• Environmental Mutagens and Carcinogens
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• v.8 no.1
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• pp.35-46
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• 1988

출생직후부터 새끼쥐에 유발시킨 납중독이 중추의 특정 신경계에 미치는 신경독성의 선택성 여부를 알아보고자 하였다. 특정 신경계의 한 예로 모노아민성 신경계를 선택하여 납중독의 지표로 모노아민성 신경계의 효소인 MAO (mono-amine oxidase)의활성을 측정하였으며, 비특정 조직의 지표로 Na+K+-ATPase의 활성을 측정하였다. Wistar계의 흰쥐에서 태어난 새끼들에게 출생직후부터 전실험기간을 통해 0.05% 혹은 0.2% 초산납 (PbAc2)용액을 식수로 공급하여 납중독을 유발시켰다. 생후 2, 4, 6 및 8주된 새끼쥐의 MAO 및 Na+K+-ATPase활성을 대뇌, 간뇌, 중뇌, 뇌교-연수 및 다섯부위에서 각기 측정하였다.

• Environmental Mutagens and Carcinogens
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• v.7 no.2
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• pp.72-84
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• 1987

어미쥐에 유발시킨 납중독이 새끼쥐의 특정 중추신경계에 미치는 신경독성의 선택성 여부를 알아보고자 하였다. 특정 신경계의 한 예로 모노아민성 신경계를 선택하여 납중독의 지표로 모노아민성 신경계의 효소인 MAO(monoamine oxidase)의 활성을 측정하였으며 비특정조직에의 지표로 Na+.K+-ATPase의 활성을 측정하였다. 임신한 Wistar계 어미쥐에게 임신전기간에 걸쳐 0.05 혹은 0.2% 초산납(PbAc2)용액을 식수로 공급하여 간접적으로 태아에 납중독을 유발시켰다. 새끼쥐는 출생직후 정상 식수를 공급해 주었다. 2, 4, 6 및 8주된 새끼쥐의 MAO 및 Na+.K+-ATPase활성을 대뇌, 간뇌, 중뇌, 뇌교-연수 및 소뇌 등 다섯부위에서 각기 측정하였다.

• Journal of the Korean Society of Food Science and Nutrition
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• v.25 no.1
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• pp.27-33
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• 1996

납중독에 대한 마늘의 antidotic effect를 조사하기 위한 4주간의 실험에서 , rat 체중 kg 당 중 (7일간) 1회초산납 100mg을 투여한 rat에 매일 마늘즙을 식이의 4%로 투여한 실험군(LG)과 초산납과 함께 중금속 해독제인 N-acetyl penicillamine을 매일 rat 체중 kg당 100mg 투여한 실험군 (LP)의 체중 증가율 비교에서 초산납만을 투여한 실험군(L)보다 LG군과 LP군 모두 유의성 있는 rat 성장률 개선효과 (각각 +13.3%과 +22.3%)를 보였다. L군 rat의 외관과 해부검사에서는 장기들(위, 간장, 신장)의 병변(damage)이 매우 미미하게 관찰되었으나 혈액검사에서 GOT, alkaline phos-phatase, blood uric acid, blood urea nitrogen, crea-tinine, bilitrubin 값이 유의적을 증가하여 납중독에 의한 장기(organs) 특히 신장 기능의 현저한 장해를 보였다. 그러나 LG군이 이들 측정값이 L군보다 유의성의 차로 낮은 값을 보여 LP군과 거의 비슷한 수준이었다. 특히 L군에서는 Pb 중독으로 인하여 hemo-globin 량이 정상 이하(10.37g/dl)로 감소되었으나 LG군에서는 L군에서와 같이 거의 정산 (12.32g/dl)을 유지하였다. L군의 혈액, 간장 및 신장의 납 합량은 각각 0.281, 0.250, 0.403ppm으로 대조군 보다 매우 높았으나 LG군은 대조군에 가깝게 그리고 LP군과는 거의 같은 수준(각각 0.182, 0.131, 0.253ppm)으로 낮아졌다. 이상의 실험 결과에서 마늘이 rat의 납중독에 미치는 효과를 N-acetyl penicillamine의 해독 효과와 비교할 때 마늘의 해독 효과라고 볼 수 있는 유의성있는 측정값들이 관찰되었다.

• 대한예방의학회:학술대회논문집
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• 1994.04a
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• pp.133-139
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• 1994

• 산업보건소식
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• no.21
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• pp.5-6
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• 1985

• Proceedings of the Korean Nutrition Society Conference
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• 2001.05a
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• pp.134.1-134
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• 2001

• Proceedings of the Korean Nutrition Society Conference
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• 2001.05a
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• pp.134.2-134
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• 2001

• Clinical and Experimental Pediatrics
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• v.48 no.9
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• pp.1009-1015
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• 2005

We encountered two children with lead poisoning who were administered herb medicinal pills recommended by their clergyman. These patients presented anemia and severe coliky abdominal pain, but no neurologic symptoms. For this reason, they were initially misdiagnosed with gastrointestinal hemorrhagic disease. However, we got a clue that they took herb medicinal pills. Finally, based on the assay of blood lead level, we made a correct diagnosis of lead poisoning in these patients. These patients underwent chelating therapy. Subsequently, the concentration of blood lead was decreased. Finally, we drew a conclusion that the possibility of lead poisoning must be considered in children who complained of colicky abdominal pain accompanying anemia. Here, we report two pediatric cases of lead poisoning with a review of literature.

• Journal of Veterinary Clinics
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• v.11 no.1
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• pp.485-505
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• 1994

Lead toxicity was evaluated in forty-five cats on a balanced diet, treated with 0(control), 10, 100(low), 1, 000, 2, 000 and 4, 000(high)ppm of lead acetate orally on a body weight basis. The objectives were to describe the gross and histopathologic changes and to demonstrate what tissue lead concentrations correlate with the known dosages of lead. In subclinical lead toxicity, greater than 80% of the absorbed lead was deposited in the bone, whereas in more acute lead toxicity, 42% of absorbed lead was deposited in the bone and 36% and 20% of absorbed lead was deposited in the kidneys and in the liver, respectively. No gross lesions were found in the nervous system. Yellow-brown colored livers appear to be associated with lead toxicity. Neuronal necrosis in the cerebrum was the most predominant histopathologic finding. Astrocytic proliferation in the cerebral gray matter was observed in 1 high dose cat. Gliosis was noted in the cerebral cortex of 6 high dose cats. Two high dose cats had demyelination in the deepest layer of the cortical gray matter of the cerebrum. Extravasation of red cells and cavitation around the vessels were found in the cerebrum of 1 high dose cat. Six high dose cats had degeneration of Purkinje cells in the cerebellum. The microscopic findings in the peripheral nerves were ambiguous. In more acute toxicity, the cats had lead inclusions in the epithelial cells of proximal tubules of the kidneys of 7 cats and hepatocytes of the liver of S cats. These inclusions could be seen wlth H&E, but were more prominent with orcein staining. Two high dose cats had granulomas and connective tissue hyperplasia between tubules of the kidneys. Periportal hepatocyte vacuolization was observed in the liver of 22 cats. Vacuolization of seminiferous tubules and a reduced number of spermatogonia(indicative of reduced spermatogenesis) were found in the testis of 5 treated cats. Cystic ovaries were observed in 3 high dose cats and poor development of oogonia was found in 2 cats. The diagnosis of lead toxicity in cats can be suspected on the basis of the histopathologic lesions described, and can be of value in contributing to a diagnosis. A reliable diagnosis of lead poisoning can be helped utilizing tissue lead analysis(post molten)

• Journal of Veterinary Clinics
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• v.10 no.1
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• pp.111-130
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• 1993

Lead toxicity was evaluated in forty-five cats on a balanced diet, Treated with 0(control), 10, 100(low), 1, 000, 2, 000, and 4, 000(high) ppm of lead acetate orally on a body weight basis. The objectives were to establish toxic dosage level of leaf in cats, to characterize changes in behavior and clinical pathology, and to demonstrate what blood lead concentrations correlate with the known dosages of lead. Some high dose cats showed projectile vomiting, hyperactivity, and seizures. The growth rates did not appear to be altered in any of the dosed groups. Normal blood lead concentration in cats were lower than that of humans, dogs, and cattle. Blood lead concentrations of 3 to 20$\mu\textrm{g}$/100$m\ell$ could be termed a 'subclinical' range in the cat. Clinical lead toxicity in cats may have blood lead concentrations ranging 20 to 120$\mu\textrm{g}$/100$m\ell$. Zinc protoporphyrin concentrations were proportional to lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverss dose response relationship for all lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverse dose response relationship for all lead dosages and appears to be a good indicator of lead exposure in cats. Urinary aminolevuliruc acid concentrations generally increased with lead dosage, but individual values varied. Hair lead concentrations rose proportionately to lead dosages. Lead at least in high doses appears to inhibit chemotactic activity of polymorphonuclear cells and monocytes. No consistent dose response relationships were observed in hemoglobin, RBC, WBC, neutrophil, lymphocyte, monocyte, and eosinophil counts. There were no consistent dose related changes in total protein, plasma protein, BUN, and ALT values. Reticulocyte counts did not increase significantly in most lead dosage levels, and are probably of little value in diagnosing lead toxicity in cats. The fact that no significant changes were found in nerve conduction velocities may support that there was no segmental demyelination resulting from lead ingestion. The lethal dose in cats appear to range from 60 to 150mg/kg body weight. A reliable diagnosis of lead poisoning can be made utilizing blood lead, ZPP, and ALAD, and hair lead.