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J Vet Sci. 2008 Sep;9(3):233-240 |
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Immunohistochemical identification and quantitative analysis of cytoplasmic Cu/Zn superoxide dismutase in mouse organogenesis
Jung-Min Yon1, In-Jeoung Baek1, Se-Ra Lee2, Mi-Ra Kim1, Beom Jun Lee1, Young Won Yun1, Sang-Yoon Nam1,* |
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1College of Veterinary Medicine and Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju 361-763, Korea
2CKD Research Institute, Chong Kun Dang Pharm., Chonan P.O. Box 74, Chonan 330-600, Korea
* synam@cbu.ac.kr |
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Cytoplasmic Cu/Zn superoxide dismutase (SOD1) is an
antioxidant enzyme that converts superoxide to hydrogen
peroxide in cells. Its spatial distribution matches that of
superoxide production, allowing it to protect cells from
oxidative stress. SOD1 deficiencies result in embryonic
lethality and a wide range of pathologies in mice, but little
is known about normal SOD1 protein expression in
developing embryos. In this study, the expression pattern
of SOD1 was investigated in post-implantation mouse
embryos and extraembryonic tissues, including placenta,
using Western blotting and immunohistochemical analyses.
SOD1 was detected in embryos and extraembryonic tissues
from embryonic day (ED) 8.5 to 18.5. The signal in
embryos was observed at the lowest level on ED 9.5-11.5,
and the highest level on ED 17.5-18.5, while levels remained
constant in the surrounding extraembryonic tissues during all
developmental stages examined. Immunohistochemical analysis
of SOD1 expression on ED 13.5-18.5 revealed its ubiquitous
distribution throughout developing organs. In particular,
high levels of SOD1 expression were observed in the
ependymal epithelium of the choroid plexus, ganglia,
sensory cells of the olfactory and vestibulocochlear epithelia,
blood cells and vessels, hepatocytes and hematopoietic
cells of the liver, lymph nodes, osteogenic tissues, and skin.
Thus, SOD1 is highly expressed at late stages of embryonic
development in a cell- and tissue-specific manner, and
can function as an important antioxidant enzyme during
organogenesis in mouse embryos.
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