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Original Article
- Manganese-induced Oxidative Stress in the Corpus Striatum of the Rat Brain
- Soo Jin Lee, Soon Oh Hong, Hyun Chul Koh
- Korean Journal of Occupational and Environmental Medicine 2002;14(1):23-33. Published online March 31, 2002
- DOI: https://doi.org/10.35371/kjoem.2002.14.1.23
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Abstract
PDF - OBJECTIVES
This study was undertaken to identify the effect of oxidative stress on the pathology of manganese intoxication through an analysis of manganese concentrations, superoxide dismutase (SOD) activities, malondialdehyde (MDA) concentrations, and the compositional changes of fatty acids from the corpus striatum of the rat brain.
METHODS
Ten Sprague-Dawley rats were equally divided into two groups. Five rats in the experimental group were administered MnCl2 intraperitoneally for 4 weeks (4 mg/kg once daily, 5 days per week) and another five rats from the control group were given normal saline. Twenty-four hours after the last injection, the rats were decapitated and, the corpus striatum was isolated from the brain.
RESULTS
In the corpus striatums of the experimental group, manganese concentrations increased significantly by 139 % (p<0.01). The SOD activities decreased significantly by 81 % (p<0.01) and the MDA concentrations increased significantly by 138 % (p<0.01) as compared to the control group. Among fatty acids, total n-6 polyunsaturated fatty acids (PUFAs) increased significantly by 325 % (p<0.01) as compared with the control group. Arachidonic acids (AA) increased by 341 % (p<0.01), and these increases were composed mostly of n-6 polyunsaturated fatty acids (PUFA). Among n-3 PUFAs, with the exception of linolenic acids, eicosapentanoic acid (EPA) decreased significantly by 72 % (p<0.05) and docosahexanoic acids (DHA) decreased by 67 % (p<0.05) as compared with the control group.
CONCLUSIONS
Our results suggest that the oxygen free radicals produced by manganese may cause compositional changes of fatty acids in the corpus striatum of the rat brain. The characteristics of the fatty acids'compositional changes by manganese were a decrease of EPAs and DHAs (n-3 PUFAs), and an increase of AAs (n-6 PUFAs). These changes coupled with the decrease of SOD activity and the increase of MDA, suggest that manganese neurotoxicity is caused by lipid peroxidation mediated with oxygen free radicals, particularly superoxide radicals.
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Original Article
- A Study of Relationship between Exposure to Manganese Chloride and Malondialdehyde in Rat Tissues
- Chul Jin Moon, Soo Jin Lee, Se Hoon Lee
- Korean Journal of Occupational and Environmental Medicine 2000;12(3):338-345. Published online September 30, 2000
- DOI: https://doi.org/10.35371/kjoem.2000.12.3.338
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Abstract
PDF
- OBJECTIVES
This research was intended to investigate the relationship between manganese and malodndialdehyde concentration in tissues of rats exposed to maganese chloride.
METHODS
The study groups were 12 manganese treated rats and 9 control rats. Manganese treated rats were given intraperitoneally manganese chloride (Mn, 4 mg/kg) daily for a period of 30 days except Sunday. Control rats were injected 1ml of saline. The plasma manganese concentrations of rats were determined by graphite furnace atomic absorption spectrometry. The tissue manganese concentration was determined by flame atomic absorption spectrometry. Malondialdehyde, the product of lipid peroxidation was determined by ultraviolet-visible spectrophotometry. The plasma malondialdehyde was determined by gas chromatography with mass-detector. Protein concentration was quantified by ultraviolet-visible spectrometry and was used for the compensation of tissue malondialdehyde and manganese concentration.
RESULTS
Manganese concentrations of plasma, brain, liver, and pancreas were very significantly higher in the manganese-treated rats than in the control rats. Malondialdehyde concentration of plasma, brain, and pacrease were significantly higher in the manganese-treated rats than in the control rats. The concentration of malondialdehyde was correlated with manganese levels in plasma, brain and pancreas.
Conclusion
Based on the results obtained as above, it was concluded that the malondialdehyde, product of lipid peroxidation was related to the cell death due to dosing excess manganese.
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