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Mitochondrial DNA A3243G mutation in noise-induced sensorineural hearing loss
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Dong Hoon Shin, Won Ki Baek, In Sung Chung
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Korean Journal of Occupational and Environmental Medicine 2000;12(3):319-326. Published online September 30, 2000
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DOI: https://doi.org/10.35371/kjoem.2000.12.3.319
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 Abstract
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- OBJECTIVES
A different sequence change, in the mitochondrial tRNA gene, has been proposed as a candidate mutation in the sensorineurnal hearing loss. The purpose of current study is to identify the association between the noise-induced sensorineurnal hearing loss and the A to G mutation at nucleotide 3243 of mitochondrial DNA.
METHODS
Subjects were established by history and chart review, and audiological and clinical data were obtained.
Blood was sampled from 101 controls, 50 noise-induced hearing loss, and 12 sensorineural deafness. The DNA of these individuals was extracted, and mitochondrial genome was analyzed by polymerase chain reaction. Subsequently, the coding sequence of mitochondrial genome was sequenced, and compared to the normal sequence, and all sequence variations were analyzed by restriction endonuclease ApaI.
RESULTS
Mitochondrial DNA mutation (3243A->G) was not detected by polymerase chain reaction (PCR) in any patients with noise-induced hearing loss, sensorineural hearing loss, and normal control without hearing loss in Koreans.
The DNA sequencing of PCR products did not revealed an A to G substitution at nucleotide 3243 of mitochondrial DNA.
CONCLUSIONS
The noise-induced sensorineural hearing loss was not associated with mitochondrial DNA mutation (3243A->G)
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Apoptosis Induced by Manganese in Basal Ganglia Primary Neuronal Cell Culture: Morphological Findings
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Dong Hoon Shin, Sang Pyo Kim, Young Wook Jung, Jae Hoon Bae, Dae Kyu Song, Won Ki Baek
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Korean Journal of Occupational and Environmental Medicine 2000;12(1):41-47. Published online March 31, 2000
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DOI: https://doi.org/10.35371/kjoem.2000.12.1.41
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Abstract
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- OBJECTIVES
Manganese is cytotoxic to the central nervous system including basal ganglia.
Its toxic mechanism is related to oxidative stress, mediated by toxic free radicals but is specultives.
In the present study, we have investigated to manifest apoptosis in manganese-induced cytotoxicity in primary neuronal cell culture of rat basal ganglia.
METHOD
To detect apoptotic neuronal cells were stained by the terminal deoxynu-cleotide(TdT)-mediated dUTP nick end-labelling(TUNEL) method and apoptotic changes in nuclei of neurons were observed by electron microscopy.
RESULTS
We showed that TUNEL immunostain showed brownish signal in the nuclei of apoptotic cells and the proportions of apoptotic cells in Manganese treatment groups were more higher than controls. On transmission electron microscopy, there were chromatine condensation with margination toward nuclear membrane and condensation of cytoplasm in the treated with luM MnC1, for 48 hours in a basal ganglia neurons.
Apoptotic bodies were found and consisted of semilunar-like condensed nuclei with relatively intact cytoplasmic organelles.
CONCLUSIONS
Apoptosis appears to be one mechanism in the manganese-induced neuronal cell death.
Manganese intoxication is a convenient model for apoptosis study.
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Apoptosis of Neuronal Cells Induced by Lead
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Seon Hee Yang, Dong Hoon Shin, Won Ki Baek
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Korean Journal of Occupational and Environmental Medicine 1999;11(2):254-263. Published online June 30, 1999
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DOI: https://doi.org/10.35371/kjoem.1999.11.2.254
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Abstract
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- Lead is a major environmental and occupational neurotoxicant. It has been shown that long-term exposure to a low level of lead impairs the development of brain. For example, it was reported that lead exposure during the childhood causes a learning difficulty and a memory deficit of children. Neurotoxic agents including the lead are believed to cause neuronal death in developing brain by two mechanisms: apoptosis and necrosis. However, the exact mechanism of neuronal death caused by lead exposure is still not known explicitly. In this study, we conducted a study to clarify a mechanism of hippocampal neuronal cell death caused by lead acetate. Hippocampal neurons were cultured for 14-16 days and treated with lead acetate of 1. 10, 100 1 microM concentrations for 12 hours. With the MTT(methyl tetrazolium test) kit, the viability of neuronal cells was measured. Next, in order to examine apoptosis caused by lead acetate, TUNEL (TdT-mediated d-UTP Nick End Labelling) assay was performed. It has been shown that lead acetate reduced the viability of neuronal cells in a dose dependent manner, especially at the concentration of 100 ~M lead acetate. TUNEL immunostain showed brownish signals in the nucleus of apoptotic cells. The proportions of apoptotic cells in the lead?acetate treated group were more higher than those in the controls and increased as lead acetate concentration increased. From above results, it may be concluded that lead in the hippocampal neuronal cells reduced cell viability and one of mechanisms in neuronal cell death by lead appears to be apoptosis.
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Citations
Citations to this article as recorded by  - Teratogenic Effects of Lead in the Developing Chick Embryos
Aqsa Shafiq, . Mahnoor, Mirza Fahad Baig, Yashal Fatima, Arooj Haer, Shakila Parveen, Muhammad Akram Tariq, Muhammad Khalil Ahmad Khan
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