Effect of thiamine pyrophosphate on ischemia-reperfusion induced oxidative damage in rat kidney

Altuner, Durdu; Cetin, Nihal; Aslan, Zeynep; Hacımüftüoğlu, Ahmet; Gülaboğlu, Mine; Isaoglu, Neslihan; Demiryılmaz, İsmail; Süleyman, Halis

doi:10.4103/0253-7613.115005

Cited by 10 publications

(4 citation statements)

References 21 publications

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“…The experimental results in this study similarly revealed that TPP prevented the increase of 8-OHGua levels with I/R. The results of this study were consistent with the results of Altuner et al 49 , who stated that TPP reduced 8-OHGua levels in renal I/R injury.…”

Section: Discussionsupporting

confidence: 92%

Effect of Thiamine Pyrophosphate Upon Oxidative Brain Injury Induced by Ischemia-Reperfusion in Rats

Yaşar¹,

Demirdögen²,

Mammadov³

et al. 2023

International J. of Pharmacology

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Background and Objective: Exposure of the brain to Ischemia-Reperfusion (I/R) may cause tissue damage through oxidative stress.Thiamine pyrophosphate (TPP), which has a protective effect against oxidative stress, is the active metabolite of vitamin B 1 . In this study, the protective effect of TPP against possible I/R damage of brain tissue was investigated. Materials and Methods: Thirty rats were randomly divided into BIR, TIR and HG groups consisting of ten rats. In the TIR group, 20 mg kgG 1 TPP was injected intraperitoneally (ip). After 1 hr, clips were placed in the common carotid arteries of the BIR and TIR groups under anesthesia. Brain tissue was subjected to ischemia for 10 min. Afterward, the clips were opened and 3 hrs of reperfusion was achieved. In the HG group, only subcutaneous incisions were made and closed. Then, the brain tissues removed by euthanasia were biochemically analyzed. Results: While, I/R increased malondialdehyde (MDA), myeloperoxidase (MPO), Tumor Necrosis Factor-" (TNF-"), Interleukin-1$ (IL-1$) and 8-Hydroxyguanine (8-OHGua) levels in brain tissues, total caused a decrease in glutathione (tGSH), glutathione peroxidase (GPO) and glutathione reductase (GSHRd) levels (p<0.001). The TPP applied before I/R significantly prevented these changes (p<0.05). Conclusion: The results of biochemical tests suggested that TPP may be beneficial in preventing possible brain damage due to I/R.

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Section: Discussionsupporting

confidence: 92%

Effect of Thiamine Pyrophosphate Upon Oxidative Brain Injury Induced by Ischemia-Reperfusion in Rats

Yaşar¹,

Demirdögen²,

Mammadov³

et al. 2023

International J. of Pharmacology

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“…It is worth noting in this regard that such alerts stem from a well-known antioxidant action of thiamine in normal cells rather than in cancer ones. Indeed, in non-malignant cells exposed to drugs including cisplatin, and other pathological conditions, such as diabetes, ischemia-reperfusion, or hemodialysis, thiamine and/or its derivatives are known to decrease DNA damage and cell death ( Schupp et al, 2008 ; Chakrabarti et al, 2011 ; Coskun et al, 2013 ; Harisa, 2013 ; Suleyman et al, 2013 ; Turan et al,2013a,b ; Vidhya et al, 2013 ; Cinici et al, 2015 ; Polat et al, 2015 ). A recent transcriptional analysis of long-term exposure of yeast cells to anticancer drug imatinib supports contribution of biosynthesis of thiamine/pyridoxal phosphate to the drug resistance in this model ( Taymaz-Nikerel et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate

et al. 2021

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Thiamine (vitamin B1) is often deficient in oncopatients, particularly those undergoing chemotherapy. However, interaction between the thiamine deficiency and anticancer action of drugs has not been characterized. A major natural thiamine derivative, thiamine diphosphate (ThDP), is a coenzyme of central metabolism, also known to affect transcriptional activity of the master metabolic regulator and genome guardian p53. A direct transcriptional target of p53, p21, regulates cell cycle dynamics and DNA damage response. Our work focuses on dependence of the action of the DNA damaging anticancer drug cisplatin on metabolic regulation through p53/p21 axes and cellular thiamine status in human lung adenocarcinoma cells A549. These cells are used as a model of a hardly curable cancer, known to develop chemoresistance to platinum drugs, such as cisplatin. Compared to wild type (A549WT), a stable line with a 60% knockdown of p21 (A549p21–) is less sensitive to antiproliferative action of cisplatin. In contrast, in the thiamine-deficient medium, cisplatin impairs the viability of A549p21– cells more than that of A549WT cells. Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin. Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH). The knockdown also changes correlations of the levels of OGDHC, GDH and GOT2 with those of the malate and isocitrate dehydrogenases. Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment. Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination.

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“…It reduces oxidative damage by balancing the antioxidant status and regulating inflammatory mediators [ 3 ] . It has been reported that silymarin reduces I/R damage in the heart, lungs, kidneys and liver, but there are no studies on the preventive effects of silymarin in organs in the supraceliac aorta I/R model [ 3 - 5 ] . The aim of this study is to examine silymarin's protective effects on end organs (heart, lungs, liver and kidneys) in a rat model of acute supraceliac aorta I/R.…”

Section: Introductionmentioning

confidence: 99%

Intraperitoneal administration of silymarin protects end organs from multivisceral ischemia/reperfusion injury in a rat model

Koçarslan

Aydın

et al. 2016

Brazilian Journal of Cardiovascular Surgery

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ObjectiveTo determine whether intraperitoneal silymarin administration has favorable effects on the heart, lungs, kidney, and liver and on oxidative stress in a rat model of supraceliac aorta ischemia/reperfusion injury.MethodsThirty male Wistar albino rats were divided equally into three groups: sham, control, and silymarin. The control and silymarin groups underwent supraceliac aortic occlusion for 45 min, followed by a 60 min period of reperfusion under terminal anesthesia. In the silymarin group, silymarin was administered intraperitoneally during ischemia at a dose of 200 mg/kg. Rats were euthanized using terminal anesthesia, and blood was collected from the inferior vena cava for total antioxidant capacity, total oxidative status, and oxidative stress index measurement. Lungs, heart, liver and kidney tissues were histologically examined.ResultsIschemia/reperfusion injury significantly increased histopathological damage as well as the total oxidative status and oxidative stress index levels in the blood samples. The silymarin group incurred significantly lesser damage to the lungs, liver and kidneys than the control group, while no differences were observed in the myocardium. Furthermore, the silymarin group had significantly lower total oxidative status and oxidative stress index levels than the control group.ConclusionIntraperitoneal administration of silymarin reduces oxidative stress and protects the liver, kidney, and lungs from acute supraceliac abdominal aorta ischemia/reperfusion injury in the rat model.

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Effect of thiamine pyrophosphate on ischemia-reperfusion induced oxidative damage in rat kidney

Cited by 10 publications

References 21 publications

Effect of Thiamine Pyrophosphate Upon Oxidative Brain Injury Induced by Ischemia-Reperfusion in Rats

Effect of Thiamine Pyrophosphate Upon Oxidative Brain Injury Induced by Ischemia-Reperfusion in Rats

Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate

Intraperitoneal administration of silymarin protects end organs from multivisceral ischemia/reperfusion injury in a rat model

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