Protective effects of antioxidant combination against D‐galactosamine‐induced kidney injury in rats

Çatal, Tunç; Saçan, Özlem; Yanardağ, Refiye; Bolkent, Şehnaz

doi:10.1002/cbf.1625

Cited by 6 publications

(8 citation statements)

References 47 publications

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“…Catal et al revealed that GPx enzyme activity had increased by the administration of the antioxidant combination consisting of beta carotene, ascorbic acid, α-tocopherol, and sodium selenate in renal damage induced by d -GAL. 72 In our opinion, the significant positive effects of PTX and CAPE on oxidative stress parameters observed in this study are attributed to their antioxidant properties.…”

Section: Discussionmentioning

confidence: 50%

The effects of pentoxifylline and caffeic acid phenethyl ester in the treatment ofd-galactosamine-induced acute hepatitis in rats

et al. 2015

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The aim of this study was to investigate histological changes in hepatic tissue and effects of pentoxifylline (PTX) and caffeic acid phenethyl ester (CAPE) on these changes using histochemical and biochemical methods in rats, in which hepatitis was established by d-galactosamine (d-GAL). Rats were divided into five groups as follows: control group, d-GAL (24 h) group, d-GAL group, d-GAL + PTX group, and d-GAL + CAPE group. In histological evaluations, the control group showed normal appearance of the liver cells. However in the d-GAL groups, focal areas consisting of inflammatory, necrotic, and apoptotic cells were detected in parenchyma. Glycogen loss was observed in the hepatocytes localized at the periphery of lobule. It was found that number of mast cells of portal areas were significantly higher in d-GAL groups compared with other groups ( p = 0.0001). In addition, the number of cells with positive staining by Ki-67 and caspase-3 were significantly increased in GAL groups compared with the control group ( p = 0.0001). In biochemical analysis, there was an increase in malondialdehyde and myeloperoxidase levels, while a decrease was observed in glutathione level and glutathione peroxidase activity in groups treated with d-GAL compared with the control group. On the other hand, it was seen that, in the groups treated with d-GAL, histological and biochemical injuries in the liver were reduced by administration of PTX and CAPE. In this study, we demonstrated the ameliorative effects of PTX and CAPE on d-GAL-induced liver injury.

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Section: Discussionmentioning

confidence: 50%

The effects of pentoxifylline and caffeic acid phenethyl ester in the treatment ofd-galactosamine-induced acute hepatitis in rats

et al. 2015

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“…Few studies have examined the effect of experimental d ‐GalN‐induced acute liver failure in different tissues . Consequently, very little information is available on the effects of d ‐GalN on the brain tissues of rats…”

Section: Discussionmentioning

confidence: 99%

“…It causes diffuse hepatic tissue damage and cellular inflammation, which are evident in the histological and biochemical profiles of tissues . Previous studies indicate that acute d ‐GalN liver toxicity results in oxidative damage in kidneys and lungs . d ‐GalN‐induced liver toxicity causes damage to the brain .…”

Section: Introductionmentioning

confidence: 99%

The effects of vitamins and selenium mixture against brain tissue induced byd‐galactosamine

Tunalı

Çatal

Bolkent

et al. 2019

J Biochem & Molecular Tox

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Brain damage is a major complication of fulminant hepatic failure. d‐Galactosamine (d‐GalN)‐induced liver toxicity causes damage to brain. The effects of vitamins and selenium mixture against d‐GalN stimulated brain injury were investigated in this study. Sprague‐Dawley female rats aged 2.0‐2.5 months were used for the study. The rats were divided into four categories. A 0.9% NaCl solution was intraperitoneally given to the experimental rats in the first group. Using gavage technique, the second group of animals were subjected to a formulation consisting of 100 mg·kg−1·day−1 vitamin C, 15 mg·kg−1·day−1 of β‐carotene, 100 mg·kg−1·day−1 of α‐tocopherol in addition to 0.2 mg·kg−1·day−1 of sodium selenate for 3 days. The third group was given a single dose of d‐GalN hydrochloride at the concentration of 500 mg·kg−1 through a saline injection. The final group was given similar concentrations of both the antioxidant combination and d‐GalN. Tissue samples were collected under ether anesthesia. The rats treated with d‐GalN showed brain damage; increased myeloperoxidase, catalase, glutathione peroxidase, glutathione‐S‐transferase, lactate dehydrogenase, and superoxide dismutase activities; and decreased glutathione levels. Treatment with vitamins and selenium combination resulted in alleviation of these alterations in the rats. These findings suggest that administration of the vitamins and selenium combination suppresses oxidative stress and protects brain cells from injury induced by d‐GalN.

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“…Group II was given Vit U (50 mg/kg/day) [ 19 ] by gavage technic for 3 days. Group III was administered GalN (500 mg/kg) [ 23 ] at a single dose intraperitoneally. Group IV was given Vit U 1 h before treatment with GalN.…”

Section: Methodsmentioning

confidence: 99%

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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Protective effects of antioxidant combination against D‐galactosamine‐induced kidney injury in rats

Cited by 6 publications

References 47 publications

The effects of pentoxifylline and caffeic acid phenethyl ester in the treatment ofd-galactosamine-induced acute hepatitis in rats

The effects of pentoxifylline and caffeic acid phenethyl ester in the treatment ofd-galactosamine-induced acute hepatitis in rats

The effects of vitamins and selenium mixture against brain tissue induced byd‐galactosamine

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

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