain mercury concentration after 71 days dosing was 11 μg/g (wet weight) in the caudate nucleus.

Accumulation and depuration of mercury in the American oyster Crassostrea virginica

To study the kinetics of mercury uptake in oysters, adult Crassostrea virginica (Gmelin) were held in seawater containing 10 μg mercury/l (ppb) or 100 μg mercury/l (ppb), added in the form of mercuric acetate, for 60 days. Mercury concentration in tissues was determined by analysis of individually homogenized oyster meats, using wet digestion and flameless absorption spectrophotometry. After 45 days, average mercury tissue concentration was 140,000 μg mercury/kg tissue (ppb) and 28,000 μg mercury/kg tissue (ppb) in the 100 ppb and 10 ppb experimental groups, respectively. After this time, concentrations dropped sharply, probably due to spawning. Clearance of mercury from tissue was studied by exposing treated adults to estuarine water (with no additions) for 30 days (100 ppb group) and 160 days (10 ppb group). Tissue concentrations in the 100 ppb mercury environment group declined from 115,000 to 65,000 ppb, and those of the 10 ppb group declined from 18,000 to 15,000 ppb, in 18 days; there-after, no further decline occurred in either group. Oysters accumulated mercury 1,400 times and 2,800 times above the environmental concentrations of 100 and 10 ppb mercury, respectively. Total self-purification was not achieved over a 6 month cleansing period.

Methyl mercury: Acute toxicity, tissue distribution and decay profiles in the guinea pig

Acute toxicity studies with methyl mercuric chloride showed that the guinea pig was quite susceptible to methyl mercury intoxication. LD50 values were 5.5 mg Hg/kg ip and 16.5 mg Hg/kg po. One to 2 weeks after dosing, several animals began to display signs of neurotoxicity. Tissue distribution and pharmacodynamic studies with radiolabeled methyl mercuric chloride ([ 203Hg]CH 3HgCl) at 1 and 10 mg Hg/kg revealed that while most tissues decreased in mercury concentration from day 1 to day 7, cerebrum, cerebellum and muscle showed a delayed uptake of the alkyl mercurial. In CNS tissue the concentration of mercury decreased in the order cerebrum > cerebellum > spinal cord. Kidney and liver consistently contained the highest levels of mercury, and plasma the lowest, during the 49-day sampling period. One week after dosing the blood: brain ratios were less than 1. The tissue concentration of mercury was generally directly proportional to the dose administered; however, mercury levels in the gall bladder were significantly higher than anticipated on 5 of the 7 sacrifice days. Most of the tissues displayed a biphasic decay profile with a half-life of 2–3 days for the initial rapid phase of decline. This initial phase was followed by a slower tissue excretion rate for which the mean half-life for mercury was 15 ± 0.9 days and 15 ± 0.8 days for the low and high dose, respectively. The similarity of these values again indicates no dose-related effects.

The Comparative Effect of Oral Ingestion of Methyl Mercury on Chicks and Rats

Two experiments with day-old chicks and one experiment with weanling rats were conducted to determine: (1) whether low levels of mercury found in some feedstuffs would result in hazardous accumulations of mercury in their tissues, and (2) the effects of feeding various dietary levels of methyl mercury to chicks and rats. Data show that feeding animal protein (fish meal) containing higher than normal levels of mercury did not result in the concentration of mercury in poultry tissues that exceeded FDA guideline levels. In fact, breast muscle concentration of mercury averaged only 0.1 p.p.m. even when the fish meal made up 17% of the diet. Significant amounts of mercury were deposited in the feathers of the test birds. At 16.9 p.p.m. dietary mercury as methyl mercuric chloride, all chicks succumbed to mercury toxicity by 17 days of age. Total mercury dose was 28.3 mg./kg. body weight. At this level of dietary mercury, brain, liver, and breast tissue of chicks at death contained 19, 47, and 15 p.p.m., respectively. Within limits, tissue concentrations of mercury were proportional to dietary levels. After 7 weeks of mercury exposure chicks retained an average of 63% of the mercury consumed. During a 21-day depletion period, chicks excreted an average of 0.66% of the total body burden of mercury per day. Thus biological half-lives can be calculated to average about 97 days for all dietary levels. Rats fed diets containing 16 p.p.m. mercury did not show outward signs of toxicity until the 6th week of treatment. After 12 weeks of mercury exposure, the total mercury dose was 84 mg./kg. body weight. None of the rats receiving lower levels of mercury showed symptoms of toxicity. Liver and brain mercury levels in rats fed 16 p.p.m. mercury averaged 26 and 12 p.p.m., respectively. Male rats generally had higher tissue levels of mercury than females. In general, rats tolerated the highest level of dietary methyl mercury for a longer period of time than chicks which consumed three times as much mercury and deposited less mercury in their tissues.

Measurement of toxic heavy metals by neutron activation analysis

Neutron activation analysis (NAA) was used to identify explicitly the causative agent in a case of suspected heavy element poisoning of livestock that conventional diagnostic techniques left unclear. NAA, using neutrons from a TRIGA Mark II Nuclear Reactor and a 25-cc germanium lithium-drifted semiconductor detector, sequentially revealed the absence of toxic concentrations of mercury in liver and kidney tissues of an affected carcass, then the absence of toxic amounts of arsenic, and finally the presence of antimony in quantities sufficient to have killed livestock.