Oxidative damage causes formation of lipofuscin-like substances in the hippocampus of the senescence-accelerated mouse after kainate treatment
- Authors
- Kim H.-C.; Bing G.; Jhoo W.-K.; Kim W.-K.; Shin E.-J.; Park E.-S.; Choi Y.-S.; Lee D.-W.; Shin C.Y.; Ryu J.R.; Ko K.H.
- Issue Date
- 2002
- Keywords
- Hippocampus; Kainic acid; Lipofuscin; Oxidative stress; Seizures; Senescence-accelerated mouse
- Citation
- Behavioural Brain Research, v.131, no.1-2, pp 211 - 220
- Pages
- 10
- Indexed
- SCOPUS
- Journal Title
- Behavioural Brain Research
- Volume
- 131
- Number
- 1-2
- Start Page
- 211
- End Page
- 220
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/22174
- DOI
- 10.1016/S0166-4328(01)00382-5
- ISSN
- 0166-4328
1872-7549
- Abstract
- We have demonstrated that seizures induced by kainic acid (KA) are, at least in part, mediated via oxidative stress in rats [Life. Sci. 61 (1997) PL373; Brain Res. 853 (2000) 215; Brain Res. 874 (2000) 15; Neurosci. Lett. 281 (2000) 65]. In order to extend our findings, we employed the rodent aging model in this study. After KA treatments (once a day for 5 days; 20, 20, 20, 20 and 40 mg/kg, i.p.), several parameters reflecting neurotoxic behaviors, oxidative stress [malondialdehyde (MDA) and protein carbonyl] and aging (lipofuscin-like substances) were compared between senile-prone (P8) and resistant (R1) strains of 9-month-old male senescence-accelerated mice (SAM). KA-induced neurotoxic signs as shown by mortality and seizure activity were more accentuated in the SAM-P8 than in the SAM-R1. Levels of MDA and carbonyl are consistently higher in the hippocampus of SAM-P8 than that of SAM-R1. Significant increases in the values of MDA and carbonyl were observed 4 h or 2 days after the final KA administration. This finding was more pronounced in the SAM-P8 than in the SAM-R1. Although a significant loss of hippocampal neurons was observed 7 days post-KA, at this time the MDA and carbonyl content had returned to near control levels. In contrast, fluorescent lipofuscin-like substances and lipofuscin granules were significantly increased 7 days after KA treatments. Therefore, our data suggests that mice in the senescence model are more susceptible to KA-induced seizures/oxidative damage, and that oxidative damage could be one of the casual factors in the accumulation of lipofuscin. © 2002 Elsevier Science B.V. All rights reserved.
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Collections - 1. Basic Science > Department of Neuroscience > 1. Journal Articles
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