• Journal of Preventive Medicine and Public Health
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• v.15 no.1
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• pp.89-94
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• 1982

Among the environmental pollutants, cadmium and lead compounds may impair human health. These compounds may inhibit the biological metabolic function of human body and may furthermore cause the disease directly or indirectly. This study was undertaken to investigate the effects of the immune response by intoxication of cadmium chloride and lead acetate. Cadmium chloride (8.8mg/kg, in saline 10ml) and lead acetate (15mg/kg, in saline 10ml) were administered by intraperitoneal injection. After 3 weeks, the rats were intoxicated with the above chemicals and immunized with sheep RBC. After 4 weeks, the immune response of rat spleen cells was measured by the Jerne's technique. The results were obtained as follows; 1. There was no change in leukocyte counts by the intoxication of cadmium chloride or lead acetate. 2. Cadmium chloride or lead acetate reduced hemoglobin contents for most intoxicated and immunized groups. 3. Hematocrits were decreased by the intoxication of cadmium chloride or lead acetate significantly. 4. It was determined that total protein, A/G (Albumin/Globulin), ${\alpha}-,\;{\beta}-\;and\;{\gamma}$-globulins in rat serum were not changed. 5. Intoxication by cadmium chloride or lead acetate reduced the number of hemolytic plaque to the sheep RBC in rat spleen cells. Therefore, antibody producing of rat spleen cells was suppressed by the intoxication of cadmium chloride and lead acetate.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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• pp.96-96
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• 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.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.10a
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• pp.137-146
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• 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.

• Biomolecules & Therapeutics
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• v.3 no.4
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• pp.288-293
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• 1995

In the present study, we tested whether lead intoxication could change the thiamine content and the activity of transketolase, one of thiamine-dependent enzymes, in the brain of rats. It was also tested whether administration of excessive thiamine can reverse the toxic manifestation of lead in the lead intoxicated rats. Four groups of Wistar rats were prepared: 1) control group, 2) lead treated group, 3) lead plus thiamine treated group and 4) thiamine deficient group. Each group of animals was divided into three subgroups based on ages: 3, 7 and 16 weeks. Lead concentration, thiamine content and the activity of transketolase in three different brain regions, i.e.,, telencephalon, brain stem and cerebellum, were measured in each group. Lead concentrations in brain regions of the lead treated group were significantly higher than those of the control group, and those of the lead plus thiamine treated group were significantly decreased from those of the lead treated group. Thiamine contents in the brain regions of the lead treated group were significantly lower than those of the control group, and those of the lead plus thiamine treated group were recovered back to those of the control group. Activities of transketolase in the brain regions of the lead treated group and the thiamine deficient group were significantly lower than those of the control group, while those of the lead plus thiamine treated group were higher than the lead treated group. The results from the present study suggest that neurotoxicity following lead intoxication in rats may be mediated, at least in part, through the changes of thiamine status and consequently thiamine-dependent biochemical reactions such as theactivity of transketolase.

• Biomolecules & Therapeutics
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• v.7 no.4
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• pp.322-328
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• 1999

In this study, it was tested whether the changes of catecholamines and its metabolites are related with the changes of blood pressure(BP) induced by different levels of lead exposure. Adult male SD rats were exposed to lead by giving drinking water containing 50(low doses), 200 and 1,000 ppm(high doses) of lead(as lead acetate) or sodium acetate(for control groups, supplying an identical amount of acetate) for 7 or 16 weeks. The systolic BP was measured in the unanesthetized state by the tail-cuff technique. Levels of catecholamines and its metabolites in urine were measured by HPLC-ECD. Rats receiving 200 and 1,000 ppm developed an elevation of systolic BP at 3 and 7 weeks compared with week 0, but blood pressure levels at 16 weeks returned to normal. For the 50 ppm lead treated group, systolic BP increased significantly at 7 weeks and 16 weeks. The concentrations of norepinephrine and VMA in the urine of lead exposed rats changed similarly to the changes of blood pressure, but blood viscosity levels in all lead treated rats increased continuously during all lead treatment periods. This result suggests that the changes of catecholamines and its metabolites in urine by lead intoxication may influence the changes of blood pressure.

• Biomolecules & Therapeutics
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• v.6 no.1
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• pp.20-24
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• 1998

In the present study, we tested whether lead intoxication induces change of the thiamine content and the seizure threshold in rats and the changes of seizure threshold are related to the changes of thiamine status. It was also tested whether administration of excessive thiamine could reverse the toxic manifestation of lead in rats. Four groups of Wistar rats were prepared: 1) control group, 2) lead treated group, 3) lead plusthiamine treated group, and 4) thiamine deficient group. Each group of animals was divided into three subgroups based on age: 3, 7 and 16 weeks. In each group, thresholds of electroshock seizure and thiamine contents in brain regions including telencephalon, brain stem, cerebellum were measured. Thiamine contents in brain regions of the lead treated group were significantly lower than those of the control group and thiamine treatment reversed the decrease back to the control level. Thresholds of the electroshock seizure of the lead treated group in 3, 7 week old rats and those of thiamine deficient group in 3 week old rats were significantly lower than those of the control group. These observations were reversed by the supplementation with thiamine. These results from the present study suggest that increased seizure sensitivity induced by lead intoxication in rats may be mediated at least in part through the changes of thiamine status.

• Journal of Animal Science and Technology
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• v.49 no.3
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• pp.415-428
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• 2007

To investigate the detoxification effect of pork on the lead toxicity, the comparison tests were performed, in which Sprague Dawley(SD) rats were clinically treated with lead during the first 7 weeks and observed the detoxification effects induced by pork feeding during the second 7 weeks. As results of lead intoxication, decreases of body weight, hemoglobin and hematocrit and the increases of weight and relative organ weight of liver and kidney were observed. Also the accumulation of lead in tibia, kidney and liver was recognized. In case of pork feeding at detoxification stage the feed efficiency was significantly increased in pork feeding group rats than the those of control rats. The pork feeding seemed to be a factor affecting relative organ weight of liver and kidney(p<0.05). It was shown that the factors affecting the accumulation of lead in liver included the lead intoxication(p<0.0005), pork feeding(p<0.0005) and interaction of above two(p<0.0005). It was observed that the content of DALAD in liver increased with significance in pork fed group compared with control group regardless of lead treatment levels. From this result, it was considered that pork feeding improved the detoxification process of SD rats intoxicated with lead.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.144-144
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• 1998

The physiological responses caused by exposure of high- and low-level lead exhibit different phase. Low-level lead continuous hypertension, but high-level lead can in the development of hypertension. In this study it was tested which difference can be caused as lead levels and, if it can be caused, whether hematological changes are related with the hypertensive effects induced by different levels of lead exposure was tested. Lead intoxication in male SD rats was induced by exposure through drinking water containing 50, 200 and 1000 ppm lead (as lead acetate). The animals of control group was supplied drinking water containing sodium acetate ad libitum. The number of each animal group was 10. Systolic blood pressures were measured in the unanesthetized state by the tail-cuff technique at 0, 3, 7 and 16 weeks. RBC, WBC, MCV, hemoglobin, hematocrit and whole blood viscosity levels were examined.

• Journal of The Korean Society of Clinical Toxicology
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• v.11 no.2
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• pp.89-95
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• 2013

Purpose: Glyphosate is widely used and its toxic exposures are not rare. Occasionally, glyphosate intoxication can lead to death. The aim of this study is to analyze clinical findings and fatality in glyphosate intoxication. Methods: Clinical data on acute glyphosate intoxication were prospectively collected at 28 hospitals nationwide between August 2005 and July 2006. The patients' clinical symptoms and characteristics of fatalities were investigated and statistical analysis was performed. Results: Among 105 patients who were finally included, gastrointestinal symptoms(59%) were the most common. A significant difference in the amount ingested was observed between patients with higher systolic blood pressure and those with systolic blood pressure less than or equal to 80 mmHg (p<0.001). The more the patients ingested, the more aggravated their mental status became (p=0.004). Seven patients(6.7%) died, and all of them had ingested greater than or equal to 200 ml. Patients who died had ingested greater amounts than the survivors (p<0.001), and their mental status was worse (p<0.001), and systolic blood pressure was lower (p<0.001). According to the result of logistic regression analysis, relative risk was 24.1-fold higher in the 'poor' mental status group compared with 'good'. Conclusion: Patients who ingested large amounts of glyphosate showed poor mental status and lower blood pressure. Statistical difference in amount ingested, mental status, and systolic blood pressure was observed between survivors and patients who died. Ingested amounts and mental status were the most important factor of the prognosis of glyphosate intoxication.

• Molecules and Cells
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• v.39 no.6
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• pp.508-513
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• 2016

To investigate the potential therapeutic effects of polyphenols in treating Pb induced renal dysfunction and intoxication and to explore the detailed underlying mechanisms. Wistar rats were divided into four groups: control groups (CT), Pb exposure groups (Pb), Pb plus Polyphenols groups (Pb+PP) and Polyphenols groups (PP). Animals were kept for 60 days and sacrificed for tests of urea, serum blood urea nitrogen (BUN) and creatinine. Histological evaluations were then performed. In vitro studies were performed using primary kidney mesangial cells to reveal detailed mechanisms. Cell counting kit-8 (CCK-8) was used to evaluate cell viability. Pb induced cell apoptosis was measured by flow cytometry. Reactive oxygen species (ROS) generation and scavenging were tested by DCFH-DA. Expression level of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-1-${\beta}$ (IL-1-${\beta}$) and IL-6 were assayed by ELISA. Western blot and qPCR were used to measure the expression of ERK1/2, JNK1/2 and p38. Polyphenols have obvious protective effects on Pb induced renal dysfunction and intoxication both in vivo and in vitro. Polyphenols reduced Pb concentration and accumulation in kidney. Polyphenols also protected kidney mesangial cells from Pb induced apoptosis. Polyphenols scavenged Pb induced ROS generation and suppressed ROS-mediated ERK/JNK/p38 pathway. Downstream pro-inflammatory cytokines were inhibited in consistency. Polyphenol is protective in Pb induced renal intoxication and inflammatory responses. The underlying mechanisms lie on the antioxidant activity and ROS scavenging activity of polyphenols.