Developmental immunohistochemistry of catalase in the human brain

Houdou, Sadataka; Kuruta, Hiromi; Hasegawa, Mitsugu; Konomi, Hiroshi; Takashima, Sachio; Suzuki, Yasuyuki; Hashimoto, Takashi

doi:10.1016/0006-8993(91)90314-l

Cited by 55 publications

(26 citation statements)

References 17 publications

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“…It is localized to peroxisomes, organelles that are present in all cell types, including cerebellar neurons (36,37). Therefore, the decrease in catalase activity can be easily correlated to the increased sensitivity to oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death

Ahlbom

Gogvadze

Chen

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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There is growing concern that prenatal exposure to excessive glucocorticoids may have deleterious effects on the development of various organs, including the nervous system. This study aimed at evaluating whether prenatal exposure to high levels of glucocorticoids might produce long-term effects on neuronal cell survival. Pregnant rats were injected i.p. with 0.1 mg͞kg dexamethasone (DEX) from day 14 postconception, and cerebellar granule cells (CGC) were prepared from 1-week-old rats from DEX-treated and control dams. After 7 days in culture, cells were exposed to H 2O2, methylmercury, or colchicine at concentrations known to induce apoptotic cell death. After exposure to H 2O2 or methylmercury, both inducing oxidative stress, the number of apoptotic cells was significantly higher in DEX-than in control-CGC. Because mitochondria play a key role in apoptosis, mitochondrial function was investigated, and a decrease in the threshold level of Ca 2؉ necessary for induction of mitochondrial permeability transition, in Ca 2؉ accumulation rate, and in oxygen consumption was detected in DEX-CGC. Moreover, the activity of the antioxidant enzyme catalase was significantly decreased in DEX-CGC. A similar decrease in catalase activity was observed in cerebellar homogenate from newborn and 40-day-old DEX-rats. In conclusion, these results indicate that prenatal exposure to high levels of glucocorticoids induces long-lasting changes in CGC rendering them more sensitive to oxidative stress. With the increasing use of multiple doses of glucocorticoids in preterm infants, the possibility that prenatal exposure to excess glucocorticoids may lead to long-term neurological consequences becomes a relevant issue.

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Section: Discussionmentioning

confidence: 99%

Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death

Ahlbom

Gogvadze

Chen

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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“…Reimer and Singh (1990) evaluated the catalase mRNA expression during mouse embryonic development; it began at E13 and increased up to E18. Furthermore, the distribution of catalase in rat and human brain has been studied from E10 to E17.5 (Nardacci et al, 2004), at adulthood (Moreno et al, 1999;, and during development (Arnold and Holtzman, 1978;Houdou et al, 1991Houdou et al, , 1993Itoh et al, 2000). In agreement with our findings, a high catalase protein level has been detected in the epithelial cells of the choroid plexus, ependyma, cerebellar nuclei (E17.5), Cx (small interneurons, E17.5, adult), hippocampal CA3 (E17.5, adult), and Bergmann glia (E17.5, adult).…”

Section: In Situ Detection Of Peroxisomes In Paraffin Sections Of Dismentioning

confidence: 99%

“…In rat and human brain, some peroxisomal matrix proteins have been localized in recent years (Houdou et al, 1991(Houdou et al, , 1993Miyawaki et al, 1995;Moreno et al, 1995Moreno et al, , 1999Itoh et al, 2000;Zaar et al, 2002;Schad et al, 2003;Nardacci et al, 2004). In these studies, however, detection of the antigen-antibody complexes was mainly done by light microscopic peroxidase-based immunohistochemistry associated with diffusion artefacts of the reaction product in the cytoplasm.…”

mentioning

confidence: 99%

Differential expression of peroxisomal matrix and membrane proteins during postnatal development of mouse brain

Ahlemeyer

Neubert

Kovacs

et al. 2007

J of Comparative Neurology

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In peroxisomal biogenesis disorders, serious neurological abnormalities can be observed in the patients and the respective knockout mouse models. As a prerequisite for a better understanding of the relationship between the absence of peroxisomes and the observed neuropathology, knowledge of the regional and cell-type specific distribution of peroxisomal proteins in mouse brain is necessary. Therefore, we investigated the expression of distinct peroxins, peroxisomal membrane and matrix proteins (e.g. Pex5p, Pex14p, Pex13p, PMP70, catalase, peroxisomal thiolase, Acox1, "SKL"-PTS1 proteins) by indirect immunofluorescence 1) in primary cultures of the medial neocortex, hippocampus, and cerebellum of newborn mice and 2) in paraffin sections of mouse brain of different ages (newborn-adult). Quantitative analysis revealed a comparable abundance (number/microm(2)) of peroxisomes in cultured neurons and astrocytes of all three brain regions. In contrast, catalase immunoreactivity was higher in cultured astrocytes than in neurons. In mouse brain tissue, the abundance of peroxisomes decreased by half during postnatal development, also exhibiting prominent differences between distinct brain regions and cell types. Catalase protein levels in neuronal peroxisomes, however, decreased much more strongly in the neocortex, CA1-3 areas of the hippocampus, dentate gyrus, cerebellar nuclei, and cerebellar cortex but remained high in Bergmann glia and other astrocytes, epithelial cells of the choroid plexus, and ependyma. Similar age-dependent changes were found for thiolase and Acox1 protein levels. Developmental changes were confirmed by Western blot analysis using enriched peroxisomal and cytosolic fractions of the brain tissue as well as by measurement of catalase activity.

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“…[1][2][3][4] Yet, antioxidants to date have not been successful therapeutic candidates for several reasons, which include the following: (1) compartmentalization of oxidation/nitration, (2) propensity of agent to scavenge preferentially reactive oxygen versus nitrogen species, (3) accessibility of antioxidants to appropriate site, 31 (4) possible benefits of avoiding excess antioxidants to maintain a balanced redox potential, 32,33 and (5) importantly, the induced toxic effects of stable products of oxidation/nitration (such as isoprostanes, isofurans, TAA [which are themselves not reactive]) after the oxidant stress subsides, 25,34 thus acting as mediators of reactive oxygen and nitrogen species in tissue injury. Accordingly, identification of the primary site of action of stable products of oxidation/nitration would be of interest physiologically and therapeutically.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4] In HI insult, the neurovascular endothelium is particularly susceptible to ensue nitro-oxidative stress, [5][6][7][8] resulting in marked microvascular degeneration, which contributes to the pathogenesis of HI brain injury. 9,10 Antioxidants and free radical scavengers have been found to be effective in reducing lesions associated with experimental neonatal HI.…”

mentioning

confidence: 99%

Fatty Acid Receptor Gpr40 Mediates Neuromicrovascular Degeneration Induced by Transarachidonic Acids in Rodents

Honoré

Kooli

Hamel

et al. 2013

ATVB

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Objective-Nitro-oxidative stress exerts a significant role in the genesis of hypoxic-ischemic (HI) brain injury. We previously reported that the ω-6 long chain fatty acids, transarachidonic acids (TAAs), which are nitrative stressinduced nonenzymatically generated arachidonic acid derivatives, trigger selective microvascular endothelial cell death in neonatal neural tissue. The primary molecular target of TAAs remains unidentified. GPR40 is a G protein-coupled receptor activated by long chain fatty acids, including ω-6; it is highly expressed in brain, but its functions in this tissue are largely unknown. We hypothesized that TAAs play a significant role in neonatal HI-induced cerebral microvascular degeneration through GPR40 activation. Approach and Results-Within 24 hours of a HI insult to postnatal day 7 rat pups, a cerebral infarct and a 40% decrease in cerebrovascular density was observed. These effects were associated with an increase in nitrative stress markers (3-nitrotyrosine immunoreactivity and TAA levels) and were reduced by treatment with nitric oxide synthase inhibitor. GPR40 was expressed in rat pup brain microvasculature. In vitro, in GPR40-expressing human embryonic kidney (HEK)-293 cells, [14 C]-14E-AA (radiolabeled TAA) bound specifically, and TAA induced calcium transients, extracellular signalregulated kinase 1/2 phosphorylation, and proapoptotic thrombospondin-1 expression. In vivo, intracerebroventricular injection of TAAs triggered thrombospondin-1 expression and cerebral microvascular degeneration in wild-type mice, but not in GPR40-null congeners. Additionally, HI-induced neurovascular degeneration and cerebral infarct were decreased in GPR40-null mice. Conclusions-GPR40 emerges as the first identified G protein-coupled receptor conveying actions of nonenzymatically generated nitro-oxidative products, specifically TAAs, and is involved in (neonatal) HI encephalopathy.

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Developmental immunohistochemistry of catalase in the human brain

Cited by 55 publications

References 17 publications

Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death

Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death

Differential expression of peroxisomal matrix and membrane proteins during postnatal development of mouse brain

Fatty Acid Receptor Gpr40 Mediates Neuromicrovascular Degeneration Induced by Transarachidonic Acids in Rodents

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