2009
DOI: 10.1007/s11011-009-9136-7
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Effects of 1,4-butanediol administration on oxidative stress in rat brain: Study of the neurotoxicity of γ-hydroxybutyric acid in vivo

Abstract: gamma-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 mental, motor, and langu… Show more

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Cited by 33 publications
(17 citation statements)
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“…Plasma levels of AOPP are also correlated with MDA and pro-inflammatory cytokines levels, suggesting the role of AOPP as a mediator in oxidative stress [36]. Antioxidant enzymes, as SOD, form the primary defense against reactive oxygen metabolites and have been shown to form an important adaptive response to peroxidative stress [37]. In the present study, SOD increased while CAT enzyme decreased significantly in spinal cord homogenate in IRI rats.…”
Section: Discussionsupporting
confidence: 53%
“…Plasma levels of AOPP are also correlated with MDA and pro-inflammatory cytokines levels, suggesting the role of AOPP as a mediator in oxidative stress [36]. Antioxidant enzymes, as SOD, form the primary defense against reactive oxygen metabolites and have been shown to form an important adaptive response to peroxidative stress [37]. In the present study, SOD increased while CAT enzyme decreased significantly in spinal cord homogenate in IRI rats.…”
Section: Discussionsupporting
confidence: 53%
“…Excessively damaged mitochondria will induce apoptosis as markedly high GHB levels in the central nervous system probably have the capacity to cause oxidative stress. However, it is uncertain whether this oxidative stress is a primary contributor to the onset of neurodegeneration, or if its manifestation is secondary in the neurodegenerative process of SSADH deficiency …”
Section: Discussionmentioning
confidence: 99%
“…Although the exact mechanisms of GHB neurotoxicity in humans are still under investigation, recent murine studies demonstrate that elevated endogenous GHB concentrations significantly increase various parameters of oxidative stress. 52 It is postulated that GHB neurotoxicity causes accumulation of lipid peroxidation byproducts (thiobarbituric acid-reactive substances), and significantly diminishes antioxidant reactivity, thereby exacerbating neurodegeneration in individuals with SSADH deficiency. Excessively damaged mitochondria will induce apoptosis as markedly high GHB levels in the central nervous system probably have the capacity to cause oxidative stress.…”
Section: Discussion Neurotoxicity and Implications In Developmentmentioning
confidence: 99%
“…Oxidation reactions damage the sulphur-hydrogen bonds of the thiol groups and thus less TNB is found in oxidized samples. Measurements were made using the same tissue homogenate that was used to protein carbonyl measurements, based on the methods described in (Aksenov and Markesbery, 2001; Sgaravatti et al, 2009) and modified for use with 96 well microtiter plates. 12 μl of sample (diluted 1:1 with homogenization buffer) or blank (no tissue) was added to two separate wells.…”
Section: Methodsmentioning
confidence: 99%