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更新于：2024-11-01

Lead Poisoning, Nervous System

神经系统铅中毒

更新于：2024-11-01

基本信息

别名

Lead Neurotoxicity Syndrome、Lead Neurotoxicity Syndromes、Lead Poisoning, Nervous System

+ [25]

简介

Injury to the nervous system secondary to exposure to lead compounds. Two distinct clinical patterns occur in children (LEAD POISONING, NERVOUS SYSTEM, CHILDHOOD) and adults (LEAD POISONING, NERVOUS SYSTEM, ADULT). In children, lead poisoning typically produces an encephalopathy. In adults, exposure to toxic levels of lead is associated with a peripheral neuropathy.

关联

项与神经系统铅中毒相关的药物

TMF

靶点-

作用机制-

在研机构

Chitkara University

原研机构-

在研适应症

神经系统铅中毒

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

项与神经系统铅中毒相关的临床试验

TCTR20180625003

/ Active, not recruitingN/AIIT

What is the best sample in detecting chronic lead poisoning: blood, hair or nail?

开始日期2018-06-29

申办/合作机构

King Chulalongkorn Memorial Hospital

[+1]

TCTR20170928001

/ Not yet recruitingN/AIIT

A comparative study of biophysical property changes between patients with chronic lead toxicity and normal control

开始日期2017-10-04

申办/合作机构-

100 项与神经系统铅中毒相关的临床结果

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100 项与神经系统铅中毒相关的转化医学

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0 项与神经系统铅中毒相关的专利（医药）

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459

项与神经系统铅中毒相关的文献（医药）

2024-12-01·IBRO Neuroscience Reports

Alchornea laxiflora (Benth.) Pax & K. Hoffman extract protects against lead-induced neurodegeneration in cockerel chickens

Article

作者: Oyagbemi, Ademola Adetokunbo ; Oladele, Omolade Abodunrin ; Nwulia, Evaristus ; Esan, Oluwaseun Olanrewaju ; Femi-Akinlosotu, Omowumi Moromoke ; Igado, Olumayowa Olawumi ; Omobowale, Temidayo Olutayo

Lead (Pb) is a ubiquitous, non-biodegradable heavy metal contaminant with a significant impact on both human and animal health. The adverse effect of lead on health and productivity of avian species has received little attention. Alchornea laxiflora (Benth) belongs to Euphorbiaceae family and grows naturally in the Nigerian rain forest. Decoction of the leaves is usually administered traditionally to treat inflammatory and infectious diseases. The ethanol extract of Alchornea laxiflora (EaAL) leaves was used in this study to ameliorate lead-induced neurodegeneration. Seven groups of 5-week-old cockerels (n=5) were treated for 6 weeks thus: Group A - Control (water only), Group B - (100 mg/kg of EaAL daily), Group C - (200 mg/kg of EaAL daily, p.o.), Group D - (1 % lead acetate in drinking water), Group E - (1 % lead acetate in drinking water and 100 mg/kg of EaAL daily), Group F - (1 % lead acetate and 200 mg/kg of EaAL daily), Group G - (1 % lead acetate and 100 mg/kg of Vitamin C). All administrations were per os birds were euthanized on day 43 by quick cervical dislocation. Histological stains (H&E and Nissl) and Black Gold II (BGII) histochemistry were used to assess alterations in the cerebrum and cerebellum. Administration of EaAL at the two concentrations resulted in a drastic reduction in the incidence of neuropathologies observed (e.g. pyknosis and multilayering of Purkinje cells, neuronal degeneration in hippocampus cerebrum and ependymal cells, distortion of meningeal epithelial cells, etc). BGII histochemistry revealed severe demyelination caused by the administration of lead acetate, while the two doses of EaAL showed significant restoration of myelin in the cerebellum. The amelioration of demyelination observed with the use of vitamin C was considerably lower than that recorded with the use of EaAL. The use of EaAL significantly ameliorated morphological alterations and demyelination caused by the administration of lead acetate, however, caution should be exercised in the administration, as individual species idiosyncrasies may arise and the tendency to pro-oxidation at 200 mg/kg when administered alone was observed in one subject.

2024-12-01·Toxicology

Ferroptosis contributes to lead-induced cochlear spiral ganglion neurons injury

Article

作者: Wu, Xuewen ; Pang, Bo ; Mei, Lingyun ; Huang, Huping ; Chen, Yongjia ; Wang, Lu ; Jiang, Mengzhu ; Bai, Yijiang ; He, Ye ; Song, Jian ; Gao, Kelei ; Zhang, Shuai

The underlying mechanisms of lead exposure-induced cochlear spiral ganglion neurons (SGNs) injury are not yet clear. This study explored whether ferroptosis is involved in lead-induced SGNs injury and investigated the mechanism of lead-induced iron overload in SGNs. A primary culture cell model of lead acetate-induced SGNs damage was established. The changes in levels of iron ions, reactive oxygen species, lipid peroxides, and glutathione in SGNs were measured after lead acetate intervention and ferroptosis inhibitors pre-treatment. The morphology of mitochondria was also observed, and the expression of ferroptosis marker genes glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), as well as iron metabolism-related proteins transferrin receptor protein 1 (TFR1), nuclear receptor coactivator 4 (NCOA4), heme oxygenase-1 (HO-1), and ferroportin (FPN) were detected. Results showed that lead acetate exposure induced SGNs injury in a time- and dose-dependent manner. Intracellular iron accumulation, increased levels of reactive oxygen species and lipid peroxide with decreased level of antioxidant capacity were occurred in SGNs after lead exposure. Meanwhile, decreased expressions of GPX4 and SLC7A11 and increased expressions of iron metabolism-related proteins (TFR1, NCOA4, and HO-1) were also found. Lead acetate intervention also caused mitochondrial shrinkage with blurred and fragmented morphology. Pre-treatment with ferroptosis inhibitors (Fer-1 and DFOM) significantly ameliorated lead-induced SGNs injury. In summary, lead exposure can induce ferroptosis in SGNs, the antioxidant defense system and iron metabolism disorder are involved in lead-induced SGNs ferroptosis. Thus, inhibiting ferroptosis may be a new strategy for preventing and treating lead exposure-related hearing loss.

2024-11-01·Radiology Case Reports

Susac syndrome: A rare pediatric case

Article

作者: Allali, Nazik ; Benbrahim, Fatima Zohra ; Belkouchi, Lina ; Chat, Latifa ; El Haddad, Siham

Susac syndrome is a rare microangiopathy of unclear etiology, likely autoimmune, characterized by a characteristic clinical triad of encephalopathy, retinopathy, and hypoacusis. The majority of cases reported in the literature involve adult patients, with its occurrence in the pediatric population being extremely rare. Magnetic resonance imaging (MRI) is essential for diagnosis and patient monitoring, revealing nearly pathognomonic features, particularly valuable given the typically incomplete clinical triad and the consistent presence of encephalopathy, often as the initial symptom. We report the case of an 11-year-old child diagnosed with Susac syndrome, highlighting the importance of considering this diagnosis in cases of childhood encephalopathy and initiating treatment as early as possible to prevent irreversible sequelae.

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