Rat liver arginase system under acetaminophen-induced toxic injury and protein deprivation

Kopylchuk, G. P.; Nykolaichuk, Ivanna; Zhuretska, O. M.

doi:10.15407/ubj89.02.092

Cited by 9 publications

(6 citation statements)

References 21 publications

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“…1). Taking into account that formation of citrulline in mitochondria occurs with the participation of ornithine transcarbamylase, a decrease in the level of the latter under these experimental conditions is obviously associated with a reduction in the level of one of the substrates of this reaction -ornithine, which was confirmed in our previous studies [11].…”

Section: Resultssupporting

confidence: 85%

“…Animals were randomly divided into 4 groups: I -animals that were kept on a balanced semisynthetic ration -control group (C) [15]; ІІ -animals that received semisynthetic low-protein ration for 28 days (1/3 of the standard daily norm of protein requirement) (LPR) [11]; ІІІ -animals with toxic acetaminophen-induced injury maintained on a balan ced diet (TI); ІV -animals with toxic acetaminophen-induced injury on the background of alimentary deprivation of protein (LPR + TI).…”

Section: Methodsmentioning

confidence: 99%

“…4). They may be caused by the deficiency of a substrate -argininosuccinate (a product of the previous reaction) and considered as one of the key mechanisms to reduce the arginine levels in hepatocytes under given conditions [11].…”

Section: Fig 1 Citrulline Level In the Mitochondrial Fraction Of Rat Liver Cells Under The Conditions Of Toxic Injury Against The Backgromentioning

confidence: 99%

“…An important regulator of the intermediate metabolism in the body is amino acid citrulline, which intracellular concentration defines the levels of L-arginine, synthesized in reactions involving enzymes argininosuccinate synthase (EC 6.3.4.5, ASS) and argininosuccinate lyase (EC 4.3.2.1, ASL) in the urea cycle [10]. Results of the previous studies [11] show that acetaminophen-induced toxic injury on the background of the alimentary deprivation of protein is accompanied by a decrease in arginine levels in hepatocytes.…”

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confidence: 99%

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Indexes of citrulline metabolism in rat liver under the toxic injury against the background of alimentary protein deficiency

Kopylchuk¹,

Nykolaichuk²,

Lylyk³

et al. 2020

Ukr.Biochem.J

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It is known that citrulline is converted into arginine in the series of metabolic transformations. Results of our previous studies showed that acetaminophen-induced toxic injury on the background of the alimentary deprivation of protein is accompanied by a decrease in arginine level in rat hepatocytes, but citrulline liver metabolism at these conditions remains incompletely clear. In this work, the content of citrulline in the rat liver mitochondrial and cytosolic fractions and the activity of citrulline-degrading enzymes -argininosuccinate synthase and argininosuccinate lyase were investigated. It was found that in the mitochondrial fraction a maximal reduction of the citrulline levels occurred after administration of acetaminophen toxic doses regardless of the protein amount in the ration, while in the cytosolic fraction the alimentary protein deficiency was a key factor in decreasing the activity of argininosuccinate synthase and arginino-succinate lyase. The data obtained indicated the disturbances of the urea cycle functioning and explained the decrease of l-arginine level in hepatocytes in conditions of acetaminophen-induced toxic injury against the background alimentary protein deficiency. K e y w o r d s: L-сitrulline, аrgininosuccinate synthetase, argininosuccinate lyase, acetaminophen, toxic injury, alimentary deprivation of protein.

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Section: Resultssupporting

confidence: 85%

Section: Methodsmentioning

confidence: 99%

Section: Fig 1 Citrulline Level In the Mitochondrial Fraction Of Rat Liver Cells Under The Conditions Of Toxic Injury Against The Backgromentioning

confidence: 99%

mentioning

confidence: 99%

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Indexes of citrulline metabolism in rat liver under the toxic injury against the background of alimentary protein deficiency

Kopylchuk¹,

Nykolaichuk²,

Lylyk³

et al. 2020

Ukr.Biochem.J

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“…[28] The present study investigated the possible protective effects of API against PMN + APAP-induced hepatic injury in rats. The suggested model in this experiment was based on the previous literature and pilot studies to elucidate the effect of a short-term nontoxic PMN regimen [4,[29][30][31][32] on a normal dose of APAP. [33][34][35][36][37][38] The current combination highlights, for the first time, the synergistic hepatotoxic effect of PMN condition with an ordinary APAP dosage.…”

Section: Discussionmentioning

confidence: 99%

Apigenin alleviated acetaminophen‐induced hepatotoxicity in low protein‐fed rats: Targeting oxidative stress, STAT3, and apoptosis signals

Mohamed

Kotb

El‐Raouf

et al. 2020

J Biochem & Molecular Tox

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Apigenin (API) is a natural flavonoid abundant in fruits and vegetables. The present study was undertaken to evaluate the effect of protein malnutrition (PMN) on acetaminophen (APAP)-induced hepatotoxicity, together with the protective effects of API, in male Wistar albino rats. In total, 64 male rats were divided into eight groups.Silymarin (SIL) (100 mg/kg, PO) as a reference standard and API (50 mg/kg, PO) were given to normal and APAP-induced hepatic injury in low protein-fed rats. The present results revealed that PMN significantly potentiated APAP-induced hepatotoxicity.Interestingly, the administration of SIL and API alleviated the induced damage, as revealed by reduced serum alanine aminotransferase and aspartate aminotransferase activities along with a significant improvement of the histopathological damage. API suppressed inflammatory response by reducing the interleukin-1β level and signal transducer and activator of transcription 3 expressions along with attenuating oxidative stress as shown by a significant reduction in liver contents of malondialdehyde and nitrite/nitrate as well as restoration of hepatic content of reduced glutathione and superoxide dismutase activity. API also counteracted apoptosis through downregulation of caspase-3 expression level. In conclusion, PMN greatly potentiated the hepatotoxic effects of APAP, and API produced a multimechanistic hepatoprotective activity that can be attributed to its antioxidant, anti-inflammatory, and antiapoptotic effects. K E Y W O R D S acetaminophen, apigenin, apoptosis, hepatotoxicity, protein malnutrition

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Sisplatin ile Karaciğer Toksisitesi Geliştirilen Ratlarda Zingeron’un Bazı Biyokimyasal Parametreler Üzerine Etkisinin Araştırılması

Kandemir¹,

Mahamadu²

2021

Kocatepe Veterinary Journal

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This study was aimed to investigate the protective effects of zingerone (ZO) on cisplatin (CP)-induced hepatotoxicity in rats. Thirty-five (35) Sprague Dawley male rats were used in the study; the animals were divided into 5 groups of 7 rats in each group. Group 1 (Control): received only oral serum physiologic (SP, for 7 days). Group 2 (CP): received a single dose of 7 mg/kg intraperitoneal (i.p.) of CP. Group 3 (ZO): Received daily oral doses of ZO at 50 mg/kg/day for 7 days. Group 4 (CP+ZO 25): Oral administration of ZO at 25 mg/kg/day was started 30 minutes after a single dose CP application and continued for 7 days. Group 5 (CP+ZO 50): Oral administration of ZO at 50 mg/kg/day was started 30 minutes after a single dose CP application and continued for 7 days. Alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) activities increased due to CP administration. Also, enzymatic antioxidants; superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and glutathione (GSH) level were shown to had decreased upon CP administration. After ZO was supported by antioxidant system and decreased malondialdehyde (MDA) levels. It was determined that CP administration increased nitric oxide (NO), 8-hydroxy-2'-deoxyguanosine (8-OHdG), cysteine aspartate specific protease-3 (caspase-3), tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB) and B-cell lymphoma-3 (Bcl-3) levels while arginase activity reduced, ZO administrations could have been the main cause of the improved effects on the parameters.

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Rat liver arginase system under acetaminophen-induced toxic injury and protein deprivation

Cited by 9 publications

References 21 publications

Indexes of citrulline metabolism in rat liver under the toxic injury against the background of alimentary protein deficiency

Indexes of citrulline metabolism in rat liver under the toxic injury against the background of alimentary protein deficiency

Apigenin alleviated acetaminophen‐induced hepatotoxicity in low protein‐fed rats: Targeting oxidative stress, STAT3, and apoptosis signals

Sisplatin ile Karaciğer Toksisitesi Geliştirilen Ratlarda Zingeron’un Bazı Biyokimyasal Parametreler Üzerine Etkisinin Araştırılması

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