Spatiotemporal evaluation of the mouse embryonic redox environment and histiotrophic nutrition following treatment with valproic acid and 1,2-dithiole-3-thione during early organogenesis

Lapehn, Samantha; Piorczynski, Ted B.; Hansen, Jason M.; Harris, Craig

doi:10.1016/j.reprotox.2021.03.001

Cited by 6 publications

(4 citation statements)

References 49 publications

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“…We evaluated the effects of VPA on these enzyme activities in rats who underwent BS followed by resuscitation. VPA reduced the concentration of GSSG in various tissues and increased the concentration of GSH and GSH/GSSG ratio as described previously (Lapehn et al, 2021;Salimi et al, 2022). Our findings about the content of antioxidant enzymes with VPA on the resuscitation of the scalded rats were consistent with those reported previously (Koroglu et al, 2021;Lapehn et al, 2021;Simon-Szabo et al, 2021).…”

Section: Sourcesupporting

confidence: 92%

“…VPA reduced the concentration of GSSG in various tissues and increased the concentration of GSH and GSH/GSSG ratio as described previously (Lapehn et al, 2021;Salimi et al, 2022). Our findings about the content of antioxidant enzymes with VPA on the resuscitation of the scalded rats were consistent with those reported previously (Koroglu et al, 2021;Lapehn et al, 2021;Simon-Szabo et al, 2021). In summary, VPA markedly alleviated lipid peroxidation, thereby improving visceral function in the scalded rats.…”

Section: Sourcesupporting

confidence: 92%

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Valproic Acid Treatment Improves Organ Function, Survival Rate, and Lipid Peroxidation in Fatally Scalded Rats

Liu,

Fu,

Jiang

et al. 2023

Pharmacognosy Magazine

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Background After hypovolemic shock caused by severe burns, lipid peroxidation is an important factor in tissue edema and multiorgan dysfunction syndrome (MODS). Many studies have shown that valproic acid (VPA) inhibits lipid peroxidation and reduces tissue and organ injury. Objectives This study investigated whether the VPA treatment of scalded rats reduced tissue edema by inhibiting lipid peroxidation, thereby improving organ function and survival rate. Materials and Methods A total of 60 male Sprague-Dawley rats (weighing: 280–300 g) with a 50% total body surface area (TBSA) full-thickness dermal burn were randomly assigned to the following 3 groups (with 20 rats per group): (I) the no infusion resuscitation (NR) group; (II) the sodium lactate Ringer’s solution (LR) group; and (III) the sodium valproate Ringer’s solution (VR) group. After scalding, the following hemodynamic parameters were measured: Copper2+-Zinc2+-superoxide dismutase (Cu2+-Zn2+-SOD) activity, thiobarbituric acid reactive substances (TBARSs), oxidized glutathione (GSSG), reduced glutathione (GSH), and antioxidant enzyme activities. Organ function parameters and water content were also measured. Another 60 male Sprague-Dawley rats were used to observe the 24-h survival rate of the rats using the same scald model and fluid resuscitation. Results VPA significantly increased the mean arterial pressure (MAP) and cardiac output (CO), and significantly decreased the pulmonary vascular permeability index (PVPI) and extravascular lung water index (ELWI). VPA also increased plasma Cu2+-Zn2+-SOD activity and decreased the plasma TBARS level. VPA reduced the TBARS level and GSSG in various tissues and increased the concentration of GSH. VPA decreased glutathione peroxidase (GPx) and catalase (CAT) activity, but significantly increased glutathione reductase (GR) activity in various tissues. VPA significantly improved organ functions and decreased water content. VPA significantly improved the survival rate, and the 24-h survival rate of the VR group was double that of the LR group. Conclusion Resuscitation with VPA reduced tissue edema, protected visceral functions, and improved the survival rate of rats with severe burn shock (BS) by alleviating lipid peroxidation.

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Section: Sourcesupporting

confidence: 92%

Section: Sourcesupporting

confidence: 92%

Valproic Acid Treatment Improves Organ Function, Survival Rate, and Lipid Peroxidation in Fatally Scalded Rats

Liu,

Fu,

Jiang

et al. 2023

Pharmacognosy Magazine

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“…It has been reported that some of the NQO1 (− / −) mice exhibit seizures, which are characterized by tail tension, bending of the front legs, rolling onto their side, salivation, and occasional spasms [ 113 ]. Interestingly, the administration of valproic acid, an antiepileptic drug, to the mouse embryo tissues after treatment with the Nrf2 antioxidant pathway inducer, 1,2-dithiole-3-thione, significantly increased the expression of NQO1 [ 225 ]. These findings indicate the implication of NQO1 in the modulation of brain excitability.…”

Section: The Involvement Of Nqo1 In Neurological Disordersmentioning

confidence: 99%

Impact of NQO1 dysregulation in CNS disorders

Yuhan,

Khaleghi Ghadiri,

Gorji

2024

J Transl Med

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NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory and degenerative processes, and tumorigenesis in the central nervous system (CNS). Impairment of the NQO1 activity in the CNS can result in abnormal neurotransmitter release and clearance, increased oxidative stress, and aggravated cellular injury/death. Furthermore, it can cause disturbances in neural circuit function and synaptic neurotransmission. The abnormalities of NQO1 enzyme activity have been linked to the pathophysiological mechanisms of multiple neurological disorders, including Parkinson's disease, Alzheimer's disease, epilepsy, multiple sclerosis, cerebrovascular disease, traumatic brain injury, and brain malignancy. NQO1 contributes to various dimensions of tumorigenesis and treatment response in various brain tumors. The precise mechanisms through which abnormalities in NQO1 function contribute to these neurological disorders continue to be a subject of ongoing research. Building upon the existing knowledge, the present study reviews current investigations describing the role of NQO1 dysregulations in various neurological disorders. This study emphasizes the potential of NQO1 as a biomarker in diagnostic and prognostic approaches, as well as its suitability as a target for drug development strategies in neurological disorders.

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“…Considering that fetuses are more vulnerable to VPA exposure during organogenesis (Lapehn, Piorczynski, Hansen, & Harris, 2021), using this drug in the first trimester of pregnancy increases the risk of congenital malformations (Gotlib, Ramaswamy, Kurlander, DeRiggi, & Riba, 2017). Administration of VPA during pregnancy is linked with a threefold increase in gross anomalies, specifically spina bifida, anencephaly, cardiac, craniofacial, skeletal and limb defects, and "valproate syndrome" (Mutlu-Albayrak, Bulut, & Caksen, 2017).…”

Section: Introductionmentioning

confidence: 99%

Valproic acid induced selective apoptosis of ocular fibrous tunic in mice fetuses

Manthos

Theotokis

Dermitzakis

et al. 2022

Birth Defects Research

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Background Valproic acid (VPA), a prescribed drug commonly used for various neurological perturbations, has been implicated in teratogenic inflictions on developing fetuses during pregnancy. The purpose of this research was to delineate the gross morphological and histological effects of VPA in the developing eye tunics and lens. Methods A time‐dependent administration of 500 mg/kg VPA to BALB/c groups of female mice was coordinated during organogenesis (gestational days 7, 8, and 9) and compared to controls that received normal saline. Seized fetuses were checked for macroscopic eye anomalies, histological malformations with Azan trichrome staining, and levels of apoptotic activity with the terminal deoxynucleotidyl transferase‐mediated nick end labeling (TUNEL) assay. Results Histochemical analysis showed that VPA‐treated groups exhibited collagen deficiency (2.5–50% decrease in aniline blue intensity) and a marked increase in TUNEL‐positive cells (p < .05) in corneal stroma and sclera/choroid layers while less was detected in retina and lens, when compared to controls. Conclusions Since the evaluation of the inner structures did not manifest major differences, we conclude that VPA teratogenic influence display eclectic toxicity, as seen by increased apoptosis to eye layers with high degree fibrous context, particularly the outer tunics.

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Spatiotemporal evaluation of the mouse embryonic redox environment and histiotrophic nutrition following treatment with valproic acid and 1,2-dithiole-3-thione during early organogenesis

Cited by 6 publications

References 49 publications

Valproic Acid Treatment Improves Organ Function, Survival Rate, and Lipid Peroxidation in Fatally Scalded Rats

Valproic Acid Treatment Improves Organ Function, Survival Rate, and Lipid Peroxidation in Fatally Scalded Rats

Impact of NQO1 dysregulation in CNS disorders

Valproic acid induced selective apoptosis of ocular fibrous tunic in mice fetuses

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