[A quantitative analysis of the distribution of proteins, labeled by H3-lysine, in chromosomes at different stages of the mitotic cycle].
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Biomedical subjects
Publications and source records attributed to I M Shapiro.
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Lead is accumulated and immobilized for long periods of time in teeth. Thus the Pb concentration of a tooth can be used as an indicator of the cumulative Pb intake of a child. Shed and extracted teeth were collected from children in Beijing, China and some industrial regions in the Middle Urals in Russia. The Pb levels in the teeth were measured in Philadelphia, PA using an X-ray fluorescence (XRF) technique. Since Pb deposits in the tooth during the entire period that it is in the child, the measured tooth Pb level was divided by the age of the child when the tooth was shed and expressed in terms of (microgram/g-yr). 10% (n = 100) of the teeth from Beijing, China had Pb levels exceeding 5.5 and 3% above 9 micrograms/g-yr. For comparison, in the 1970s when urban environmental Pb levels were elevated, the tooth Pb levels in Philadelphia children were similar, i.e. 10% (n = 298) of the teeth had Pb levels exceeding 7.5 and 6% were above 9 micrograms/g-yr. Children in a more rural setting, Bennington, VT, had no detectable tooth Pb (n = 200). The Pb levels in the teeth from the Urals were much higher; 50% (n = 134) of the teeth had Pb levels exceeding 7.5 and 10% exceeding 17.8 micrograms/g-yr. The tooth Pb levels observed in the teeth from Beijing, and more so from the Urals, indicate that these children are residing in Pb polluted environments. Further studies are required to determine the extent of the Pb pollution and to explore the possibility that there are associated Pb-related health deficits.
Cumulative lead exposure in 193 inner-city black children was assessed by measuring lead concentrations in the primary and circumpulpal dentine of their deciduous teeth. Lead concentrations for these children were comparable to the concentrations reported in population studies of low-income children living in inner-city areas. Analysis of the children's neuropsychological test performance showed that elevated lead levels were associated with deficits in visual-motor functioning and perceptual integration, right-left orientation, and verbal abstraction; other verbal abilities and motor functioning were not affected. Possible alternative explanations for these findings were evaluated by examining the relationships between lead and maternal intelligence, family socioeconomic status, and perinatal indicators of neurological impairment. None of these relationships was significant. It was concluded that, even at levels usually regarded as asymptomatic, lead in the environment represents a hazard to inner-city children.
Eighteen patients with known past occupational lead exposure underwent parenteral diagnostic chelation with ethylenediaminetetraacetic acid and x-ray fluorescent determination of in vivo skeletal lead stores at the distal styloid process of the ulna and at the temporal base bone using a cobalt 57 source and measuring lead Ka x-rays. X-ray fluorescent lead measurements in both locations correlated with results of diagnostic chelation. Using a post-chelation urinary excretion of greater than 600 micrograms lead/24 h as the definition of "high-" lead stores, sensitivity of x-ray fluorescence at the wrist and temple was 56% and 39%, respectively.
Chick epiphyseal plate mitochondria observed in vitro suggest that energy dependent Ca++ uptake was maximal in the presence of ATP and a respiratory substrate. However, nucleotides other than ATP had no effect on this type of cation uptake. The observation that Ca++ accumulation was sensitive to the presence of 2,4-DNP and a number of respiratory inhibitors suggested that the mechanism of cation accumulation was similar to that described in tissues that do not undergo biological mineralization. Non-energy supported Ca++ acumulation was studied in the presence of rotenone and antimycin A. Under these conditions, the amount of Ca++ bound by skeletal tissue mitochondria was greater than bound by mitochondria obtained from noncalcifying tissues. Following isopycnic centrifugation, the Ca++ loaded mitochondria banded at different sucrose densties but the Ca++ affinity of mitochondria at each density band was similar. Hence, no particular mitochondrial species seems to be responsible for cation transport.
Mercury exposure in dental offices may represent a health hazard. Previous studies evaluated mercury exposure through blood, urine or hair analysis. The mercury content of body fluids in hair depends on the time since mercury exposure, mode of intake and its excretion, and sequestration by different tissues. Utilizing an x-ray fluorescence technique, the mercury burden in bone, liver, lung, spleen, and kidney was measured in vitro. The x-ray fluorescence, XRF, and chemical assays of the mercury content of these samples correlated. The XRF technique was used to assay the mercury content of tissues irradiated in vivo. It was found that the mercury signal arising at a depth in tissue was reduced as the thickness of overlying material increased. Thus, the XRF assay for tissues in vivo is confined to organs near the surface. The mercury content of the superficial layers of the head and wrist were determined in situ for a dental population. Concentrations as low as 20 micrograms/g could be detected with an exposure of 60 mR. Of the 298 dentists evaluated, 28% had greater than 20 micrograms/g of mercury in the head.
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The major goal of this investigation was to determine if the sensitivity of lymphocytes and monocytes to mercury (Hg++) was related to intracellular glutathione (GSH) levels and the thiol redox status [GSH/glutathione disulfide (GSSG)]. To isolate cells based upon their GSH content, T and B-cells were stained with monochlorobimane (MCB) and separated into high and low fluorescent groups by FACS analysis. Cells with high GSH fluorescence were found to be resistant to both the cytotoxic and immunotoxic effects of HgCl2 as evidenced by cell viability and their responsiveness to mitogen, respectively. In contrast, cells with low levels of GSH were extremely sensitive to mercury. To further examine the relationship between GSH level and mercury exposure, T-cells, B-cells and monocytes were treated with different doses of HgCl2 for 12 hrs. All cells exhibited a dose-dependent decrease in GSH content with a concomitant reduction in GSSG levels. However, the GSH/GSSG ratio in these cells remained constant, or increased following exposure to mercury. GSH levels were also reduced in monocytes following exposure to HgCl2; in this case, GSSG levels remained constant and a decline in the GSH/GSSG ratio was observed. For all cell types, mercury did not inhibit the activities of GSH reductase and GSH peroxidase, enzymes responsible for oxidation/reduction of GSH and GSSG, respectively. Results of the study clearly show that susceptibility to the immunotoxic effects of HgCl2 is, in part, dependent upon GSH levels and further that mercury inhibits GSH generation by lymphocytes and monocytes.(ABSTRACT TRUNCATED AT 250 WORDS)