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The Redox Dysregulation Visualized by Electron Microscopic Localization of Cerium Perhydroxide in The Kidney of (Nzb X Nzw)F1 Mice.

Published online by Cambridge University Press:  02 July 2020

Megumi Nishikawa
Affiliation:
Dept. of Anat. Developmental Biol., 8-1 Kawada-cho, Shinjuku-ku, Tokyo162Japan
Li-Li Chen
Affiliation:
Ophthalmol., Tokyo Women's Medical College, 8-1 Kawada-cho, Shinjuku-ku, Tokyo162Japan
Rie Igarashi
Affiliation:
Inst. of Medical Science, St. Marianna Univ. of Medicine, 2-16-1, Sugau, Miyamae-ku, Kawasaki216Japan
Tomoko Nakazawa
Affiliation:
Dept. of Anat. Developmental Biol., 8-1 Kawada-cho, Shinjuku-ku, Tokyo162Japan
Eizo Aikawa
Affiliation:
Dept. of Anat. Developmental Biol., 8-1 Kawada-cho, Shinjuku-ku, Tokyo162Japan
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Extract

Redox dysregulation is known as pathogenesis of renal involvement in autoimmune lupus mice [1,2]. However, the behavior of reactive oxygen species (ROS) is still unclear [3]. The purpose of this study is to make clear the localization of hydrogen perhydroxide which is generated as intermediate substances of radical reactions.

Modified Brigg's method [4] was used to determine the generation of ROS in renal tissues of (NZB x NZW)F1 mice. The renal specimens were incubated with a standard medium, which consisted of 0. IM tris-malate buffer (pH7.4) with 7% sucrose, lmM CeCl3 and lOmM aminotriazole at 37° C for 30 min and ultrathin sections were prepared and examined by electron microscopy. Lecithinized-recombinant-superoxide dismutase (SOD) was used as redox regulator, which is ROS inhibitor. SOD (1000 U/kg) was injected 3 times a week, tail-intravenously to Fl mice from 4 to 60 weeks of age. The mRNA of inflammatory cytokines and IkB was detected by RT-PCR method.

Type
Pathology
Copyright
Copyright © Microscopy Society of America 1997

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References

1.Shah, S.V.et al.,Kidney Int. 35(1989)1093.10.1038/ki.1989.96CrossRefGoogle Scholar
2.Johnson, R.J.et al., Wilson Brenner Stem (1991)87.Google Scholar
3.Chaim, O. J.et al., lmmunogenetics 36(1992)182.Google Scholar
4.Ohno, Y. et al., Blood 60a(1982)253.10.1182/blood.V60.1.253.253CrossRefGoogle Scholar