Proceedings of the Korean Society of Applied Pharmacology
/
1995.10a
/
pp.137-146
/
1995
In this study, it was tested whether lead intoxication could change thiamine content and the thiamine related biochemical factor such as activity of transketolase in the brain, and whether the changes of the myelin composition :s well as the seizure threshold induced by lead intoxication in rats be related to these changes of thiamine status and thiamine related biochemical factors. In addition, it was also tested whether administration of excessive thiamine can reverse the toxic manifestation of lead in lead intoxicated animals. Five groups of Wistar rats were prepared: 1)Control group, 2)lead treated group, 3)thiamine treated group, 4)lead plus thiamine treated group and 5)thiamine deficiency group. Each group of animals was divided into three subgroups based on ages: 3, 7 and 10 weeks of age subgroups. Lead concentration, thiamine content, the activity of transketolase and myelin composition in brain areas and threshold of electric shock seizure were tested in each group. Lead concentrations in all brain regions of lead treated group were higher than those of control group, and those of lead plus thiamine treated group were significantly lower than those of lead treated group. Thiamine contents in the brain regions of lead treated group were significantly lower than those of control group, and those of lead plus thiamine treated group were recovered back to those of control group. Activities of transketolase of lead treated group were significantly lower than those of control group, while those of lead plus thiamine treated group were recovered back to those of control group. The cases of which was observed with the concomitant changes of thiamine content and transketolase activity in myelin content or constituent of all the brain regions tested were total amount of myelin protein in the cerebellum of 3 week old rats, and phospholipid in the cerebellum of 3 week old rats and the telencephalon of 16 week old rats. Thresholds of the electroshock seizure of lead-treated group and thiamine-deficient group in 3, 7 week old rats were significantly lower than those of control group, while those of the lead plus thiamine-treated group were similar to those of control group. Changes of the electroshock seizure threshold induced by lead intoxication were observed in 3 week and 7 week old animals with the concomitant decrement of thiamine content in all the brain regions tested. These observations were reversed by the supplementation with thiamine to those animals. However, the changes of seizure threshold induced by lead intoxication corelated with the changes of thiamine contents as well as. transketolase due to lead intoxication. The changes of myelin phospholipid as one of myelin composition and those of myelin Protein content only in the cerebellum of 3 week old rats correlated with the changes of the seizure threshold as well as thiamine content due to lead intoxication. The results from the present study may indicate that neurotoxicity of lead in rats may be mediated at least in part through the changes of thiamine status. Such changes of thiamine status may induce the changes of myelin composition such as myelin phospholipid and those of myelin protein content especially in the cerebellum of 3 week old rats which may eventually affect the threshold of seizure.
Ahn, Kyu Dong;Lee, Jong Chun;Cho, Kwang Sung;Kim, Jin Ho;Lee, Sung Soo;Lee, Byung Kook
Journal of Korean Society of Occupational and Environmental Hygiene
/
v.11
no.2
/
pp.111-117
/
2001
A cross-sectional study was performed to evaluate associations between lead biomarkers, lead-related symptoms, and ${\delta}$-aminolevulinic acid dehydratase (ALAD) genotype among 598 lead workers and 144 control office workers in storage battery industries, secondary smelting and litharge making industries. Lead inhibits the second enzymes, ALAD, in the heme synthesis pathway. ALAD gene, which codes for one of three isozymic proteins (termed ALAD1-1, ALAD1-2, and ALAD2-2), seems to modify the toxicokinetics of lead. The result as follows; The percents of total workers whose genotype of ALAD1-1 and ALAD1-2 were 88.4% and 11.6%, respectively. The zinc protoporphyrin in blood (ZPP) and ${\delta}$-aminolevulinic acid in urine (ALAU) of lead workers with ALAD1-2 were significantly lower than those of lead workers with ALAD1-1, but there were no significant difference between two genotype for blood lead, age, and work duration. The proportion of ALAD1-2 genotype in control office workers was 13.2%. The proportions of ALAD1-2 genotype of lead workers were 14.0%(their mean air lead level below $0.024mg/m^3$), 10.4%($0.025-0.049mg/m^3$), 11.8%($0.050-0.099mg/m^3$), and 9.4%(above $0.100mg/m^3$), respectively. In the logistic analysis of 15 lead related symptoms, 'arthralgia'(S7) symptom of ALAD1-2 was significantly lower (OR=0.481; 95% CI=0.248-0.932) than that of ALAD1-1, but 'feeling of irritation'(S11) of ALAD1-2 was significantly higher(OR=1.636; 95% CI=1.035-2.586) than that of ALAD1-1 after controlling possible confounder (blood lead, work duration, smoking and drinking habit).
To investigate the ultrastructural changes of kidney and clarify to a cause of its changes in lead intoxicated rats, the 0.5% lead acetate administed orally to the rats and those were sacrifled at 2 day, 1, 2, 4, 6 and 8 week after the treatment of lead acetate. Each extirpated kidney was histopathologically examined under the electron microscopy and histochemical examination was also carried out. Concomitantly, the activity of free radical metabolizing enzyme was determined. The blood levels of lead concentration showed a gradual increase from the first group reaching the plateau at the one or two week group with the slightly decreasing value throughout the whole course of the experiment. And the urinary ALA concentration showed a gradual increase from the first group to the 8 week group. In the kidney tissue of rat sacrified at 6 week, the proximal tubular cells showed dilatation of endoplasmic reticulum, mitochondrial swelling, increased numbers of secondary lysosomes and myelin figure-like residual bodies on electron microscope and oxygen free radicals are identified by histochemistry on light microscope whereas there were no differences in the activity of catalase and glutathione peroxidase between the lead acetate treated group and control group. But the activity of xanthine oxidase was more increased in lead acetate treated rats than control group. Furthermore, the superoxide dismutase activity was significantly increased in the experimental group than the control group. In conclusion, it is assumed the kidney damage in lead intoxicated rat may be induced by free radicals.
Bressler, Joseph P.;Olivi, Luisa;Kim, Yong-Bae;Bannon, Desmond;Ko, Hong-Sook;Cheong, Jae-Hoon
Biomolecules & Therapeutics
/
v.13
no.1
/
pp.1-6
/
2005
Lead and cadmium are potent environmental toxicants that affect populations living in Europe. Americas, and Asia. Identifying transporters for lead and cadmium could potentially 1 help us better understand possible risk factors. The iron transporter, divalent metal transporter 1 (DMT1), mediates intestinal transport of cadmium, and lead in yeast and fobroblasts overexpressing DMT1. In human intestinal cells knocking down expression of DMT1 attenuated uptake of cadmium and iron but not lead. A possible explanation is the expression of a second transporter for lead in intestine. In astrocytes, however, DMT1 appears to transport lead in an extracellular buffer at pH value. At neutral pH, transport was not mediated by DMT1 but rather by a transporter that is stimulated by bicarbonate and inhibited by 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonic acid. The identity of this lead transporter will beverified by future study.
Nerve conduction impairment in lead neuropathy has been empirically linked to altered nerve myo-inositol metabolism. In most cases of neuropathy, abnormal myo-inositol metabolism is associated with abnormal $Na^+/K^+$ATPase provides a potential mechanism to relate defects of the myo-inositol metabolism in the peripheral nerve treated with lead. Therefore, the effect of lead on the rat sciatic nerve $Na^+/K^+$ATPase and other ATPase of sciatic nerve was studied. ATPase activity was measured enzymatically in sciatic nerve homogenates from 2-wk lead treated neuropathy rats and age-mached controls administered myo-inositol. $Na^+/K^+$ATPase components were assessed by ouabain inhibition or the omission of sodium and potassium ions. Lead reduced 50% reduction in the $Na^+/K^+$ATPase activity in homogenates of sciatic nerve. The 50% reduction in the $Na^+/K^+$ ATPase activity was selectively prevented by myo-inositol treatment. This study suggests that the toxic mechanism of the lead on peripheral nerve may be through reduction in $Na^+/K^+$ATPase activity which has been linked to axonal transport slowing in the rat model of lead neuropathy, via direct changes by the perturbation of the intracelluar sodium or potasium level.
Analyses of lead and zinc were made by means of standard addition method using atomic absorption spectrophotometer(Baird Ltd., Model A5100) with flameless method for lead and flame method for zinc. The blood samples used were merely diluted with triton x-100, because it was simple, rapid and minimal risk of contamination. Mean recovery rate for lead added to the blood ranged from 97.7 to 101.3% with coefficient of variation ranging from 1.9 to 10.7%, and that for the added zinc ranged from 99.0 to 102.2% with coefficient of variation ranging from 2.1 to 9.1%. In repeated measurements of zinc in the blood, good reproducibility and interindividual variation were proved(p<0.01). In comparison of the lead and zinc concentrations in the blood determined by the standard addition method and standard method, there were good correlations between 2 sets of data (r=0.9731 for lead and r=0.9785 for zinc), although lead levels were estimated higher by the former method(p<0.01) and zinc levels by the latter method(p<0.01). It can be concluded that lead and zinc levels in blood standard addition method is reliable for determination of lead and zinc in the blood with good accuracy and reproducibility.
Under the condition of water electrolysis in aqueous hydrochloric acid as the electrolyte, the lead removal from the lead-loaded activated carbon packed on the anode was investigated. The adequate flow condition is a total flow rate of 10 mL/min in the same flow rate ratio to both electrodes. The increase of current decreases pH values at the anode and the decrease of pH leads to the lead removal. This work shows that the water electrolysis is an efficient method for the lead removal from the lead-loaded activated carbon with a reduction in quantity of the chemical used in comparison with the acid rinse.
Proceedings of the Korean Society of Applied Pharmacology
/
1995.04a
/
pp.96-96
/
1995
It was recognized that lead intoxication reduces thiamine content in the brain of rat and this change produces the alterations of thiamine-related biochemical reactions. In the present study, it was tested whether the changes of myelin composition as well as seizure threshold induced by lead intoxication in rats may be related to these changes of thiamine status and thiamine related biochemical factors. Wistar rats were divided into five groups: Control group, Lead-treated group, Lead plus Thiamine-treated group, Thiamine-deficient group, Pyrithiamine-treated group. Each group was divided into three subgroups: 3, 7 and 16 week old group. Myelin protein and phospholipid, one of the compositions of myelin lipid, were measured in the myelin isolated from rat brain. Threshold of electric shock seizure was tested in each group. The amount of each myelin composition in lead-treated group and thiamine-deficient group was significantly lower than those of all the brains in control group, but recovery by supplementation with thiamine during lead intoxication was occurred only in the cerebellum of 3 week old animal. Thresholds of the electric shock seizure of lead treated group and thiamine deficient group in 3 and 7 week old rats were significantly lower than those of control group, while those of lead plus thiamine treated group were similar to those of control group.
The color change of lead-containing pigments is one of the most serious diseases in watercolor, oil paintings and wall paintings. These pigments have a tendency to darken or brighten. It was proved that oxidation of lead containing pigments in the formation of brown-colored lead dioxide is a photochemical reaction under high humidity conditions. Therefore, we carried out some analogic experiments on the color change of three typical lead containing pigments ; $Pb_3O_4$, Pbo and $PbCo_3{\cdot}Pb(OH)_2$ at the conditions of illuminations under the high humidity ($2PbCo_3{\cdot}Pb(OH)_2$ R. H.). The reason for the chemical reactions are discussed and the results of these experiments are shown in some spectrograms, micrographs and X-ray micro-diffraction patterns. Important conclusions were drawn in our research. Due to the formation of brown $PbO_2$, red lead $(Pb_3O_4)$ and massicot (PbO) turned brown or dark when they were illuminated light under high humidity. We noticed that the brightening of red lead occurred d to admixture with chalk or lead white in egg yolk or linseed oil medium on exposure to light. Lead white used in oil paintings turned yellowish on dark.
Pathologic lead points are found in a few intussusception patients. To evaluate the pathologic lead points in childhood intussusception, a retrospective review of 227 operated cases of intussusception treated at the Yeungnam University Hospital from January 1986 to April 1999. The patients were divided into 2 groups; idiopathic group 209 cases, (92.1 % and lead points group 18 cases, 7.9 %). Intussusception developed between age two months and six months in both groups. Enteroenteric type of intussusception was relatively more frequent in the lead point group than in idiopathic group. The lead points were veil (10 cases, 52.6 %), Meckel's diverticulum(3 cases, 15.8 %), lymphoma(3 cases, 15.8 %), ectopic pancreas(2 cases, 10.5 %), Henoch-Sch$\ddot{o}$nlein purpura(1 cases, 5.3 %). The bowel resection rate was 44.4 % in the lead point group and 8.6% in idiopathic group. The recurrence rate was 5.56 % in lead points group and 1.44 % in idiopathic group.
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