Vitamin U ameliorates glycoprotein components, enzyme and tissue factor activities of amiodarone toxicity in liver

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In this study, we aimed to evaluate whether edaravone (EDA) has a protective role against valproic acid (VPA)-induced lung damage via its antioxidative activity. Male Sprague-Dawley rats were split into four groups. Control (n = 8) rats; rats given EDA (30 mg kg −1 day −1 ; n = 10); rats given only (VPA, 500 mg kg −1 day −1 ; n = 10); rats given VPA + EDA (in the same dose and time) for 7 days. EDA and VPA were applied intraperitoneally. After 8 days, lung tissues were immediately taken from the rats. In lung homogenates, reduced glutathione, total antioxidant status levels, and superoxide dismutase, glutathione peroxidase, sodium/potassium ATPase, paraoxonase1, and carbonic anhydrase activities significantly abated, whereas catalase, glutathione reductase, glutathione-S-transferase activities insignificantly decreased in the VPA-treated group. In contrast, lipid peroxidation, reactive oxygen species, and total oxidant status levels, glycoprotein and protein carbonyl contents, nitric oxide, hydroxyproline levels, and xanthine oxidase, lactate dehydrogenase, arginase, and prolidase activities significantly increased in the VPA-given group. Administration of EDA caused the reverse effects. As a consequence, EDA prevented oxidative stress-mediated lung injury via its robust antioxidant effects.

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The effects of edaravone, a free‐radical scavenger in lung injury induced by valproic acid demonstrated via different biochemical parameters

Bayrak

Yılmaz

Cakmak

et al. 2021

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“…In addition to that, Raukas et al [58] reported that they found elevated mitochondrial OSI in brain tissues of Alzheimer's disease patients. Vit U, whose antioxidant activity has been proven on many toxicity models, [59,60] showed reversing effect on the distorted activities of antioxidants and oxidant levels of the brain tissues of the PTZ administered group.…”

Section: Discussionmentioning

confidence: 94%

The protective effect of vitamin U on pentylenetetrazole‐induced brain damage in rats

Bayrak

Türkyılmaz

Yanardağ

2022

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Pentylenetetrazole (PTZ) is preferred for experimental epilepsy induction. PTZ damages brain and other organs by elevating oxidative substances. Vitamin U (Vit U) is sulfur derivative substance that proved to be an excellent antioxidant.The current study was intended to determine the protective role of Vit U on PTZ-induced brain damage. Male Sprague-Dawley rats were separated into four groups. The Control group (Group I), was given saline for 7 days intraperitoneally (i.p); Vit U (Group II) was given as 50 mg/kg/day for 7 days by gavage; PTZ was injected into animals (Group III) at a single dose of 60 mg/kg, by i.p; PTZ + Vit U group (Group IV) was administered PTZ and Vit U in same dose and time as aforementioned. After the experiment was terminated, brain tissues were taken for the preparation of homogenates. In the PTZ group, glutathione and lipid peroxidation levels, alkaline phosphatase, myeloperoxidase, xanthine oxidase, acetylcholine esterase, antioxidant enzyme activities, total oxidant status, oxidative stress index, reactive oxygen species, and nitric oxide levels were increased. However, total antioxidant capacity was decreased in the PTZ group.Vit U ameliorated these effects in the PTZ-induced brain damage. Consequently, we can suggest that Vit U protected brain tissue via its antioxidant feature against PTZ kindling epilepsy.

“…This sulfur‐based compound help in the stabilization of the mucosal barrier by holding the main structure together, and in turn decreasing glycoprotein levels, eliminating the ROS levels, which was also proven on livers of antiarrhythmic drug‐induced toxicity. [ 48 ]…”

Section: Discussionmentioning

confidence: 99%

“…This sulfur-based compound help in the stabilization of the mucosal barrier by holding the main structure together, and in turn decreasing glycoprotein levels, eliminating the ROS levels, which was also proven on livers of antiarrhythmic drug-induced toxicity. [48] The antioxidant enzymes, CAT, SOD, GPx, GR, and GST are the first line for all cell defenses against to ROS. These enzymes work alternately for cell protection by scavenging free radicals and using GSH-like substances as cosubstrate.…”

Section: (A) (B)mentioning

confidence: 99%

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

Topaloglu¹,

Türkyılmaz

Yanardağ

2022

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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.