The effect of vitamin U on the lung tissue of pentyleneterazole-induced seizures in rats

Oktay, Şule; Bayrak, Gamze; Alev, Burçin; Ipekci, Hazal; Üstündağ, Ünsal Veli; Türkyılmaz, İsmet Burcu; Pişiriciler, Rabia; Emekli-Alturfan, Ebru; Tunalı-Akbay, Tuğba; Yanardağ, Refiye; Yarat, Ayşen

doi:10.1007/s00210-017-1447-3

Cited by 7 publications

(12 citation statements)

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“…[38] Several studies revealed that excessive generation of free-radical intermediates including reactive oxygen species (ROS) are associated with VPA administration, possibly as a consequence of VPA biotransformation, alterations in GSH homeostasis, and/or depletion of cofactors required for antioxidant defense. [14,39,40] Additionally, MPO produces ROS such as hydroxyl radicals, singlet oxygen, and ozone, which are the most important and clinically relevant oxidants. [41] Oztay et al [42] noted that ROS pro- Thus, it is accepted that increased LPO and MPO activity in tissues are excellent markers of induced oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

“…Vit U attenuated oxidative stress by increasing activities of antioxidant enzymes in the lens, liver, and kidney of rats. Recently, Oktay et al [ 14 ] reported the protective role of Vit U against oxidative stress‐induced lung damage, which may occur during seizures in epileptic rats, by increasing GSH level and activities of SOD and CAT. In the current study, Vit U also diminished VPA‐induced oxidative damage in rat lungs by increasing the GSH level and activities of GST and GPx in addition to activities of SOD and CAT.…”

Section: Discussionmentioning

confidence: 99%

“…[ 12,13 ] It is reported to be a beneficial agent for reducing organ damage in VPA‐induced hepatotoxicity and in the lung tissue of epileptic rats, by decreasing oxidative stress. [ 14,15 ] In addition, Vit U was referred to as a novel free‐radical scavenger due to the sulfhydryl groups in its chemical composition. [ 16 ] Nuclear factor‐erythroid‐2‐related factor 2 (Nrf2) is a transcription factor controlling the expression of many antioxidant enzymes in addition to the recycling and release of glutathione (GSH).…”

Section: Introductionmentioning

confidence: 99%

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The protective effect of vitamin U on valproic acid‐induced lung toxicity in rats via amelioration of oxidative stress

Öztay

Tunalı

Kayalar

et al. 2020

J Biochem & Molecular Tox

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Vitamin U (Vit U) is a novel free-radical scavenger. The protective effect of Vit U on valproic acid (VPA)-induced lung damage was examined. Rats were divided into four groups: control rats; rats given Vit U (50 mg/kg/d, by gavage) for 15 days; rats treated with VPA (500 mg/kg/d, intraperitoneally) for 15 days; and rats were given VPA + Vit U (in same dose and time). On the 16th day of the experiment, the lungs were collected from rats. Lung structure, pulmonary oxidant/antioxidant parameters and Nrf2, α-SMA, and collagen-1 were evaluated by microscopic and biochemical analysis. Additionally, it was determined the interactions of Vit U with Nrf2 and Keap1 by in silico analysis. VPA administration increased lipid peroxidation and the activity of lactate dehydrogenase and myeloperoxidase. However, it decreased the glutathione level, and the activities of glutathione peroxidase, glutathione-Stransferase, catalase, and superoxide dismutase. VPA-mediated oxidative stress prompted structural distortion and fibrotic alterations in the lung. Vit U supplementation reversed structural and biochemical alterations, induced antioxidant system through Nrf2 activation, and attenuated fibrosis by reducing collagen expression in VPA-administered rats. However, Vit U pretreatment was unable to reduce α-SMA levels in the lung of VPA-treated rats. Molecular docking analysis showed the binding of Vit U to ETGE motif leads to dissociation of Nrf2 from the Nrf2/Keap1 complex and its transfer to nuclei. In conclusion, Vit U attenuated VPA-induced tissue damage by restoring antioxidative systems through amelioration of Nrf2 activity in the lung under oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The protective effect of vitamin U on valproic acid‐induced lung toxicity in rats via amelioration of oxidative stress

Öztay

Tunalı

Kayalar

et al. 2020

J Biochem & Molecular Tox

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“…This might be associated with the duration of administration of MMSC (three consecutive days). Oktay et al, stated that the administration of MMSC (50 mg/kg/day) to intact animals for 7 days caused an insignificant elevation of NO levels (7). In GalN injected groups, the levels of NO were remarkably elevated as compared to intact rats.…”

Section: Discussionmentioning

confidence: 99%

“…It is being studied as a source of anti-peptic ulcer dietary factors. As of its clinical importance, MMSC had several biofunctions such as cytoprotective agents against gastrointestinal disorders (6) and anti-epileptic effects (7). Besides, MMSC plays an important role by acting as a radical scavenger, as well as anti-fibrotic and anti-inflammatory agent under oxidative stress conditions (8).…”

Section: Introductionmentioning

confidence: 99%

The Protective Effects of S-Methyl Methionine Sulfonium Chloride on Brain Tissue Damage in D-Galactosamine-Induced Hepatotoxicity

Bayrak¹,

Mahmarzayeva²,

Türkyılmaz³

et al. 2022

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Objective: The objective of the current work is to examine the protective effects of S-methyl methionine sulfonium chloride (MMSC) on brain in galactosamine (GalN)-induced hepatotoxicity in rats. Materials and Methods:A total of twenty two female Sprague-Dawley rats were randomly assigned into four groups as follows: Group I (n=5), intact control animals; Group II (n=6), animals that received 50 mg/kg/day of MMSC by gavage technique for 3 consecutive days; Group III (n=5), animals injected with a single dose of 500 mg/kg of GalN intraperitoneally (i.p.); and Group IV (n=6) are animals injected with the same dose of GalN (i.p.) 1 hour after MMSC treatment. At the end of the experiments (after 6 hours of the last GalN treatment), all animals were sacrificed under anaesthesia, and brain tissues were dissected out. Results:A statistically remarkable increase in lipid peroxidation, hydroxyproline, and nitric oxide levels, was detected while a notable decline in the activities of sodium/potassium ATPase was observed in GalN group in comparison with control rats. In contrast, all alterations observed were reversed when MMSC was given to GalN groups. Conclusion:Consequently, it may be considered that MMSC has a protective role on brain in GalN-induced hepatotoxicity in rats.

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Gastroprotective effect of vitamin U in D‐galactosamine‐induced hepatotoxicity

Topaloglu¹,

Türkyılmaz

Yanardağ

2022

J Biochem & Molecular Tox

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Galactosamine (GalN) is a well‐known agent for inducing viral hepatitis models in rodents, but it can cause toxicity on different organs. Vitamin U (Vit U) has been proved as a powerful antioxidant on many toxicity models. The present study was designed to investigate the protective effects of Vit U on GalN‐induced stomach injury. Rats were divided into four groups as follows: control (group I), Vit U given animals (50 mg/kg per day; group II), GalN administered animals (500 mg/kg at a single dose; group III), GalN + Vit U given animals (at the same dose and time, group IV). At the end of the 3rd day, animals were killed, and stomach tissues were taken. They were homogenized and centrifuged. In comparison to the control group, glutathione, total antioxidant capacity levels, catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione‐S‐transferase, and Na+/K+‐ATPase activities of GalN group were found to be decreased. On the contrary, lipid peroxidation, advanced oxidized protein products, hexose‐hexosamine, fucose, sialic acid, reactive oxygen species levels, as well as the activities of myeloperoxidase, xanthine oxidase, and lactate dehydrogenase were elevated. Administration of Vit U reversed these abnormalities in the GalN group. It can be concluded that Vit U exerts its unique antioxidant effect and prevents GalN‐induced gastric damage.

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The effect of vitamin U on the lung tissue of pentyleneterazole-induced seizures in rats

Cited by 7 publications

References 50 publications

The protective effect of vitamin U on valproic acid‐induced lung toxicity in rats via amelioration of oxidative stress

The protective effect of vitamin U on valproic acid‐induced lung toxicity in rats via amelioration of oxidative stress

The Protective Effects of S-Methyl Methionine Sulfonium Chloride on Brain Tissue Damage in D-Galactosamine-Induced Hepatotoxicity

Gastroprotective effect of vitamin U in D‐galactosamine‐induced hepatotoxicity

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