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PubMedDate not supplied

Use of the Topliss scheme for the design of more effective chelating agents for cadmium decorporation.

The Topliss scheme, which designates a special series of substituents for use in sequence in the search for suitably substituted aromatic compounds with biological properties superior to the parent unsubstituted aromatic compound, has been applied to the design of new chelating agents for the decorporation of cadmium from its deposits in vivo. Substituted benzylamines have been used in the syntheses of the corresponding substituted sodium N-benzyl-D-glucamine-N-carbodithioates, i.e., RC6H4CH2N(CS2Na)CH2(CHOH)4CH2OH (or RBGDTC): CF3BGDTC, R = 3-CF3; MeBGDTC, R = 4-CH3; MeOBGDTC, R = 4-OCH3; ClBGDTC, R = 4-Cl. Examination of the behavior of these compounds as agents for the mobilization of cadmium from its deposits in vivo shows that such substitution can have an appreciable effect on the organ selectivity for cadmium removal, as well as the efficacy. Of the four compounds suggested by the Topliss scheme for pilot studies, two were much more effective than the parent compound (BGDTC), and of these the best one, sodium N-(4-methoxybenzyl)-D-glucamine-N-carbodithioate (MeOBGDTC) reduced kidney cadmium levels to 30% and liver cadmium levels to 50% of those obtained with the parent compound. Sodium N-[3-(trifluoromethyl)benzyl]-D-glucamine-N-carbodithioate (CF3BGDTC) was also found to be superior to the parent compound in reducing the liver cadmium levels, though it was equivalent in reducing renal cadmium levels.

Animals↗

PubMed1996

Different growth response of Euglena gracilis to Hg, Cd, Cr and Ni compounds.

The toxicity of inorganic mercury, nickel, chromium and cadmium on the unicellular photosynthetic flagellate Euglena gracilis, strain Z (E.g.) has been tested. Under the conditions used each metal impaired the growth rate of E.g., and had a very strong effect on cell motility. The degree of cytotoxicity and motility decreased from mercury iodide to cadmium chloride to cadmium nitrate to potassium dichromate to nickel sulfate. No mutagenic effects of the metals investigated have been observed. Adverse effects of metal compounds can be tested on the eukaryotic species of Euglena gracilis used as an intermediate model system between bacterial and animal model.

Journal Article↗

PubMed1997

Gadolinium chloride reduces cytochrome P450: relevance to chemical-induced hepatotoxicity.

The Kupffer cell inhibitor, gadolinium chloride (GdCl3), protects the liver from a number of toxicants that require biotransformation to elicit toxicity (i.e. 1,2-dichlorobenzene and CCl4), as well as compounds that do not (i.e. cadmium chloride and beryllium sulfate). The mechanism of this protection is thought to result from reduced secretion of inflammatory and cytotoxic products from Kupffer cells (KC). However, since other lanthanides have been shown to decrease cytochrome P450 (P450) activity, the following studies were designed to determine if GdCl3 pretreatment alters hepatic P450 levels or activity. The toxicological relevance of GdCl3-mediated alterations in P450 activity was also estimated by determining the effect of GdCl3 pretreatment on the susceptibility of primary cultured hepatocytes to CCl4 and cadmium chloride (CdCl2). Male and female Sprague-Dawley rats were given GdCl3 (i.v., 10 mg/kg). Twenty-four hours later, livers were either processed for preparation of microsomes or for primary cultures of hepatocytes. Gadolinium chloride treatment reduced total hepatic microsomal P450 as well as aniline hydroxylase activity by approximately 30% in males and 20% in females. In hepatocytes isolated from rats pretreated with GdCl3, the toxicity caused by CCl4, but not CdCl2 was reduced. Interestingly, when GdCl3 was administered in vitro to microsomes, there was no effect on either the microsomal P450 difference spectra or p-hydroxylation of aniline. However, when GdCl3 was incubated with isolated hepatocytes, the cytotoxicity of CCl4 (but not CdCl2) was partially attenuated. These results suggest that, in addition to its inhibitory effects on KC, GdCl3 produces other effects which may alter the susceptibility of hepatocytes to toxicity caused by certain chemicals.

Analysis of Variance↗

PubMed1977

Biliary excretion of cadmium in rat. I. Dose-dependent biliary excretion and the form of cadmium in the bile.

Biliary excretion of cadmium was studied in rats after intravenous injection of different doses of cadmium chloride (0.1-2 mg Cd/kg). The rate of bile flow was not affected by cadmium injection and cadmium was excreted into bile during the first 2 hr after injection. The biliary excretion of cadmium increased with increasing dose of CdCl2. Cumulative biliary excretion of cadmium for 5 hr was 0.065% of the administered dose for groups injected with 0.1 mg Cd/kg as compared to 16.9% of the administered dose for 2 mg Cd/kg. During the 5 hr experimental period, most of the cadmium in liver cytosol was bound to high-molecular-weight proteins and less than 10% was bound to the metallothionein fraction. The biliary cadmium was recovered as a low-molecular-weight compound (less than 4,000) in experiments with various doses of cadmium and no cadmium was attached to high-molecular-weight proteins or metallothionein in the bile. The low-molecular-weight cadmium complex in bile was partially characterized as Cd-glutathione by thin-layer chromatography and amino acid analysis.

Animals↗

PubMed1997

Synthesis, Crystal Structure, and Second-Order Optical Nonlinearity of Bis(2-chlorobenzaldehyde thiosemicarbazone)cadmium Halides (CdL(2)X(2); X = Br, I).

The new Schiff base ligand 2-chlorobenzaldehyde thiosemicarbazone (L, 1) has been synthesized and characterized by spectral techniques and single-crystal X-ray analysis. Crystals of 1 are monoclinic, space group P2(1)/n with a = 12.964(4) Å, b = 5.131(5) Å, c = 4.970(1) Å, beta = 94.32(2) degrees, and Z = 4. The thiosemicarbazone moiety adopts a configuration with N(1) cis to N(3) and places the E configuration about both the bonds C(1)-N(2) and C(2)-N(3). The monodentate behavior of the neutral ligand (L) has been investigated in two cadmium halides CdL(2) Br(2) (2) and CdL(2)I(2) (3). Compound 2 crystallizes in space group Cc witha = 8.175(1) Å, b = 14.176(1) Å, c = 21.073(1) Å, beta = 94.02(1) degrees, and Z = 4. Compound 3 crystallizes in space group P&onemacr; with a = 10.9577(1) Å, b = 16.174(1) Å, c = 7.878(1) Å, alpha = 100.50(1) degrees, beta = 109.39(1) degrees, gamma = 83.67(1) degrees, and Z = 2. The coordination geometry about the cadmium(II) atom in compound 2 conforms to a tetrahedral configuration with two sulfur atoms from two unequivalent neutral ligands and two bromide atoms. Whereas the coordination geometry about the cadmium(II) atom in compound 3 is (4 + 1) distorted trigonal bipyramidal with two iodide atoms and one sulfur atom in the equatorial plane, the other thiosemicarbazone sulfur and the iodide atom I(1a) of an adjacent moiety occupy the axial positions. Compound 2 exhibits powder SHG efficiencies ca. 20 times that of urea, whereas compound 3 does not exhibit any SHG efficiency. Theory and experiment suggested that intermolecular contact is the main factor controlling the SHG efficiencies of compounds.

Journal Article↗

PubMed2000

Implication of free radicals and glutathione in the mechanism of cadmium-induced expression of stress proteins in the A549 human lung cell-line.

Cellular mechanisms underlying the expression of stress proteins (HSP) were studied in the human cell-line A549 submitted to a pollutant, cadmium, in the presence of several agents which modulate the glutathione level and, supposedly, the effects of this metal in the cell. It was observed that HSP 90, HSP 72 and HSP 27 are significantly over-expressed after exposure to cadmium chloride for 24 h. Low cadmium concentrations (i.e. from 1 to 10 microM) also triggered a slight accumulation of glutathione, whereas this compound was depleted after exposure to higher cadmium concentrations (25-100 microM). When 50 microM diethyl-maleate, which traps glutathione, was added together with cadmium, the over-expression of HSP 72 and HSP 90 was much stronger. Treatment of cells with 20 or 40 mM N-acetyl-L-cysteine, which traps free radicals, was found to increase by 30% the glutathione level and to suppress the HSP over-expression. From our results, it is suggested that HSP induction by cadmium in A549 cells is due, at least in part, to the oxidative stress consisting in formation of reactive oxygen species and inhibition of peroxides detoxification. Due to this oxidative status within the cell, more proteins would be damaged inducing the HSP over-expression.

Acetylcysteine↗

PubMed1987

A comparative study of the effects of inhaled cadmium chloride and cadmium oxide: pulmonary response.

The effects of aerosols of cadmium chloride (CdCl2) and cadmium oxide (CdO) on pulmonary biochemical function were compared. Rats and rabbits were exposed to 0.25, 0.45, or 4.5 mg Cd/m3 for 2 h. Pulmonary toxicity was determined histologically and biochemically. Cadmium chloride and CdO showed a deposition response that was linearly related to the chamber concentration. Both compounds caused multifocal, interstitial pneumonitis 72 h after exposure, but the CdO lesion was more severe with proliferation of fibrocytic-like cells as well as pneumocytes. Comparing the two Cd compounds at the highest concentration (4.5 mg Cd/m3), the biochemical responses in the rat were similar. The majority of the effects occurred 72 h after exposure, with significant increases in lung weight, lung-to-body weight ratio, GSH reductase, GSH transferase, and G-6-PDH. However, GSH peroxidase was inhibited immediately after the CdO exposure. Cadmium oxide-related alterations in the parameters studied could easily be distinguished from those of CdCl2 at the exposure concentration of 0.45 mg Cd/m3. The response pattern in the rabbit resembled that of the rat. In both species Cd had a consistent inhibitory effect on pulmonary GSH peroxidase, even at the lowest concentration of 0.25 mg Cd/m3. Based on these findings, inhaled CdO appeared to be more toxic to the lung than inhaled CdCl2.

Aerosols↗

PubMed2006

Evaluation of immunotoxic and immunodisruptive effects of inorganic arsenite on human monocytes/macrophages.

A trivalent inorganic arsenic, arsenite, has been causing chronic inflammation in humans through the consumption of contaminated well water. The total peripheral blood arsenic concentrations of chronic arsenic-exposed patients, who had inflammatory-like immune responses, are less than 1 microM, thus, nM concentrations may be very important regarding the chronic inflammatory effects by arsenite. However, there are few reports about the biological effects of low concentrations of arsenite in mammalian cells, especially in normal immune effector cells. In this study, we examined whether arsenite has any biological and/or toxicological effects on the differentiation of human peripheral blood monocytes into macrophages using the colony-stimulating factor (CSF) in vitro compared with that of other metallic compounds, and found that arsenite sensitively inhibited the CSF-induced in vitro maturation of monocytes into macrophages at nM levels, and it also induced small, nonadhesive and CD14-positive abnormal macrophage generation from monocytes with granulocyte-macrophage CSF (GM-CSF) at 50-500 nM without cell death. The addition of other metallic compounds, including chromium, selenium, mercury, cadmium, nickel, copper, zinc, cobalt, manganese and other human pentavalent arsenic metabolites, such as inorganic arsenate, monomethylarsonic acid and dimethylarsinic acid, could not induce the same abnormal cell generation from monocytes with CSFs at any concentration and any additional time schedules; they showed only simple cytolethality in monocytes and macrophages at any concentration and any additional time schedules; they showed only simple cytolethality in monocytes and macrophages at n-mM levels accompanied by cell death. This work may have implications in the arsenic-induced chronic inflammation in humans.

Arsenites↗

PubMed2003

Blue dimetallic complexes of two heavy metal ions Cd(II) and Hg(II) with an extended nitrogen donor ligand. Preparation, spectral characterization, and crystallographic studies.

In methanol, the metal salts CdCl2.H2O and HgCl2 react instantaneously with the deprotonated ligand, L-, producing molecular dimetallic ink-blue complexes of general formula M2Cl2L2, M=Cd(II), (1) and Hg(II), (2) (HL=2-[2-(pyridylamino)phenylazo]pyridine). Crystal structures of these two complexes are reported. The coordination sphere around each Cd(II) ion in 1 is a distorted square pyramidal. The metal ion (Cd1) sits above the basal plane of three nitrogen atoms, N(1), N(3), and N(4). The second cadmium ion (Cd2) in this compound lies below the plane of three nitrogen atoms, N(6), N(8), and N(9). The apical positions are occupied by two Cl atoms. Secondary intramolecular interactions between the metal ions and the anionic secondary amine nitrogen atoms (N(4) and N(9)) are noted. The geometry of each Hg(II) ion in the mercury complex, Hg2Cl2L2.0.5H2O, is also distorted square based pyramid with the metal ions lying out of planes of the three nitrogen atoms of the chelating ligands. Secondary Hg(1)...N(1A) (deprotonated amine) interactions are noted. The separation between the two Hg(II) ions in this complex is within the sum of their van der Waals radii. Solution properties of these blue complexes are reported. The origin of the intense blue color in these complexes is the intraligand transitions that occur near 615 nm. 1H NMR of Hg2Cl2L2.0.5H2O indicates that it undergoes exchange in solution with the coordinated ligands.

Journal Article↗

PubMedDate not supplied

[The antimutagenic activity of biomass extracts from the cultured cells of medicinal plants in the Ames test].

Antimutagenic activity of 20 and 40% ethanol extracts from the biomass of Rhodiola rosea, Polyscias filicifolia, Panax ginseng and Ungernia victoris cultured cells have been studied. DDDTDP, ethidium bromide, benz(a)pyrene, benzidine served as model mutagens for Salmonella typhimurium TA 98 strain (the latter two were tested in presence of metabolic activation system); for S. typhimurium TA 100 strain these were tio-tefa, bichromate potassium and sodium azide and heavy metal compounds (chlorides of manganese, zinc, cadmium, lead acetate) for both strains. Higher capacity of the extracts from the biomass of R. rosea and P. filicifolia to counteract gene mutations induced by various mutagens was demonstrated (ca. 90% inhibition in isolated cases). In the experiment with the metabolic activation most effective proved to be the extracts from the P. ginseng biomass (up to 34% and 47% mutagenicity inhibition).

Antimutagenic Agents↗

PubMed1990

[Studies on protective effect of selenium on the nephrotoxicity of cis-diamminedichloroplatinum (CDDP) in mice].

Protective effect of sodium selenite (Se) on the nephrotoxicity of cis-diamminedichloroplatinum (CDDP) was studied in mice. The administration of CDDP alone at doses of 50 mumols/kg caused the increase of blood urea nitrogen (BUN) and urinary N-acetylglucosaminidase (NAG) and the degeneration of proximal tubule cells pathologically. The co-administration of Se, especially at doses of 20 mumols/kg/day, inhibited the increase of BUN and urinary NAG and depressed the degeneration of proximal tubule cells. The administration of CDDP at doses of 20 mumols/kg caused a mild reduction of transplanted Lewis lung carcinoma and a decrease of metastasis to lung. The co-administration of Se at doses of 8 mumols/kg didn't inhibit the antitumor effect of CDDP against Lewis lung carcinoma. Co-administration of Se didn't influence concentration of CDDP in plasma, blood cells, kidney and liver. In mice fed Se deficient diet, the nephrotoxicity of CDDP increased and activities of glutathione peroxidase (G-Px) in blood and kidney decreased. In mice co-administered with Se, G-Px activities didn't increase. These results suggest that co-administration of Se may allow use of CDDP at higher doses in cancer chemotherapy. Interaction between CDDP and Se differs from that between mercury and Se, and cadmium and Se(formation of compound). Intake of Se is related to appearance of the nephrotoxicity of CDDP. G-Px may be related to a part of the protective effect of Se on the nephrotoxicity of CDDP.

Acetylglucosaminidase↗

PubMed1990

[Studies on the mechanism of protective effect of selenium on nephrotoxicity of cis-diamminedichloroplatinum (CDDP) in mice].

The mechanism of protective effect of sodium selenite (Se) on the nephrotoxicity of cis-diamminedichloroplatinum (CDDP) was studied with mice. CDDP and Se concentrations in the plasma, blood cell, kidney and liver were measured in mice given CDDP alone and those given both CDDP and Se. The nephrotoxicity of CDDP was observed in mice fed Se deficient diet (SDD). The activities of glutathione peroxidase (G-Px) in the plasma, blood cells, kidney and liver were measured in mice mentioned above. Co-administration of Se did not influence on the concentration of CDDP in the blood, kidney and liver. In mice fed SDD, the nephrotoxicity of CDDP increased and G-Px activities of the blood and kidney decreased. In mice given Se, G-Px activities was not increased. These results suggest that interaction between CDDP and Se differs from that between mercury and Se, or between cadmium and Se (formation of compound). Intake of Se is related to the appearance of the nephrotoxicity of CDDP. G-Px may be related partially to the protective effect of Se on the nephrotoxicity of CDDP.

Animals↗

PubMed1989

Multinuclear NMR studies of the divalent metal binding site of NADP-dependent isocitrate dehydrogenase from pig heart.

The metal activator site of NADP-dependent isocitrate dehydrogenase from pig heart has been probed by using 113Cd and 25Mg NMR as well as manganese paramagnetic relaxation of nuclei in the fast-exchanging ligands alpha-ketoglutarate and adenosine 2'-monophosphate. Cadmium NMR shows that cadmium, bound to the enzyme in the presence of isocitrate, has a resonance at 9 ppm relative to cadmium perchlorate, while the free Cd-isocitrate complex has a resonance at -23 ppm. Comparison with model compounds and previously studied proteins indicates that cadmium is coordinated with six oxygen ligands. Measurements as a function of cadmium concentration give a dissociation constant of 66 microM and a dissociation rate constant of 1.5 X 10(4) s-1 at pH 7.0. 25Mg NMR demonstrates that the line width of the magnesium resonance is increased upon binding to isocitrate dehydrogenase. A further increase in line width is observed upon addition of isocitrate. Measurement of line widths as a function of temperature reveals that in the binary complex between magnesium and enzyme, exchange is the major contributor to broadening while in the ternary complex containing isocitrate, the intrinsic relaxation in the bound state is also important, suggesting an increase in the dissociation rate constant for magnesium from the ternary complex. Paramagnetic relaxation studies of nuclei of alpha-ketoglutarate, bicarbonate, and adenosine 2'-monophosphate locate the divalent metal within the active site. The results with adenosine 2'-monophosphate show that atoms in the adenosine moiety of the coenzyme are at least 8 A from the metal site.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

[Determination of tetradecyl pyridyl bromide in waste water by flame atomic absorption spectrometry].

A indirect method for the determination of tetradecyl pyridyl bromide (TPB) was established (TPB) by flame atomic absorption spectrometry (FAAS). TPB was combined with cadmium tetrathocyanate to make neutral ion association compounds, which are extracted into xylene. The concentration of TPB can be indirectly determined by the absorption of cadmium in xylene layer with flame atomic absorption spectrometry. The linear range of TPB is 0.03-0.80 mg/L. The sensitivity is 0.0212 mg/L x 1%. When the method was applied to the analysis of waste water, the recovery is from 98% to 104% and the RSD is less than 9.16%.

Hydrocarbons, Brominated↗

PubMed2001

Infrared studies on Co and Cd complexes of sulfamethoxazole.

In this study, the new Co and Cd complexes of sulfamethoxazole (SMX) (drug substance) [4-amino-N-(5-methyl-3-isoxazolyl) benzenesulfonamide] have been prepared for the first time and their infrared spectra have been investigated. The infrared spectra of the samples were recorded in the range 4000-400 cm(-1) and their fundamental vibrational wave numbers were obtained. The vibrational assignments were determined by using the group frequency tables and compared with the wave numbers of SMX found in the literature. The SMX wave numbers observed in the infrared spectra of the metal complexes were compared with those of free SMX. Investigations of the infrared spectra of the metal complexes indicated the vibrations due to the amino and sulfonamido groups are shifted with respect to the free molecule in line with their coordination to the metal. In the cadmium complex, the active binding sites of SMX are the sulfonamide nitrogen and sulfonic oxygen; in cobalt compound, the metal atom coordinates through the sulfonamide and amino nitrogens. The low energy calculations were also carried out by using geometry optimization. It is shown that the proposed structure for the metal complexes of SMX derived from the infrared spectra are consistent with the theoretical results.

Cadmium Compounds↗

PubMed2006

Phytochelatin-cadmium-sulfide high-molecular-mass complexes of Euglena gracilis.

High-molecular-mass PC complexes (PC-HMWCs) constituted by phytochelatins (PCs), cadmium and sulfide are synthesized by several organisms after exposure to cadmium. In this study, PC-HMWCs were isolated from photoheterotrophic Euglena gracilis and purified to homogeneity, resulting in compounds of molecular mass 50-380 kDa depending on the CdCl2 and sulfate concentrations in the culture medium. In contrast with plants and some yeasts, PC-HMWCs from E. gracilis mainly comprise (57-75%) monothiol molecules (Cys, gamma-glutamylcysteine, GSH) and, to a lesser extent (25-43%), PCs. A similar acid-soluble thiol compound composition was found in whole cell extracts. The -SH/Cd2+ and S2-/Cd2+ ratios found in purified PC-HMWCs were 1.5 and 1.8, respectively; the (-SH + S2-)/Cd2+ ratio was 3.2. PC-HMWCs of molecular mass 60 and 100 kDa were also localized inside Percoll-purified chloroplasts, in which cadmium and PCs were mainly compartmentalized. Cadmium and sulfur-rich clusters with similar sulfur/cadmium stoichiometries to those of the purified PC-HMWCs were detected in the chloroplast and throughout the cell by energy dispersive microanalysis and atomic resolution electron microscopy. The presence of PC-HMWCs in primitive photosynthetic eukaryotes such as the protist, E. gracilis, suggests that their function as the final cadmium-storage-inactivation process is widespread. Their particular intracellular localization suggests that chloroplasts may play a major role in the cadmium-resistance mechanism in organisms lacking a plant-like vacuole.

Animals↗

PubMed1999

A Daphnia magna first-brood chronic test: An alternative to the conventional 21-Day chronic bioassay?

In this study a comparison was made of the results obtained in Daphnia magna chronic bioassays after first-brood release and after 21 days of exposure, using inhibition of normal reproduction and growth as effect criteria and EC10, EC20, EC50, no-observed-effect concentration (NOEC), and lowest-observed-effect concentration (LOEC) as statistical parameters. Test substances were sodium bromide (NaBr), 3,4-dichloroaniline (DCA), cadmium, and parathion. For NaBr, DCA, and cadmium, toxicity evaluated after the first-brood release was similar to toxicity evaluated after 21 days, using reproduction as end point. Parathion did not affect either reproduction or growth. Thus, LC50, NOEC, and LOEC were calculated using mortality as the endpoint for parathion. Results indicate that the period until release of the first brood is sufficient to predict the toxicity of some chemicals to D. magna. Values estimated on the basis of a logistic model (EC10, EC20, and EC50) were more appropriate than NOECs and LOECs for evaluating toxicity of the test substances. Furthermore, classic endpoints used for the evaluation of chronic toxicity (inhibition of normal reproduction and growth) may not be adequate to evaluate the sublethal toxicity of compounds that induce cumulative effects leading to mortality within the test period and causing no observable effects on the reproduction and growth of the species. Endpoints indicative of biochemical stress or effects on specific targets of the test compound may be useful in sublethal toxicity evaluation.

Aniline Compounds↗

PubMed2001

Use of in vitro assays to assess hematotoxic effects of environmental compounds.

The number of chemicals being introduced into the environment increases and many of these substances may pose a health risk to exposed individuals. Many environmental toxicants with a potential toxicity to the hematopoietic system have been identified by animal experiments. Owing to the risks of severe chronic hematopoietic disorders, it is important to screen chemicals for their hematotoxicity. The aim of this work was to identify, through the use of in vitro techniques, targets for hematotoxic effects. Our study focused on myeloid and erythroid hematopoietic progenitors and stromal stem cells as possible targets. The in vitro assays showed that various hematotoxic compounds exert different effects on these cell populations. In vitro exposure of murine bone marrow cells to various inorganic (cadmium, lead) and organic (benzene metabolites, lindane. benzo-[a]-pyrene (BaP), PCB (polychlorinated biphenyl) congeners) environmental chemicals indicated that hematopoietic or stromal bone marrow cells were targets for most of the chemicals. Stromal cells were more affected by lead, cadmium, and BaP compared to myeloid cells. Benzene and phenol gave no response, but the metabolites catechol and hydroquinone were equally toxic to the stromal and the myeloid progenitor cells. Among the PCBs tested, PCB126 was most toxic. Human progenitor cells derived from cord blood were exposed in vitro to catechol, hydroquinone, lead nitrate, and PCBs. Human hematopoietic cells were sensitive to the tested compounds. Human erythroid progenitors are more susceptible to lead exposure than are myeloid progenitors. Based on the in vitro tests, humans are more sensitive to lead, catechol, and PCB126 than are mice. In contrast to the murine data, humans responded with individual differences to lead and PCB126.

3T3 Cells↗