Gotowe bibliografie tematyczne / Induces nephrotoxicity

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Gotowa bibliografia na temat „Induces nephrotoxicity”

Autor: Grafiati
Data publikacji: 2 czerwca 2025
Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Induces nephrotoxicity"

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Gómez-Sierra, Tania, Omar Noel Medina-Campos, José D. Solano, María Elena Ibarra-Rubio, and José Pedraza-Chaverri. "Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells." Molecules 25, no. 19 (2020): 4442. http://dx.doi.org/10.3390/molecules25194442.

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Isoliquiritigenin (IsoLQ) is a flavonoid with antioxidant properties and inducer of endoplasmic reticulum (ER) stress. In vitro and in vivo studies show that ER stress-mediated hormesis is cytoprotective; therefore, natural antioxidants and ER stress inducers have been used to prevent renal injury. Oxidative stress and ER stress are some of the mechanisms of damage involved in cisplatin (CP)-induced nephrotoxicity. This study aims to explore whether IsoLQ pretreatment induces ER stress and produces hormesis to protect against CP-induced nephrotoxicity in Lilly Laboratories Cell-Porcine Kidney
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Lou, Qiang, Yanzhong Hu, Yuanfang Ma та Zheng Dong. "Heat shock factor 1 induces crystallin-αB to protect against cisplatin nephrotoxicity". American Journal of Physiology-Renal Physiology 311, № 1 (2016): F94—F102. http://dx.doi.org/10.1152/ajprenal.00201.2016.

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Cisplatin, a wildly used chemotherapy drug, induces nephrotoxicity that is characterized by renal tubular cell apoptosis. In response to toxicity, tubular cells can activate cytoprotective mechanisms, such as the heat shock response. However, the role and regulation of the heat shock response in cisplatin-induced nephrotoxicity remain largely unclear. In the present study, we demonstrated the induction of heat shock factor (Hsf)1 and the small heat shock protein crystallin-αB (CryAB) during cisplatin nephrotoxicity in mice. Consistently, cisplatin induced Hsf1 and CryAB in a cultured renal pro
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Becerra-Torres, Sergio L., César Soria-Fregozo, Fernando Jaramillo-Juárez, and José L. Moreno-Hernández-Duque. "Allium sativum aqueous extract prevents potassium dichromate-induced nephrotoxicity and lipid oxidation in rats." Journal of Pharmacy & Pharmacognosy Research 2, no. 1 (2011): 45–52. http://dx.doi.org/10.56499/jppres14.020_2.2.45.

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Context: The potassium dichromate (K2Cr2O7) induces nephrotoxicity by oxidative stress mechanisms. Aims: To study the potential protection of an aqueous extract of Allium sativum against the K2Cr2O7-induced nephrotoxicity and lipid oxidation in rats. Methods: Twenty four hours after treatment, biomarkers such as proteinuria, creatinine clearance, malondialdehyde production, specific enzyme activity of gamma glutamyl transpeptidase and alanine aminopeptidase, and renal clearance of para-aminohippuric acid and inulin were measured. Results: The K2Cr2O7 caused significant renal dysfunction, but A
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Wei, Qingqing, Guie Dong, Tianxin Yang, Judit Megyesi, Peter M. Price, and Zheng Dong. "Activation and involvement of p53 in cisplatin-induced nephrotoxicity." American Journal of Physiology-Renal Physiology 293, no. 4 (2007): F1282—F1291. http://dx.doi.org/10.1152/ajprenal.00230.2007.

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Cisplatin, a widely used chemotherapy drug, induces acute kidney injury, which limits its use and efficacy in cancer treatment. However, the molecular mechanism of cisplatin-induced nephrotoxicity is currently unclear. Using pharmacological and gene knockout models, we now demonstrate a pathological role for p53 in cisplatin nephrotoxicity. In C57BL/6 mice, cisplatin treatment induced p53 phosphorylation and protein accumulation, which was accompanied by the development of acute kidney injury. p53 was induced in both proximal and distal tubular cells and partially colocalized with apoptosis. P
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Min, Hye Sook, Ji Eun Lee, Jung Yeon Ghee, et al. "A Novel Dipeptidyl Peptidase-4 Inhibitor DA-1229 Ameliorates Tubulointerstitial Fibrosis in Cyclosporine Nephrotoxicity in Mice." Life 11, no. 3 (2021): 251. http://dx.doi.org/10.3390/life11030251.

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Cyclosporine A (CyA) is an immunosuppressive agent that induces nephrotoxicity with long-term treatment. The roles of DPP-4 and its inhibitors in cyclosporine nephrotoxicity are not fully understood. Therefore, we investigated the effects of a novel DPP-4 inhibitor, DA-1229, on the progression of renal disease in an experimental cyclosporine nephrotoxicity model. Chronic cyclosporine nephrotoxicity was induced in six-week-old male ICR mice by subcutaneous injections of CyA at a dose of 30 mg/kg for four weeks. Animals were treated with DA-1229 at a dose of 300 mg/kg per day in food for four we
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Negrette-Guzmán, Mario, Sara Huerta-Yepez, Omar Noel Medina-Campos, et al. "Sulforaphane Attenuates Gentamicin-Induced Nephrotoxicity: Role of Mitochondrial Protection." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–17. http://dx.doi.org/10.1155/2013/135314.

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Sulforaphane (SFN), an isothiocyanate naturally occurring in Cruciferae, induces cytoprotection in several tissues. Its protective effect has been associated with its ability to induce cytoprotective enzymes through an Nrf2-dependent pathway. Gentamicin (GM) is a widely used antibiotic; nephrotoxicity is the main side effect of this compound. In this study, it was investigated if SFN is able to induce protection against GM-induced nephropathy both in renal epithelial LLC-PK1 cells in culture and in rats. SFN prevented GM-induced death and loss of mitochondrial membrane potential in LLC-PK1 cel
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Pandhita, Bashar Adi Wahyu, Deliana Nur Ihsani Rahmi, Nielda Kezia Sumbung, et al. "A glance at molecular mechanisms underlying cisplatin-induced nephrotoxicity and possible renoprotective strategies: a narrative review." Medical Journal of Indonesia 28, no. 3 (2019): 292–9. http://dx.doi.org/10.13181/mji.v28i3.2690.

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Cisplatin is a platinum-based drug that is usually used for the treatment of many carcinomas. However, it comes with several devastating side effects, including nephrotoxicity. Cisplatin toxicity is a very complex process, which is exacerbated by the accumulation of cisplatin in renal tubular cells via passive diffusion and transporter-mediated processes. Once cisplatin enters these cells, it induces the formation of reactive oxygen species that cause cellular damage, including DNA damage, inflammation, and eventually cell death. On a small scale, these damages can be mitigated by cellular ant
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Chaim, Olga Meiri, Youssef Bacila Sade, Rafael Bertoni da Silveira, et al. "Brown spider dermonecrotic toxin directly induces nephrotoxicity." Toxicology and Applied Pharmacology 211, no. 1 (2006): 64–77. http://dx.doi.org/10.1016/j.taap.2005.05.015.

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Pazarci, Percin, Serkan Özler, and Halil Mahir Kaplan. "Effect of alpha-linolenic acid on aminoglycoside nephrotoxicity and RhoA/Rho-kinase pathway in kidney." PeerJ 12 (October 18, 2024): e18335. http://dx.doi.org/10.7717/peerj.18335.

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Aminoglycoside nephrotoxicity stands as a primary contributor to the development of acute intrinsic renal failure. Distinctive characteristic associated with this nephrotoxicity is the occurrence of tubular necrosis, which is why it is commonly referred to as acute tubular necrosis. Studies have demonstrated that inhibiting rhoA/rho-kinase pathway is beneficial for kidney damage induced by diabetes and renal ischemia. Comparable pathological conditions can be observed in aminoglycoside nephrotoxicity, like those found in diabetes and renal ischemia. Gentamicin, an aminoglycoside, is known to a
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Park, Moon Soo, Maryely De Leon, and Prasad Devarajan. "Cisplatin Induces Apoptosis in LLC-PK1 Cells via Activation of Mitochondrial Pathways." Journal of the American Society of Nephrology 13, no. 4 (2002): 858–65. http://dx.doi.org/10.1681/asn.v134858.

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ABSTRACT. Cisplatin, a commonly used chemotherapeutic agent, has a major limitation because of its nephrotoxicity. Recent studies have shown that cisplatin causes apoptotic cell death in renal tubule cells, but the underlying molecular mechanisms remain to be elucidated. In this study, cisplatin was found to induce apoptosis in a dose- and duration-dependent manner in cultured proximal tubule (LLC-PK1) cells, as evidenced by DNA laddering and TdT-mediated dUTP nick end-labeling assay. Pretreatment with the specific caspase 9 inhibitor LEHD-CHO completely prevented the apoptosis, whereas the ca
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Rozprawy doktorskie na temat "Induces nephrotoxicity"

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Paquette, Melanie. "Dietary composition alters gentamicin-induced nephrotoxicity in rats." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=30827.

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Macronutrient composition of food was shown to have a potent impact in modulating circadian rhythms of gentamicin toxicity. In the present study, adult female Sprague-Dawley rats fully adapted to isocaloric 20 casein-containing, 20% soy-containing (both semi-purified with 10% safflower oil and 58.55% carbohydrate) or a standard chow diet (non-purified with 18.1% mixed proteins, 4.5% fat and 57.3% carbohydrate) were chronically treated for 10 days with a nephrotoxic dose of gentamicin sulfate (40 mg/kg/day, i.p.) or a saline solution given in the middle of their resting period or in the middle
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McWilliam, Stephen. "Novel approaches to aminoglycoside-induced nephrotoxicity in children." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2049479/.

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Background: Aminoglycoside antibiotics are commonly used in paediatric clinical practice, especially for the treatment of neonatal sepsis and pulmonary exacerbations in cystic fibrosis (CF). However, megalin-mediated endocytosis of the aminoglycosides by renal proximal tubule epithelial cells leads to toxicity, and may result in acute kidney injury and chronic kidney disease. Current approaches to identify and prevent toxicity are limited. Several novel biomarkers have shown utility in preclinical studies for the identification of aminoglycoside-induced nephrotoxicity, but clinical data and an
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Alghamdi, Saeed Saeed. "The role of cytochrome P4502E1 in solvent-induced nephrotoxicity." Thesis, Queen Mary, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405934.

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MacFarlane, Marion. "The role of cysteine conjugate #beta#-lyase in haloalkene-induced nephrotoxicity." Thesis, University of Surrey, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328376.

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Nakamura, Takanori. "Disruption of multidrug and toxin extrusion MATE1 potentiates cisplatin-induced nephrotoxicity." Kyoto University, 2011. http://hdl.handle.net/2433/142112.

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Filipski, Kelly K. "Contribution of organic cation transporter 2 (OCT2) to cisplatin-induced nephrotoxicity." View the abstract Download the full-text PDF version, 2009. http://etd.utmem.edu/ABSTRACTS/2009-022-Filipski-index.htm.

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Thesis (Ph.D.)--University of Tennessee Health Science Center, 2009.<br>Title from title page screen (viewed on August 6, 2009). Research advisor: Alex Sparreboom, Ph.D. Document formatted into pages (ix, 79 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 74-78).
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Cockburn, Elinor M. "The relevance of prostanoid metabolism in the development of drug-induced nephrotoxicity." Thesis, University of Aberdeen, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.481095.

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The enzymes prostaglandin synthetase (PGS) and lipoxygenase can cooxidise a variety of xenobiotics to reactive intermediates during the metabolism of arachidonic acid (AA). PGS exhibited a gradient of activity within the kidney which was greatest in the papilla and least in the cortex. Rabbit and rat renal microsomes metabolised the model compound, tetramethylphenylenediamine (TMPD), in the presence of AA by pathways which were predominantly PGS and lipoxygenase-dependent, respectively. Therefore, both enxymes may play a role in the development of site-specific nephrotoxicity within the kidney
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Tort, Piella A. "Development of novel proximal tubule in vitro models to predict drug-induced nephrotoxicity." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3004444/.

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Drug-induced nephrotoxicity is a dose limiting factor and a common side effect of many drugs such as antibiotics, cancer chemotherapeutics or diagnostic agents and represents 20-25% of all cases of acute kidney injury (AKI). Due to a lack of representative animal models and metabolically competent renal cell lines, only 10.5% of the drug-induced nephrotoxicity cases can be predicted in preclinical studies. Furthermore, it has been recently accepted that mitochondria represent an important target for a broad spectrum of renal toxins. However, the supraphysiological glucose concentrations used i
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Wadey, Rebecca. "Characterisation of tools for studying renal mineral ion homeostasis and drug-induced nephrotoxicity." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/71398/.

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The complex interplay between regulatory factors of kidney mineral ion homeostasis are difficult to investigate in vivo. In addition, preclinical drug safety testing is limited by lack of translational tools for screening novel drugs for nephrotoxicity. At Cardiff University, my PhD project aimed to characterise tools to address these needs. At AstraZeneca, the use of tissue biomarkers as tools for assessing kidney injury in retrospective studies where urine biomarker samples are not available, was evaluated. To enable studies of mineral ion homeostasis, an in vitro human primary renal cell mo
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Lassila, Markus. "Cyclosporine A-induced hypertension and nephrotoxicity in spontaneously hypertensive rats on high-sodium diet." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/biola/vk/lassila/.

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Książki na temat "Induces nephrotoxicity"

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Clarke, Hilary. In vivo and in vitro studies on cyclosporine-induced nephrotoxicity. University College Dublin, 1997.

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Larsson, Roger. Metabolic activation by peroxidases: A role for prostaglandin synthase in phenacetin induced nephrotoxicity. [s.n.], 1986.

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Shirali, Anushree, and Mark A. Perazella. Drug-induced nephropathies. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0362.

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Pharmacological therapy with prescription medications and other drugs is the mainstay of modern medical practice. In addition, an increasing number of people use over-the-counter and complementary treatments for management of acute and chronic disease. The kidney faces constant exposure to some of these medications and drugs since it receives significant blood flow from the systemic circulation and importantly participates in excretion of many of these substances. Some of these agents have the innate potential for nephrotoxicity, which is modified by patient- as well as drug-related factors. A
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Betul Apaydin Yildirim, M.A. Tunc, S. Yildirim, et al. The effect of Vitis vinifera L. cv. Merlot seed extract on gentamicin-induced nephrotoxicity in broilers. Verlag Eugen Ulmer, 2017. http://dx.doi.org/10.1399/eps.2017.199.

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Macpherson, Nicol Alexander. Aminoaciduria as a marker of renal tubular damage : the mechanism of cyclosporin and gentamicin induced nephrotoxicity. 1992.

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Rásonyi, Thomas. Mechanistic investigations in ochratoxin A induced nephrotoxicity and their relevance for the sex specific renal tumor induction in rats. 1995.

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World Health Organization (WHO). Principles and Methods for the Assessment of Nephrotoxicity Associated with Exposure to Chemicals. World Health Organization, 1991.

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Sever, Mehmet Şükrü, and Raymond Vanholder. Acute kidney injury in polytrauma and rhabdomyolysis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0252_update_001.

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The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves spec
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Części książek na temat "Induces nephrotoxicity"

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Charbonneau, Michel, Josef Strasser, Edward A. Lock, Max J. Turner, and James A. Swenberg. "1,4-Dichlorobenzene-Induced Nephrotoxicity: Similarity with Unleaded Gasoline (UG)-Induced Renal Effects." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_85.

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Porter, Vera R., and Dora B. Weiner. "Historical Perspective on Cadmium-Induced Nephrotoxicity." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_7.

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Ohshiro, Takeshi, Kiyoshi Mukai, and Takesada Mori. "Endotoxin-Haemoglobin Induced Nephropathy and Haptoglobin Administration." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_103.

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Hannemann, J., and K. Baumann. "Lipid Peroxidation as a Mechanism of Cisplatin-Induced Nephrotoxicity." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_51.

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Raguenez-Viotte, G., C. Dadoun, A. M. Van den Bossche, and J. P. Fillastre. "Celiptium Induced Lipid Peroxidation and Toxicity in Rat Renal Cortex." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_68.

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Carvounis, Christos P., and Peter Cushley. "Effects of Glycerol-Induced Acute Renal Failure on Renal Phosphorus Handling." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_100.

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Cal, J. C., F. Larue, P. Dormmua, and J. Cambar. "Protective Effect of Low Concentrations of Mercury Against HgCl2-Induced Nephrotoxicity." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_12.

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Goyer, R. A., C. R. Weinberg, W. M. Victery, and C. R. Miller. "Lead Induced Nephrotoxicity: Kidney Calcium as an Indicator of Tubular Injury." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_2.

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Powell, C. J., M. Dobrota, and E. Holtz. "Studies on the Mechanism of Radiological Contrast Media Induced Renal Failure." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_72.

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Rankin, G. O., D. J. Yang, V. J. Teets, H. C. Shih, and P. I. Brown. "Role of Biotransformation in Acute N-(3,5-Dichlorophenyl)Succinimide-Induced Nephrotoxicity." In Nephrotoxicity. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_92.

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Streszczenia konferencji na temat "Induces nephrotoxicity"

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Şener, Dila. "Protective role of curcumin in benzo(a)pyrene induced nephrotoxicity." In 15th International Congress of Histochemistry and Cytochemistry. LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-150.

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Özdaşçı, Abdullah. "Protective Effect of Origanum majorana Against Nephrotoxicity Induced by gentamicin." In 15th International Congress of Histochemistry and Cytochemistry. LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-240.

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Rimin, I. Nyoman Ehrich Lister, Sukirman Lie, and Ali Napiah Nasution. "Syzygium polyanthum Ethanol Extract Ameliorates Benzene-induced Nephrotoxicty in Rats." In 2021 IEEE International Conference on Health, Instrumentation & Measurement, and Natural Sciences (InHeNce). IEEE, 2021. http://dx.doi.org/10.1109/inhence52833.2021.9537185.

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Yu, Li-Rong, Zhiguang Li, Yuan Gao, and Tao Chen. "Abstract LB-438: Proteomic analysis of aristolochic acid-induced nephrotoxicity in rats." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-438.

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Patel, Vishal N., and David C. Kaelber. "Azathioprine-Induced Comorbidity Network Reveals Patterns and Predictors of Nephrotoxicity and Neutrophilia." In 2012 IEEE Second International Conference on Healthcare Informatics, Imaging and Systems Biology (HISB). IEEE, 2012. http://dx.doi.org/10.1109/hisb.2012.28.

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Koleva, Iliana, Veselin Ivanov, Yanka Karamalakova, and Galina Nikolova. "C-reactive protein and ROS promote chronic ochratoxin-induced H nephrotoxicity in mice." In RAD Conference. RAD Centre, 2021. http://dx.doi.org/10.21175/rad.abstr.book.2021.1.2.

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Ceylan, Tayfun. "Protective effect of Caffeic acid phenethyl ester against cisplatin-induced nephrotoxicity in rats." In 15th International Congress of Histochemistry and Cytochemistry. LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-239.

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Rial Domínguez, Y., C. Cremades Artacho, I. Carro Méndez, et al. "5PSQ-080 Cisplatin-induced nephrotoxicity and electrolyte imbalances in hyperthermic intraperitoneal chemotherapy (HIPEC)." In 29th EAHP Congress, Copenhagen, Denmark, 12-13-14 March 2025, Person centred pharmacy — Navigating digital health. British Medical Journal Publishing Group, 2025. https://doi.org/10.1136/ejhpharm-2025-eahp.377.

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Ismail, Treefa, and Falah Aziz. "The Protective Effect of Omega-3 Oil Against Cadmium Chloride Induced Nephrotoxicity in Rat." In 4th International Scientific Conference of Cihan University-Erbil on Biological Sciences. Cihan University-Erbil, 2017. http://dx.doi.org/10.24086/bios17.15.

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Soodvilai, Sirima, Sunhapas Soodvilai, Warayuth Sajomsang, Theerasak Rojanarata, Prasopchai Patrojanasophon, and Praneet Opanasopit. "Chitosan Polymeric Micelles for Prevention of Cisplatin-Induced Nephrotoxicity and Anticancer Activity of Cisplatin." In ICBET 2020: 2020 10th International Conference on Biomedical Engineering and Technology. ACM, 2020. http://dx.doi.org/10.1145/3397391.3397438.

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Artykuły w czasopismach Rozprawy doktorskie
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