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Blood cells mercury

The impacts of contaminants on the structure of the immune system can be assessed by examining white blood cell (WBC) numbers and the mass and cellularity of immune organs, although these indicators are usually not as sensitive as measures of immune function. Avian immunotoxicity studies frequently assess total and (or) differential WBC counts [79], and immunosuppression can be indicated by reduced numbers of WBCs or elevated WBC numbers caused by recurrent infections. An elevated heterophil to lymphocyte ratio can indicate altered immune status in response to corticosteroid stress hormones or other factors [78,7 9], Exposure to lead shot or lead acetate has been shown to alter total and (or) differential WBC numbers in Japanese quail (Coturnix coturnix) and mallards [81-83], In western grebes (Aechmophorus occidentalis) from California, concentrations of mercury in the kidney were positively correlated with heterophil... [Pg.393]

The mercuric ion, Hg2 +, which is obtained after oxidation in the red blood cells and other tissues, is able to form many stable complexes with biologically important molecules or moieties such as sulphydryl groups. The affinity of mercury for sulphydryl groups is a major factor in the understanding of the biochemical properties of mercuric compounds, resulting in interference with membrane structure and function and with enzyme activity. [Pg.190]

After injection into mice, mercuric chloride has been found to be distributed equally between erythrocytes and plasma in blood for up to 1 day after the administration [12, 13]. There is, however, a gradual increase in red blood cell/plasma ratio. In the erythrocytes, mercury is probably bound to sulphydryl groups on the hemoglobin molecule [14], though the binding is readily reversible [15]. There is possibly also a binding to glutathione [16]. [Pg.191]

Immunosuppressive effects have been obtained in vitro with mercuric chloride. A marked inhibition of the mixed lymphocyte reaction in mice as well as PFC (plaque forming cell) response to SRBC (sheep red blood cells) by mercuric chloride [166] has been reported. Chronic exposure to mercury of rabbits gave immunosuppression, measured as low antibody titres to viral agents [167], A suppression of antibody production in chickens exposed to mercuric chloride has also been reported [168]. Furthermore, an inhibition of mitogenic response to PHA in lymphocytes by mercuric chloride has been obtained [169],... [Pg.201]

O. Ertas and H. Tezel, A validated cold vapour-AAS method for determining mercury in human red blood cells, J. Pharm. Biomed. Anal., 36(4), 2004, 893-897. [Pg.144]

Elemental mercury vapor is relatively lipid soluble and is readily absorbed from the lungs following inhalation and is oxidized in the red blood cells to Hg2+. Elemental mercury may also be transported from red blood cells to other tissues such as the CNS. Elemental mercury readily passes across the blood-brain barrier into the CNS and also into the fetus. The metallic compound is only poorly absorbed from the gastrointestinal tract, however. [Pg.387]

Although elemental mercury is rapidly oxidized to mercury(II) in erythrocytes (red blood cells), which have a strong affinity for mercury, a large fraction of elemental mercury absorbed through the pulmonary route reaches the brain prior to oxidation and enters that organ because of the lipid solubility of mercury(O). This mercury is subsequently oxidized in the brain and remains there. Inorganic mercury(II) tends to accumulate in the kidney. [Pg.235]

Absorption varies significantly according to the form of exposure (elemental, inorganic, or organic). Inhaled mercury vapor crosses through the alveolar cells readily, is 75% absorbed, and is carried by the red blood cells. Catalase in these cells oxidizes elemental mercury almost at once to the divalent state. Alcohol inhibits the catalase activity however, in the seconds it takes for a complete blood circulation cycle, a significant amount of free mercury can cross the blood-brain barrier. [Pg.1621]

Once absorbed, metallic and inorganic mercury enter an oxidation-reduction cycle. Metallic mercury is oxidized to the divalent inorganic cation in the red blood cells and lungs of humans and animals. Evidence from animal studies suggests that the liver is an additional site of oxidation. Absorbed divalent cation from exposure to mercuric compounds can, in turn, be reduced to the metallic or monovalent form and released as exhaled metallic mercury vapor. In the presence of protein sulfhydryl groups, mercurous mercury (Hg+) disproportionates to one divalent cation (Hg+2) and one molecule at the zero oxidation state (Hg°). The conversion of methylmercury or phenylmercury into divalent inorganic mercury can probably occur soon after absorption, also feeding into the oxidation-reduction pathway. [Pg.50]

In volunteers who inhaled a tracer dose of metallic mercury vapor for 20 minutes, approximately 2% of the absorbed dose was deposited per liter of whole blood after the initial distribution was complete (Cherian et al. 1978). Uptake into the red blood cells was complete after 2 hours, but plasma uptake was not complete until after 24 hours. Mercury concentration in red blood cells was twice that measured in the plasma. This ratio persisted for at least 6 days after exposure. However, the ratios of 1-2 have been reported for metallic mercury vapor (Miettinen 1973). [Pg.194]

After exposure to mercury vapor, mercury is distributed throughout the body in different chemical and physical states. Metallic mercury dissolves in the blood upon inhalation, and some remains unchanged (Magos 1967). Metallic mercury in the blood is oxidized to its divalent form in the red blood cells (Halbach and Clarkson 1978). The divalent cation exists as a diffusible or nondiffusible form. The nondiffusible form is mercuric ions that bind to protein and are held in high-molecular weight complexes, existing in equilibrium with the diffusible form. [Pg.196]

In the plasma, the mercuric ion is predominantly nondiffusible and binds to albumin and globulins (Berlin and Gibson 1963 Cember et al. 1968 Clarkson et al. 1961). Following mercuric salt administration, levels of mercuric ions in the plasma are similar to levels of mercuric ions in the red blood cells. Binding of mercury also occurs in tissues, and retention varies, with the brain retaining mercury the longest. [Pg.196]

Organic Mercury. Distribution of organic mercury compounds in humans and animals is similar to that of metallic mercury. Methylmercury distributes readily to all tissues, including the brain and fetus, after absorption from the gastrointestinal tract. The uniform tissue distribution is due to methylmercury s ability to cross diffusion barriers and penetrate all membranes without difficulty (Aberg et al. 1969 Miettinen 1973). Thus, tissue concentrations tend to remain constant relative to blood levels. About 90% of the methylmercury in blood is found in the red blood cells (Kershaw et al. 1980). The mean mercury concentrations in red blood cells were 27.5 ng/g and 20.4 ng/g in males and females, respectively, exposed to mercury, primarily from mercury-contaminated fish (Sakamoto et al. 1991). Because of this uniform distribution in tissues, blood levels are a good indicator of tissue concentrations independent of dose (Nordberg 1976). [Pg.199]

Following acute mercury vapor intoxication of two humans, it was found that, despite chelation therapy with multiple chelators (2,3-dimercaptopropanol [BAL] followed by 2,3-dimercaptosuccoinic acid [DMSA]), relatively high concentrations of mercury remained in the plasma for a very long time (Houeto et al. 1994). The authors suggested that this could be explained by the progressive release of mercury from red blood cells and tissues after oxidation. In a group of chloralkali workers exposed to metallic mercury vapor for 1-24 years (median, 10 years), a decrease in the mercury concentration (following... [Pg.208]

The rate of mercury excretion was also slower in younger animals (7 or 15 days) than in older animals (24 and 56 days) (Thomas et al. 1982). This age-dependent difference in the rate of mercury excretion may reflect differences in the sites of mercury deposition (i. e., hair, red blood cells, skin). In neonatal rats, the excretion of methylmercury is longer than in adult rats because of the inability of the neonatal liver to secrete the toxicant into the bile. Therefore, the immaturity of the transport system in neonatal rats affects the elimination of mercury. [Pg.216]

Mercury is unusual in its ability to induce delayed neurological effects. This is especially prevalent with exposure to alkyl mercury compounds. In such cases, the onset of adverse effects may be delayed for months after the initial exposure. The delayed effects of methyl- and dimethylmercury reported in human poisonings are thought, in part, to result from binding to red blood cells, and subsequent slow release. Methylmercury also forms a complex in plasma with the amino acid cysteine, which is structurally similar to the essential amino acid methionine (Aschner and Clarkson 1988). Clarkson (1995) proposed that methylmercury can cross the blood-brain barrier "disguised" as an amino acid via a carrier-mediated system (i.e., transport is not solely the result of methylmercury s lipid solubility). [Pg.248]

Following exposure and absorption, metallic mercury is distributed primarily to the kidneys. Elemental mercury is highly soluble in lipids and easily crosses cell membranes (Gossel and Bricker 1984), particularly those of the alveoli (Florentine and Sanfilippo 1991). Once in the blood, this form of mercury can distribute throughout the body, as well as penetrate the blood-brain barrier, thus accumulating in the brain (Berlin et al. 1969). The body burden half-life of metallic mercury is about 1-2 months (Clarkson 1989). The kidney is also the primary organ of accumulation for compounds of inorganic mercury, but the liver, spleen, bone marrow, red blood cells, intestine, and respiratory mucosa... [Pg.363]

Preston, RL Mount Desert Island Biological Salsbury Cove, ME Mercury interaction with the taurine transport system of red blood cells. NIEHS... [Pg.394]

Sakamoto M, Nakano A, Kinjo Y, et al. 1991. Present mercury levels in red blood cells of nearby inhabitants about 30 years after the outbreak of Minamata disease. Ecotoxicol Environ Safety 22 58-66. [Pg.642]

Organic mercury is the most readily absorbed (90-95% from the gastrointestinal tract), and after absorption distributes especially to the brain, particularly the posterior cortex. All the forms of mercury will cross the placenta and gain access to the foetus, although elemental mercury and organic mercury show greater uptake. The concentrations in certain foetal tissues, such as red blood cells, are greater than in maternal tissue. [Pg.644]


See other pages where Blood cells mercury is mentioned: [Pg.353]    [Pg.353]    [Pg.106]    [Pg.387]    [Pg.119]    [Pg.2612]    [Pg.2613]    [Pg.116]    [Pg.249]    [Pg.249]    [Pg.273]    [Pg.1278]    [Pg.1607]    [Pg.153]    [Pg.185]    [Pg.204]    [Pg.205]    [Pg.227]    [Pg.232]    [Pg.297]    [Pg.330]    [Pg.340]    [Pg.345]    [Pg.359]    [Pg.522]    [Pg.143]    [Pg.166]    [Pg.3]    [Pg.160]   
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