Oxidative damage causes formation of lipofuscin-like substances in the hippocampus of the senescence-accelerated mouse after kainate treatment

Hyoung Chun Kim, Guoying Bing, Wang Kee Jhoo, Won-Ki Kim, Eun Joo Shin, Eon Sup Park, Yong Soon Choi, Dong Wook Lee, Chan Young Shin, Jae Ryun Ryu, Kwang Ho Ko

Research output: Contribution to journalArticle

39 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)211-220
Number of pages10
JournalBehavioural Brain Research
Volume131
Issue number1-2
DOIs
Publication statusPublished - 2002 Apr 11
Externally publishedYes

Fingerprint

Lipofuscin
Kainic Acid
Hippocampus
Malondialdehyde
Seizures
Oxidative Stress
Brain
Heat-Shock Proteins
Rodentia
Neurons
Mortality

Keywords

  • Hippocampus
  • Kainic acid
  • Lipofuscin
  • Oxidative stress
  • Seizures
  • Senescence-accelerated mouse

ASJC Scopus subject areas

  • Behavioral Neuroscience

Cite this

Oxidative damage causes formation of lipofuscin-like substances in the hippocampus of the senescence-accelerated mouse after kainate treatment. / Kim, Hyoung Chun; Bing, Guoying; Jhoo, Wang Kee; Kim, Won-Ki; Shin, Eun Joo; Park, Eon Sup; Choi, Yong Soon; Lee, Dong Wook; Shin, Chan Young; Ryu, Jae Ryun; Ko, Kwang Ho.

In: Behavioural Brain Research, Vol. 131, No. 1-2, 11.04.2002, p. 211-220.

Research output: Contribution to journalArticle

Kim, Hyoung Chun ; Bing, Guoying ; Jhoo, Wang Kee ; Kim, Won-Ki ; Shin, Eun Joo ; Park, Eon Sup ; Choi, Yong Soon ; Lee, Dong Wook ; Shin, Chan Young ; Ryu, Jae Ryun ; Ko, Kwang Ho. / Oxidative damage causes formation of lipofuscin-like substances in the hippocampus of the senescence-accelerated mouse after kainate treatment. In: Behavioural Brain Research. 2002 ; Vol. 131, No. 1-2. pp. 211-220.
@article{6758e557e12642caa43ecfe3fe0271bf,
title = "Oxidative damage causes formation of lipofuscin-like substances in the hippocampus of the senescence-accelerated mouse after kainate treatment",
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.",
keywords = "Hippocampus, Kainic acid, Lipofuscin, Oxidative stress, Seizures, Senescence-accelerated mouse",
author = "Kim, {Hyoung Chun} and Guoying Bing and Jhoo, {Wang Kee} and Won-Ki Kim and Shin, {Eun Joo} and Park, {Eon Sup} and Choi, {Yong Soon} and Lee, {Dong Wook} and Shin, {Chan Young} and Ryu, {Jae Ryun} and Ko, {Kwang Ho}",
year = "2002",
month = "4",
day = "11",
doi = "10.1016/S0166-4328(01)00382-5",
language = "English",
volume = "131",
pages = "211--220",
journal = "Behavioural Brain Research",
issn = "0166-4328",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Oxidative damage causes formation of lipofuscin-like substances in the hippocampus of the senescence-accelerated mouse after kainate treatment

AU - Kim, Hyoung Chun

AU - Bing, Guoying

AU - Jhoo, Wang Kee

AU - Kim, Won-Ki

AU - Shin, Eun Joo

AU - Park, Eon Sup

AU - Choi, Yong Soon

AU - Lee, Dong Wook

AU - Shin, Chan Young

AU - Ryu, Jae Ryun

AU - Ko, Kwang Ho

PY - 2002/4/11

Y1 - 2002/4/11

N2 - 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.

AB - 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.

KW - Hippocampus

KW - Kainic acid

KW - Lipofuscin

KW - Oxidative stress

KW - Seizures

KW - Senescence-accelerated mouse

UR - http://www.scopus.com/inward/record.url?scp=0037061544&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037061544&partnerID=8YFLogxK

U2 - 10.1016/S0166-4328(01)00382-5

DO - 10.1016/S0166-4328(01)00382-5

M3 - Article

C2 - 11844588

AN - SCOPUS:0037061544

VL - 131

SP - 211

EP - 220

JO - Behavioural Brain Research

JF - Behavioural Brain Research

SN - 0166-4328

IS - 1-2

ER -