Induction after Administering Paraquat of Heme Oxygenase-1 and Heat Shock Protein 70 in the Liver of Senescence-accelerated Mice

Nakanishi, Yusuke; Yasumoto, Kyoden

doi:10.1271/bbb.61.1302

Cited by 19 publications

(9 citation statements)

References 7 publications

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“…(Nakanishi and Yasumoto 1997) investigated age-associated changes in the induction of heme oxygenase and HSP 70 in the liver of senescent mice after the administration of paraquat, and found that HO-1 and HSP70 induction in response to paraquat decreased significantly with age. Moreover, the amount of HSP70 induced was lower in mice that were prone to accelerated senescence than in mice of the same age that were resistant to accelerated senescence.…”

Section: Discussionmentioning

confidence: 99%

Heme oxygenase 1 expression in rat liver during ageing and ethanol intoxication

et al. 2007

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Heme oxygenase 1 (HO-1) expression is recognized as a marker of cellular response to oxidative stress; since ageing is believed to be related to oxidative "wear and tear", HO-1 may represent a candidate biomarker of ageing. In our study, the hepatic expression of HO-1 mRNA, evaluated by RT-PCR in 2.5-24 month-old rats, was higher at 6 months than at 2.5 months of age, but thereafter increased no further: on the contrary, a declining trend was observed. However, while 2.5 month-old rats responded to acute ethanol intoxication by displaying increased expression of liver HO-1 mRNA, and 6 month-old rats exhibited a mild response, 18 month-old rats did not show any response; this phenomenon suggests that during development and ageing the transcriptional response to oxidative stress decreases. In our view, the finding that HO-1 expression did not increase progressively during ageing may be explained by a decreased transcriptional ability to respond to stress in older animals, rather than by a reduction in oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Heme oxygenase 1 expression in rat liver during ageing and ethanol intoxication

et al. 2007

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“…Impaired HO-1 induction has been frequently observed in various tissues of old rodents and by variety stimulators. Compared with that in young rodents, HO-1 induction declined in the liver of old rodents in response to iron [171], heat stress [172], and paraquat [173]; in hippocampus by hypoxia [167]; in aorta of old rats by H 2 O 2 and glucose [159]; in the carotid body [174], the gastrointestinal tract [175], and retinal pigment epithelium of old mice [158]. It should be noted that the age-related decline of HO-1 induction in rodents occurs independently of the basal HO-1 level.…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress response and Nrf2 signaling in aging

Zhang¹,

Davies

Forman

2015

Free Radical Biology and Medicine

678

504

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Increasing oxidative stress, a major characteristic of aging, has been implicated in variety of age-related pathologies. In aging, oxidant production from several sources is increased while antioxidant enzymes, the primary lines of defense, are decreased. Repair systems, including the proteasomal degradation of damaged proteins also declines. Importantly, the adaptive response to oxidative stress declines with aging. Nrf2/EpRE signaling regulates the basal and inducible expression of many antioxidant enzymes and the proteasome. Nrf2/EpRE activity is regulated at several levels including transcription, post-translation, and interaction with other proteins. This review summarizes current studies on age-related impairment of Nrf2/EpRE function and discusses the change of Nrf2 regulatory mechanisms with aging.

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“…And 24 fragments are strain specific or differential expression. Most of those genes are associated with aging and senile phenotypic pathologies, which include heat shock protein 8 (Hspa8) (Nakanishi and Yasumoto, 1997), ubiquitin specific protease 14 (USP14) (Gray et al, 2003), protein L-isoaspartate (D-aspartate) O-methyltransferase (DeVry and Clarke, 1999), glial cell line derived neurotrophic factor family receptor alpha 1 (GDFR1) (Remy et al, 2001), RAB14 (Longo, 2003), FBJ osteosarcoma oncogene B (FOSB) (Kalinichev et al, 2000)., ubiquinol-cytochrome c reductase complex 7.2 kD, (Dillin et al, 2002), 60S ribosomal protein L21 (Zhang et al, 2002), phenylalkylamine Ca2+ antagonist (emopamil) binding protein (Roy et al, 1999), fucosyltransferase 9 (Ameno et al, 2001), ferritin heavy chain (Ammendola et al, 1992) Note. Clones1-4 are aging specific expression fragments.…”

Section: Discussionmentioning

confidence: 99%

Seeking for Senile-Related Gene Expression in Cerebral Tissue of Senescence-Accelerated Mouse

Zhang

Wang²,

Cheng

et al. 2004

Cell Mol Neurobiol

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1. A better understanding of the molecular effect on aging in the brain may help reveal important aspects of organism aging, as well as the processes that lead to aging-related brain dysfunction. In this study, the aging-specific expression genes of the murine cerebrum were investigated by using the technique of DDRT-PCR in two senescence-accelerated mouse strains, SAMP10/Ta and SAMR1TA. 2. Through comparing gene expression profile among the age, 2, 4, 12, and 18 month of the SAMP10/Ta strain, four differential fragments have been found, and comparing gene expression profile between the two mouse strains, 24 fragments have been detected, 7 and 17 of them belong to SAMP10/Ta and SAMR1TA, respectively. 3. Sequencing analysis indicated that most of those fragments are homologous with some of certain gene cDNA that are related with senile. The data obtained from this study suggest that many genes are involved in the senile process and accelerate senescence phenotypic pathologies in SAMP10/Ta.

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Induction after Administering Paraquat of Heme Oxygenase-1 and Heat Shock Protein 70 in the Liver of Senescence-accelerated Mice

Cited by 19 publications

References 7 publications

Heme oxygenase 1 expression in rat liver during ageing and ethanol intoxication

Heme oxygenase 1 expression in rat liver during ageing and ethanol intoxication

Oxidative stress response and Nrf2 signaling in aging

Seeking for Senile-Related Gene Expression in Cerebral Tissue of Senescence-Accelerated Mouse

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