γ-Hydroxybutyric acid induces oxidative stress in cerebral cortex of young rats

@article{Sgaravatti2007HydroxybutyricAI,
  title={$\gamma$-Hydroxybutyric acid induces oxidative stress in cerebral cortex of young rats},
  author={{\^A}ngela Malysz Sgaravatti and Mirian Bonaldi Sgarbi and Carla G. Testa and Karina Durigon and Carolina Didonet Pederzolli and Cristina C. Prestes and Angela T.S. Wyse and Clovis Milton Duval Wannmacher and Moacir Wajner and Carlos Severo Dutra-filho},
  journal={Neurochemistry International},
  year={2007},
  volume={50},
  pages={564-570}
}
View on Elsevier
doi.org
45 Citations
Background Citations
15
Results Citations
2

45 Citations

Effects of 1,4-butanediol administration on oxidative stress in rat brain: Study of the neurotoxicity of γ-hydroxybutyric acid in vivo

Results indicate that 1,4-BD induces in vivo oxidative stress by stimulating lipid peroxidation and decreasing the non-enzymatic antioxidant defenses in cerebral cortex of young rats.

Promotion of Lipid and Protein Oxidative Damage in Rat Brain by Ethylmalonic Acid

In the present work, the in vitro effect of EMA on oxidative stress parameters in rat cerebral cortex is investigated and it is presumed that oxidative stress may represent a pathomechanism involved in the pathophysiology of the neurologic symptoms manifested by patients affected by disorders in which EMA accumulates.

Evaluation of the Effects of Fructose on Oxidative Stress and Inflammatory Parameters in Rat Brain

The present data indicate that fructose provokes oxidative stress in the cerebral cortex, which induces oxidation of lipids and proteins and changes of CAT and SOD activities, and it seems reasonable to propose that antioxidants may serve as an adjuvant therapy to diets or to other pharmacological agents used for patients, to avoid oxidative damage to the brain.

Evidence for oxidative stress in tissues derived from succinate semialdehyde dehydrogenase-deficient mice

The data showing an imbalance between tissue antioxidant defences and oxidative attack strongly indicate that oxidative stress is involved in the pathophysiology of SSADH deficiency in mice, and likely the corresponding human disorder.

Induction of oxidative stress by the metabolites accumulating in 3-methylglutaconic aciduria in cerebral cortex of young rats.

Oxidative stress induction by cis-4-decenoic acid: Relevance for MCAD deficiency

The data indicate that oxidative stress is induced by cDA in rat brain in vitro and that oxidative damage might be involved in the pathophysiology of the encephalopathy in MCADD.

Neurotoxic effects induced by gammahydroxybutyric acid (GHB) in male rats.

The results show for the first time that the repeated administration of GHB, especially at very low doses, produces neurotoxic effects, which is very relevant because its abuse, especially by young persons, could produce considerable neurological alterations after prolonged abuse.

Succinic semialdehyde dehydrogenase: biochemical-molecular-clinical disease mechanisms, redox regulation, and functional significance.

The current review summarizes some 30 years of research on this protein and disease, addressing pathological mechanisms in human and mouse at the protein, metabolic, molecular, and whole-animal level.

Long-chain 3-hydroxy fatty acids accumulating in LCHAD and MTP deficiencies induce oxidative stress in rat brain

Medium-chain fatty acids accumulating in MCAD deficiency elicit lipid and protein oxidative damage and decrease non-enzymatic antioxidant defenses in rat brain

References

SHOWING 1-10 OF 43 REFERENCES

Significance of γ-hydroxybutyric acid in the brain

Murine succinate semialdehyde dehydrogenase deficiency

A murine knockout model of SSADH deficiency is developed and may represent a useful model in which to explore the effect of GABA and GHB accumulation on central nervous system development and function, potentially implicating the GABAA receptor in pathogenesis.

Significant behavioral disturbances in succinic semialdehyde dehydrogenase (SSADH) deficiency (Gamma-Hydroxybutyric aciduria)

Vigabatrin and newer interventions in succinic semialdehyde dehydrogenase deficiency

Succinic semialdehyde dehydrogenase (SSADH) deficiency is a rare disorder characterized by an inborn error of the catabolism of the inhibitory neurotransmitter GABA. Because of the deficiency of…

Inhibition of Rat Brain Lipid Synthesis In Vitro by 4-Hydroxybutyric Acid

Evaluated the in vitro influence of 4HB on lipid synthesis and CO2 production from [U-14C] acetate in cerebral cortex of 30-day-old Wistar rats found an impairment of mitochondrial metabolism by 4HB which may secondarily inhibit lipid synthesis.

Therapeutic intervention in mice deficient for succinate semialdehyde dehydrogenase (gamma-hydroxybutyric aciduria).

The data indicate that, at a minimum, GHB and GABA(B) receptors are involved in the pathophysiology of SSADH deficiency and that the poor clinical efficacy of VGB in this disease may relate to an inability to decrease brain GHB concentrations.

Increased guanidino species in murine and human succinate semialdehyde dehydrogenase (SSADH) deficiency.

Succinic semialdehyde dehydrogenase deficiency in children and adults

Preliminary human cerebrospinal fluid measurements are consistent with neurometabolic aberrations documented in the murine animal model, with elevations in γ‐aminobutyric acid, γ-hydroxybutyrate, and homocarnosine, and low glutamine.

Inhibition of succinic semialdehyde dehydrogenase activity by alkenal products of lipid peroxidation.

Inherited disorders of GABA metabolism

Only succinic semialdehyde dehydrogenase deficiency manifests organic aciduria, which may account for the higher number of patients identified with this disorder; identification of additional patients with some of the other disorders will require increased request for analysis of cerebrospinal fluid metabolites by paediatrics and neurometabolic specialists.