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

  title={Effects of 1,4-butanediol administration on oxidative stress in rat brain: Study of the neurotoxicity of $\gamma$-hydroxybutyric acid in vivo},
  author={{\^A}ngela Malysz Sgaravatti and Alessandra Selinger Magnusson and Amanda S. Oliveira and Caroline Paula Mescka and Fernanda Rech Zanin and Mirian Bonaldi Sgarbi and Carolina Didonet Pederzolli and Angela T.S. Wyse and Clovis Milton Duval Wannmacher and Moacir Wajner and Carlos Severo Dutra-filho},
  journal={Metabolic Brain Disease},
Abstractγ-Hydroxybutyric acid (GHB) is a naturally occurring compound in the central nervous system (CNS) whose tissue concentration are highly increased in the neurometabolic-inherited deficiency of succinic semialdehyde dehydrogenase (SSADH) activity or due to intoxication. SSADH deficiency is biochemically characterized by increased concentrations of GHB in tissues, cerebrospinal fluid, blood and urine of affected patients. Clinical manifestations are variable and include retardation of… 

Learning and memory impairment induced by 1,4-butanediol is regulated by ERK1/2-CREB-BDNF signaling pathways in PC12 cells.

The results suggest that 1,4-BD may affect synaptic plasticity via the ERK1/2-CREB-BDNF pathway, leading to Ach release reduction and ultimately to learning and memory impairment.

K+ channel blocker-induced neuroinflammatory response and neurological disorders: immunomodulatory effects of astaxanthin

Kaliotoxin is able to induce neurological disorders by blocking the K+ ion channel, and ATX suppresses this alterations with down regulation of IL-6, TNF-α and NF-κB expression in the brain.

A potential protective effect of α-tocopherol on vascular complication in spinal cord reperfusion injury in rats

α-TOL administration significantly prevents the damage caused by spinal cord IRI in rats with subsequent recovery of both motor and sensory functions and improves the oxidative stress level with subsequent reduction of the incidence of neurological deficits due to spinal Cord IRI conditions.



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

Significance of γ-hydroxybutyric acid in 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.

Central effects of 1,4-butanediol are mediated by GABA(B) receptors via its conversion into gamma-hydroxybutyric acid.

The results suggest that the sedative/hypnotic effect of 1,4-butanediol is mediated by its conversion in vivo into GHB which, in turn, binds to GABA(B) receptors.

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

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.

Determination of aldehydic lipid peroxidation products: malonaldehyde and 4-hydroxynonenal.