Skip to main content
Erschienen in: Metabolic Brain Disease 5/2021

22.02.2021 | Original Article

Oral administration of D-galactose increases brain tricarboxylic acid cycle enzymes activities in Wistar rats

verfasst von: Josiane Budni, Arleide Braga Brandão, Sabrina da Silva, Michelle Lima Garcez, Francielle Mina, Tatiani Bellettini-Santos, Gabriel Casagrande Zabot, Eduarda Behenck Medeiros, Giselli Scaini, Jade de Oliveira, Emílio Luiz Streck, João Quevedo

Erschienen in: Metabolic Brain Disease | Ausgabe 5/2021

Einloggen, um Zugang zu erhalten

Abstract

D-galactose (D-gal) is a carbohydrate widely distributed in regular diets. However, D-gal administration in rodents is associated with behavioral and neurochemical alterations similar to features observed in aging. In this regard, this study aimed to investigate the effects of D-gal exposure, in different periods, in rats’ brain regions’ activities of creatine kinase (CK) and tricarboxylic acid (TCA) cycle enzymes. Male adult Wistar rats received D-gal (100 mg/kg, gavage) for 1, 2, 4, 6 or 8 weeks. CK and TCA enzymes’ activities were evaluated in rats’ prefrontal cortex and hippocampus. In general, the results showed an increase in citrate synthase (CS) and succinate dehydrogenase (SDH) activities in animals treated with D-gal compared to the control group in the prefrontal cortex and hippocampus. Also, in the fourth week, the malate dehydrogenase (MD) activity increased in the hippocampus of rats that received D-gal compared to control rats. In addition, we observed an increase in the CK activity in the prefrontal cortex and hippocampus in the first and eighth weeks of treatment in the D-gal group compared to the control group. D-gal administration orally administered modulated TCA cycle enzymes and CK activities in the prefrontal cortex and hippocampus, which were also observed in aging and neurodegenerative diseases. However, more studies using experimental models are necessary to understand better the impact and contribution of these brain metabolic abnormalities associated with D-gal consumption for aging.
Literatur
Zurück zum Zitat Garcez ML, de Carvalho CA, Mina F, Bellettini-Santos T, Schiavo GL, da Silva S, Campos ACBF, Varela RB, Valvassori SS, Damiani AP, Longaretti LM, de Andrade VM, Budni J (2018) Sodium butyrate improves memory and modulates the activity of histone deacetylases in aged rats after the administration of d-galactose. Exp Gerontol 113:209–217. https://doi.org/10.1016/j.exger.2018.10.005CrossRefPubMed Garcez ML, de Carvalho CA, Mina F, Bellettini-Santos T, Schiavo GL, da Silva S, Campos ACBF, Varela RB, Valvassori SS, Damiani AP, Longaretti LM, de Andrade VM, Budni J (2018) Sodium butyrate improves memory and modulates the activity of histone deacetylases in aged rats after the administration of d-galactose. Exp Gerontol 113:209–217. https://​doi.​org/​10.​1016/​j.​exger.​2018.​10.​005CrossRefPubMed
Zurück zum Zitat Garcez ML, Cassoma RCS, Mina F, Bellettini-Santos T, da Luz AP, Schiavo GL, Medeiros EB, Campos ACBF, da Silva S, Rempel LCT, Steckert AV, Barichello T, Budni J (2021) Folic acid prevents habituation memory impairment and oxidative stress in an aging model induced by D-galactose. Metab Brain Dis 36(2):213–224. https://doi.org/10.1007/s11011-020-00647-7CrossRefPubMed Garcez ML, Cassoma RCS, Mina F, Bellettini-Santos T, da Luz AP, Schiavo GL, Medeiros EB, Campos ACBF, da Silva S, Rempel LCT, Steckert AV, Barichello T, Budni J (2021) Folic acid prevents habituation memory impairment and oxidative stress in an aging model induced by D-galactose. Metab Brain Dis 36(2):213–224. https://​doi.​org/​10.​1007/​s11011-020-00647-7CrossRefPubMed
Zurück zum Zitat Lowry OH, Rosebrough NJ, Farr AL et al (1951) Protein measurement with the Folin phenol reagent. J Biol Chem 193(1):265–275CrossRefPubMed Lowry OH, Rosebrough NJ, Farr AL et al (1951) Protein measurement with the Folin phenol reagent. J Biol Chem 193(1):265–275CrossRefPubMed
Zurück zum Zitat Reddy PH, McWeeney S, Park BS et al (2004) Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer’s disease. Hum Mol Genet 13(12):1225–1240. https://doi.org/10.1093/hmg/ddh140CrossRefPubMed Reddy PH, McWeeney S, Park BS et al (2004) Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer’s disease. Hum Mol Genet 13(12):1225–1240. https://​doi.​org/​10.​1093/​hmg/​ddh140CrossRefPubMed
Zurück zum Zitat Selvaraji S, Poh L, Natarajan V et al (2019) Negative conditioning of mitochondrial dysfunction in age-related neurodegenerative diseases. Cond Med 2(1):30–39PubMedPubMedCentral Selvaraji S, Poh L, Natarajan V et al (2019) Negative conditioning of mitochondrial dysfunction in age-related neurodegenerative diseases. Cond Med 2(1):30–39PubMedPubMedCentral
Metadaten
Titel
Oral administration of D-galactose increases brain tricarboxylic acid cycle enzymes activities in Wistar rats
verfasst von
Josiane Budni
Arleide Braga Brandão
Sabrina da Silva
Michelle Lima Garcez
Francielle Mina
Tatiani Bellettini-Santos
Gabriel Casagrande Zabot
Eduarda Behenck Medeiros
Giselli Scaini
Jade de Oliveira
Emílio Luiz Streck
João Quevedo
Publikationsdatum
22.02.2021
Verlag
Springer US
Erschienen in
Metabolic Brain Disease / Ausgabe 5/2021
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI
https://doi.org/10.1007/s11011-021-00682-y

Weitere Artikel der Ausgabe 5/2021

Metabolic Brain Disease 5/2021 Zur Ausgabe

Leitlinien kompakt für die Neurologie

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Neurologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.