In order to investigate the neurotoxic effect of methylmercury (MM) on cultured mouse spinal motoneuron cell line, NSC-19, neurotoxic effect of MM was evaluated by MTT assay after neurons were incubated with various concentrations of methylmercuric chloride (MMC) for 24 hours. In addition, neuroprotective effect of vitamin E against MMC-induced neurotoxicity was examined by MTT assay and neurofilament enzymeimmunoassay (EIA) in these cultures. The results were as follows : 1. MTT50 value was a concentration of 20µM methylmercuric chloride. 2. Methylmercuric chloride was toxic on cultured spinal motor neurons, NSC-19 cells in a time-and dose-dependent manner by severe decrease of cell viability. 3. Methylmercuric chloride induced the decrease of cell number and the loss of neuritis on these cultures. 4. Vitamin E remarkably increased the viabilily of cultured neurons damaged by methylmercury-induced neurotoxicity at a concentration of 250µM vitamin E. From above the results, it is suggested that methylmercury induces severe toxic effect on cultured mouse spinal motor neurons, NSC-19 cells, and the selective antioxidants such as vitamin E are effective in the neurotoxicity induced by methylmercury in these cultures.
Animals ; Antioxidants ; Cell Count ; Cell Culture Techniques ; Cell Line ; Cell Survival ; Intermediate Filaments ; Mice ; Motor Neurons* ; Neuritis ; Neurons ; Neuroprotective Agents ; Vitamin E* ; Vitamins*

To evaluate the effect of midkine (MK), neurotrophic factor on cultured mouse spinal motor neuron, NSC-19 which was inhibited by glucose oxidase (GO)-induced oxygen radicals, MTT assay and neurofilament enzymeimmunoassay were carried out after NSC-19 cells were preincubated with various concentrations of midkine for 2 hours prior to exposure of glucose oxidase. The results were as follows : 1. MK increased the rate of cell viability and neurofilamental development in a dose-dependent manner on motoneurons inhibited by glucose oxidase-induced oxygen radicals. 2. MTT50 value was 25 mU/ml GO. 3. GO-induced oxygen radicals were toxic on cultured motor neurons in a time and dose-dependent manner. 4. GO-induced oxygen radicals induced the decrease of cells in number and the loss of neurites in cultured mouse spinal motor neurons. From above the results, it is concluded that oxygen radicals are toxic in cultured mouse spinal motor neurons, and selective neurotrophic factors such as MK enhance the viability of motor neurons inhibited by oxygen radicals.
Animals ; Cell Survival ; Glucose ; Glucose Oxidase ; Intermediate Filaments ; Mice ; Motor Neurons* ; Nerve Growth Factor ; Nerve Growth Factors ; Neurites ; Oxidative Stress* ; Reactive Oxygen Species

To elucidate the neurotoxic mechanism of methylmercury on cultured bovine oligodendrocytes, neurotoxic effect was estimated by MTT assay after cultures were exposed to various concentrations of methylmercuric chloride (MMC). In addition, neuroprotective effect of antioxidant, allopurinol agonist MMC-induced neurotoxicity was examined on these cultures. Exposure of cultured bovine oligodendrocytes to MMC showed less than 50% of the cell viability 24 hours after treatment with 35µM of MMC. And also, allopurinol blocked the neurotoxicity induced by MMC on these cultures. These results suggest that oxygen radicals involve in MMC-mediated neurotoxicity, and also seletive antioxidants such as allopurinol are effective in blocking the neurotoxicity induced by MMC on cultured bovine oligodendrocytes.
Allopurinol* ; Antioxidants ; Cell Survival ; Neuroprotective Agents ; Oligodendroglia ; Reactive Oxygen Species

No abstract available.
HLA-A2 Antigen* ; Isoelectric Focusing*

No abstract available.
Animals ; Fibroblasts* ; Fluorouracil* ; Rats*

No abstract available.
Alleles* ; Gene Frequency* ; HLA-DR Antigens* ; Polymerase Chain Reaction*

No abstract available.
Animals ; Liver* ; Metals, Heavy* ; Rats*

In order to examine the neurotoxic mechanism of oxygen radicals on cultured bovine oligodendrocytes, cytoxic effect of oxygen radicals was examined when cultures were treated with various concentrations of xanthine oxidase (XO) and hypoxanthine (HX) in culture medium. In addition, the neuroprotective effect of iron-chelators against the neurotoxicity induced by oxygen radicals was evaluated by MTT assay. Cell viability was remarkably decreased in a time-dependent manner after exposure of cultured bovine oligodendrocytes to 20mU/ml XO and 0.1mM HX for 4 hours. In the neuroprotective effect of iron-chelators on oxidant-induced neurotoxicity, tetrakis (2-pyridylmethyl)ethylenediamine (TPEN) blocked the neurotoxicity induced by oxygen radicals, while DFX was not effective in blocking oxidant-induced neurotoxicity in these cultures. These results suggest that oxygen radicals are toxic in cultured bovine oligodendrocytes, and also selective iron-chelators such as TPEN are effective in blocking the neurotoxicity induced by oxygen radicals.
Allopurinol* ; Cell Survival ; Hypoxanthine ; Neuroprotective Agents ; Oligodendroglia ; Reactive Oxygen Species ; Xanthine Oxidase

No abstract available.
DNA* ; HLA-DR Antigens* ; Polymerase Chain Reaction*

During inflammation of the colon, cells of the gut mucosa express numerous inflammatory mediators including interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta(IL-1beta). These cytokines have been implicated as contributing factors in the inflammatory process, which may result in colitis during inflammatory bowel disease (IBD). Gliotoxin is a fungal metabolite of an epipolythiodioxopiperazine analogue with immunosup-pressive properties in vivo and in vitro, but the effects of gliotoxin on IBD have not been largely evaluated. Therefore, this study evaluated the potential of gliotoxin to protect against TNBS-induced colitis. One microgram of gliotoxin in 100microliter of vehicle was intra-rectally administered into mice exhibiting trinitrobenzene sulfonic acid (TNBS)-induced colitis. IL-8 secretion was measured using an enzyme-linked immu-nosorbent assay (ELISA), myeloperoxidase (MPO) activity was evaluated spectrophotometically, and IkappaB degradation was analyzed on Western blots. Gliotoxin treatment of mice bearing TNBS-induced colitis improved macro-and micro-pathological findings and dramatically decreased MPO activity, a marker of leukocyte infiltration. Furthermore, gliotoxin decreased IkappaB degradation and IL-8 induction caused by TNF-alpha or IL-1beta in HT-29 cells. These findings suggest that gliotoxin partially protects against TNBS-induced colitis through the sup-pression of IL-8 induction and IkappaB degradation by inflammatory mediators such as TNF-alpha or IL-1beta.
Animals ; Blotting, Western ; Colitis* ; Colon ; Crohn Disease ; Cytokines ; Down-Regulation* ; Gliotoxin* ; HT29 Cells ; Humans ; Inflammation ; Inflammatory Bowel Diseases ; Interleukin-8 ; Leukocytes ; Mice ; Mucous Membrane ; Peroxidase ; Tumor Necrosis Factor-alpha