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Kainate-induced mitochondrial oxidative stress contributes to hippocampal degeneration in senescence-accelerated mice.
Cell Signal. 2008 Apr; 20(4):645-58.CS

Abstract

We have demonstrated that kainate (KA) induces a reduction in mitochondrial Mn-superoxide dismutase (Mn-SOD) expression in the rat hippocampus and that KA-induced oxidative damage is more prominent in senile-prone (SAM-P8) than senile-resistant (SAM-R1) mice. To extend this, we examined whether KA seizure sensitivity contributed to mitochondrial degeneration in these mouse strains. KA-induced seizure susceptibility in SAM-P8 mice paralleled prominent increases in lipid peroxidation and protein oxidation and was accompanied by significant impairment in glutathione homeostasis in the hippocampus. These findings were more pronounced in the mitochondrial fraction than in the hippocampal homogenate. Consistently, KA-induced decreases in Mn-SOD protein expression, mitochondrial transmembrane potential, and uncoupling protein (UCP)-2 expression were more prominent in SAM-P8 than SAM-R1 mice. Marked release of cytochrome c from mitochondria into the cytosol and a higher level of caspase-3 cleavage were observed in KA-treated SAM-P8 mice. Additionally, electron microscopic evaluation indicated that KA-induced increases in mitochondrial damage and lipofuscin-like substances were more pronounced in SAM-P8 than SAM-R1 animals. These results suggest that KA-mediated mitochondrial oxidative stress contributed to hippocampal degeneration in the senile-prone mouse.

Authors+Show Affiliations

Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon 200-701, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18248956

Citation

Shin, Eun-Joo, et al. "Kainate-induced Mitochondrial Oxidative Stress Contributes to Hippocampal Degeneration in Senescence-accelerated Mice." Cellular Signalling, vol. 20, no. 4, 2008, pp. 645-58.
Shin EJ, Jeong JH, Bing G, et al. Kainate-induced mitochondrial oxidative stress contributes to hippocampal degeneration in senescence-accelerated mice. Cell Signal. 2008;20(4):645-58.
Shin, E. J., Jeong, J. H., Bing, G., Park, E. S., Chae, J. S., Yen, T. P., Kim, W. K., Wie, M. B., Jung, B. D., Kim, H. J., Lee, S. Y., & Kim, H. C. (2008). Kainate-induced mitochondrial oxidative stress contributes to hippocampal degeneration in senescence-accelerated mice. Cellular Signalling, 20(4), 645-58. https://doi.org/10.1016/j.cellsig.2007.11.014
Shin EJ, et al. Kainate-induced Mitochondrial Oxidative Stress Contributes to Hippocampal Degeneration in Senescence-accelerated Mice. Cell Signal. 2008;20(4):645-58. PubMed PMID: 18248956.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Kainate-induced mitochondrial oxidative stress contributes to hippocampal degeneration in senescence-accelerated mice. AU - Shin,Eun-Joo, AU - Jeong,Ji Hoon, AU - Bing,Guoying, AU - Park,Eon Sub, AU - Chae,Jong Seok, AU - Yen,Tran Phi Hoang, AU - Kim,Won-Ki, AU - Wie,Myung-Bok, AU - Jung,Bae-Dong, AU - Kim,Hyun Ji, AU - Lee,Sung-Youl, AU - Kim,Hyoung-Chun, Y1 - 2007/12/14/ PY - 2007/10/08/received PY - 2007/11/27/revised PY - 2007/11/27/accepted PY - 2008/2/6/pubmed PY - 2008/5/9/medline PY - 2008/2/6/entrez SP - 645 EP - 58 JF - Cellular signalling JO - Cell Signal VL - 20 IS - 4 N2 - We have demonstrated that kainate (KA) induces a reduction in mitochondrial Mn-superoxide dismutase (Mn-SOD) expression in the rat hippocampus and that KA-induced oxidative damage is more prominent in senile-prone (SAM-P8) than senile-resistant (SAM-R1) mice. To extend this, we examined whether KA seizure sensitivity contributed to mitochondrial degeneration in these mouse strains. KA-induced seizure susceptibility in SAM-P8 mice paralleled prominent increases in lipid peroxidation and protein oxidation and was accompanied by significant impairment in glutathione homeostasis in the hippocampus. These findings were more pronounced in the mitochondrial fraction than in the hippocampal homogenate. Consistently, KA-induced decreases in Mn-SOD protein expression, mitochondrial transmembrane potential, and uncoupling protein (UCP)-2 expression were more prominent in SAM-P8 than SAM-R1 mice. Marked release of cytochrome c from mitochondria into the cytosol and a higher level of caspase-3 cleavage were observed in KA-treated SAM-P8 mice. Additionally, electron microscopic evaluation indicated that KA-induced increases in mitochondrial damage and lipofuscin-like substances were more pronounced in SAM-P8 than SAM-R1 animals. These results suggest that KA-mediated mitochondrial oxidative stress contributed to hippocampal degeneration in the senile-prone mouse. SN - 0898-6568 UR - https://www.unboundmedicine.com/medline/citation/18248956/Kainate_induced_mitochondrial_oxidative_stress_contributes_to_hippocampal_degeneration_in_senescence_accelerated_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0898-6568(07)00369-5 DB - PRIME DP - Unbound Medicine ER -