Prenatal alcohol–induced neuroapoptosis in rat brain cerebral cortex: protective effect of folic acid and betaine

Söğüt, İbrahim; Uysal, Onur Kadir; Oğlakçı, Ayşegül; Yücel, Ferruh; Kartkaya, Kazım; Kanbak, Güngör

doi:10.1007/s00381-016-3309-6

Cited by 22 publications

(14 citation statements)

References 44 publications

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“…Our results are similar to the previous studies which show that ethanol can trigger apoptosis (Cohen et al 2009;Sogut et al 2017). Tang et al also demonstrated that proper doses of boric acid (160 mg/L most) prevents apoptosis and brain development damage in ostrich chick brains (Tang et al 2016).…”

Section: R a F Tsupporting

confidence: 92%

The antioxidant and antiapoptotic effect of boric acid on hepatoxicity in chronic alcohol-fed rats

Söğüt

Paltun

Tunçdemi̇r

et al. 2018

Can. J. Physiol. Pharmacol.

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The harmful use of alcohol is a worldwide problem involving all ages. This study aims to investigate chronic alcohol exposure related hepatotoxicity on the rat liver and possible hepatoprotective effects of boric acid. Rats were separated into 4 different groups: control, ethanol, ethanol+boric acid, and boric acid. We measured (i) malondialdehyde (MDA), total sialic acid (TSA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels, which are known to be the markers of alcohol damage; and also (ii) caspase-3, tumor necrosis factor-alpha (TNF-α), and the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) as the markers of apoptosis. In the ethanol group, MDA, TSA, and TNF-α levels increased whereas SOD and CAT levels decreased compared with the control group. Ethanol+boric acid group MDA, TSA, caspase-3, and TNF-α levels decreased whereas SOD and CAT levels increased compared with the ethanol group. Using histopathological evaluation of light microscope images, immunohistochemical caspase-3 and TNF-α activity in the ethanol+boric acid group were shown to be decreased compared with that in the ethanol group. Our results revealed that ethanol is capable of triggering oxidative stress and apoptosis in the rat liver. We propose that boric acid is an effective compound in protecting the rat liver against ethanol.

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Section: R a F Tsupporting

confidence: 92%

The antioxidant and antiapoptotic effect of boric acid on hepatoxicity in chronic alcohol-fed rats

Söğüt

Paltun

Tunçdemi̇r

et al. 2018

Can. J. Physiol. Pharmacol.

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“…The methyl donor and osmolyte betaine (trimethylglycine) was reduced in quantity in the brain extracts of chronically alcohol-exposed mice. Betaine is derived from the diet or choline metabolism and has been shown to have protective effects on the brain (e.g., see refs − ). Betaine is also well known as an osmolyte, and this may be one of its roles in the brain (e.g., ref ).…”

Section: Discussionmentioning

confidence: 99%

Metabolic Phenotyping Study of Mouse Brains Following Acute or Chronic Exposures to Ethanol

et al. 2020

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The chronic and acute effect of ethanol administration on the metabolic phenotype of mouse brain was studied in a C57BL/6 mouse model of ethanol abuse using both untargeted and targeted ultra performance liquid chromatography-tandem mass spectrometry. Two experiments based on either chronic (8 week) exposure to ethanol of both male and female mice or acute exposure of male mice for 11 days, plus 2 oral gavage doses of 25% ethanol, were undertaken. Marked differences were found in amino acids, nucleotides, nucleosides, and related metabolites as well as a number of different lipids. Using untargeted metabolite profiling, acute ethanol exposure found significant decreases in several metabolites including nucleosides, fatty acids, glycerophosphocholine, and a number of phospholipids, while chronic exposure resulted in increases in several amino acids with notable decreases in adenosine, acetylcarnitine, and galactosylceramides. Similarly, targeted metabolite analysis, focusing on the hydrophilic fraction of the brain tissue extract, identified significant decreases in the metabolism of amino acids and derivatives, as well as purine degradation especially after chronic exposure to ethanol.

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“…To our knowledge there is no published literature linking folic acid deficiency and formic acid to FASD, although numerous studies suggest alcohol-mediated oxidative stress as the possible mechanism (Dreosti 1993;Brocardo et al 2011;Muralidharan et al 2015;Gupta et al 2016;Sarmah et al 2016;Sogut et al 2017). Thus, treatment using nutrients that have antioxidant properties, such as folic acid, appear promising.…”

Section: Discussionmentioning

confidence: 99%

FASD: folic acid and formic acid — an unholy alliance in the alcohol abusing mother

Kapur

Baber

2018

Biochem. Cell Biol.

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Alcohol consumption during pregnancy remains a significant cause of preventable birth defects and developmental disabilities; however, the mechanism of toxicity remains unclear. Methanol is present as a congener in many alcoholic beverages and is formed endogenously. Because ethanol is preferentially metabolized over methanol, it has been found in the sera and cerebro-spinal fluid of alcoholics. Toxicity resulting from methanol has been attributed to formic acid. Formic acid is present in significantly higher quantities in the biofluids of alcoholics. These higher levels can be cytotoxic and cause neuronal cell death. However, the adverse effects can be mitigated by adequate levels of hepatic folic acid, because formic acid elimination depends on folic acid. During pregnancy, folate concentrations are at least 2-fold higher in cord blood then in maternal blood, owing to increased folate requirements. The reverse has been demonstrated in pregnancies with alcohol abuse, suggesting downregulation of folate transporters and low fetal folate levels. Moreover, formic acid can cross the placenta and its adverse effects can be mitigated by folic acid. Thus, the combination of low fetal folate levels and presence of formic acid form a potent cytotoxic combination that may play a significant role in the etiology of fetal alcohol spectrum disorder.Key words: formic acid, methanol, folic acid, FASD, neurotoxicity.Résumé : La consommation d'alcool pendant la grossesse demeure une cause significative de déficiences congénitales et développementales évitables, mais le mécanisme responsable de sa toxicité est encore flou. Le méthanol est présent comme congénère dans plusieurs boissons alcooliques et il est formé de manière endogène. Puisque l'éthanol est préférentiellement métabolisé par rapport au méthanol, ce dernier a été trouvé dans le sérum et le liquide céphalorachidien des personnes alcooliques. La toxicité résultant du méthanol a été attribuée à l'acide formique. L'acide formique est présent en quantité significativement plus élevée dans les liquides biologiques des patients alcooliques. Ces niveaux plus élevés peuvent être cytotoxiques et causer la mort neuronale. Cependant, ces effets nocifs peuvent être atténués par des niveaux appropriés d'acide folique hépatique, car l'élimination d'acide formique dépend de l'acide folique. Durant la grossesse, les concentrations de folate sont au moins deux fois plus élevées dans le cordon ombilical que dans le sang maternel à cause des besoins accrus en folate. L'inverse a été démontré chez les femmes enceintes qui abusent d'alcool, suggérant une régulation à la baisse des transporteurs du folate et de faibles niveaux foetaux de folate. En outre, l'acide formique peut traverser le placenta et ses effets nocifs peuvent être atténués par l'acide folique. Ainsi, de faibles niveaux foetaux de folate et la présence d'acide formique forment une combinaison cytotoxique puissante qui peut jouer un rôle significatif dans l'étiologie de troubles du spectre de l'alcoolisation foet...

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Prenatal alcohol–induced neuroapoptosis in rat brain cerebral cortex: protective effect of folic acid and betaine

Cited by 22 publications

References 44 publications

The antioxidant and antiapoptotic effect of boric acid on hepatoxicity in chronic alcohol-fed rats

The antioxidant and antiapoptotic effect of boric acid on hepatoxicity in chronic alcohol-fed rats

Metabolic Phenotyping Study of Mouse Brains Following Acute or Chronic Exposures to Ethanol

FASD: folic acid and formic acid — an unholy alliance in the alcohol abusing mother

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