AI Article Synopsis

  • The study examined how high doses of ethanol affect the activity of enzymes involved in GABA metabolism in brain mitochondria during six stages of postnatal development.
  • After administering a high dose of ethanol, the activity of these enzymes in various brain regions (cerebral cortex, cerebellum, hypothalamus, and brain stem) was observed to increase.
  • Notably, GABA-T activity decreased significantly in the 10- and 21-day-old animals, whereas, in other developmental periods, its activity was found to increase.

Article Abstract

The activity of the enzymes of GABA- GDK and GABA-T metabolism in the brain mitochondria in 6 periods of postnatal development under the conditions of high dose of ethanol was studied. It has been revealed that after the impact of high dose of ethanol (3.5 g/kg of 25% solution, intraperitoneally) the enzymes' activities in initial mitochondrial fractions of cerebral cortex, cerebellum, hypothalamus and brain stem increases. The activity of GABA-T in 10- and 21-days animals significantly decreases, while in other periods on the contrary it increases.

Download full-text PDF

Source

Publication Analysis

Top Keywords

brain mitochondria
8
high dose
8
dose ethanol
8
[glutamate decarboxylase
4
decarboxylase gaba-aminotransferase
4
gaba-aminotransferase activity
4
activity brain
4
mitochondria conditions
4
conditions ethanol
4
ethanol exposure
4

Similar Publications

Objective: To evaluate the therapeutic effects of Kuanxiong Aerosol (KXA) on ischemic stroke with reperfusion and elucidate the underlying pharmacological mechanisms.

Methods: In vivo pharmacological effects on ischemic stroke with reperfusion was evaluated using the transient middle cerebral artery occlusion (t-MCAO) mice model. To evaluate short-term outcome, 30 mice were randomly divided into vehicle group (n=15) and KXA group (n=15).

View Article and Find Full Text PDF

Background: Neuroinflammation is one of the essential pathogeneses of cognitive damage suffering from sepsis-associated encephalopathy (SAE). Lots of evidences showed the microglia presented mitochondrial fragmentation during SAE. This study investigated the protective effects and novel mechanisms of inhibiting microglia mitochondrial fragmentation via mitochondrial division inhibitor 1 (Mdivi-1) on cognitive damage in SAE.

View Article and Find Full Text PDF

Failure to repair damaged NAD(P)H blocks de novo serine synthesis in human cells.

Cell Mol Biol Lett

January 2025

Enzymology and Metabolism Group, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, L-4367, Belvaux, Luxembourg.

Background: Metabolism is error prone. For instance, the reduced forms of the central metabolic cofactors nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotide phosphate (NADPH), can be converted into redox-inactive products, NADHX and NADPHX, through enzymatically catalyzed or spontaneous hydration. The metabolite repair enzymes NAXD and NAXE convert these damaged compounds back to the functional NAD(P)H cofactors.

View Article and Find Full Text PDF

Alzheimer disease is a neurodegenerative pathology-modifying mitochondrial metabolism with energy impairments where the effects of biological sex and DNA repair deficiencies are unclear. We investigated the therapeutic potential of dietary ketosis alone or with supplemental nicotinamide riboside (NR) on hippocampal intermediary metabolism and mitochondrial bioenergetics in older male and female wild-type (Wt) and 3xTgAD-DNA polymerase-β-deficient (3xTg/POLβ) (AD) mice. DNA polymerase-β is a key enzyme in DNA base excision repair (BER) of oxidative damage that may also contribute to mitochondrial DNA repair.

View Article and Find Full Text PDF

α-Ketoisocaproic Acid Disrupts Mitochondrial Bioenergetics in the Brain of Neonate Rats: Molecular Modeling Studies of α-ketoglutarate Dehydrogenase Subunits Inhibition.

Neurochem Res

January 2025

Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.

Brain accumulation of the branched-chain α-keto acids α-ketoisocaproic acid (KIC), α-keto-β-methylvaleric acid (KMV), and α-ketoisovaleric acid (KIV) occurs in maple syrup urine disease (MSUD), an inherited intoxicating metabolic disorder caused by defects of the branched-chain α-keto acid dehydrogenase complex. Patients commonly suffer life-threatening acute encephalopathy in the newborn period and develop chronic neurological sequelae of still undefined pathogenesis. Therefore, this work investigated the in vitro influence of pathological concentrations of KIC (5 mM), KMV (1 mM), and KIV (1 mM) on mitochondrial bioenergetics in the cerebral cortex of neonate (one-day-old) rats.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!