Differential roles of hydrogen peroxide and hydroxyl radical in cisplatin-induced cell death in renal proximal tubular epithelial cells

Baek, Su Mi; Kwon, Chae Hwa; Kim, Jae Ho; Woo, Jae Suk; Jung, Jin Sup; Kim, Yong Keun

doi:10.1016/s0022-2143(03)00111-2

Cited by 152 publications

(112 citation statements)

References 38 publications

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“…Cisplatin is one of the most active cytotoxic agents used in the treatment of cancer, and induces mitochondrial dysfunctions, particularly the inhibition of the electron transfer system, thereby resulting in enhanced ROS production (30,31) and subsequent tissue damages. Therefore, the administration of antioxidants prior to cisplatin treatment has been used to protect against nephrotoxicity and hepatotoxicity (32).…”

Section: Discussionmentioning

confidence: 99%

Isoliquiritigenin Inhibits Tumor Growth and Protects the Kidney and Liver Against Chemotherapy-Induced Toxicity in a Mouse Xenograft Model of Colon Carcinoma

et al. 2008

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Abstract. A growing amount of attention has been focused on the investigation of the effects of chemopreventive agents on the inhibition of cancer cell growth and toxicity in combination with chemotherapeutics. The objective of this study was to determine whether isoliquiritigenin (ISL) has the potential to serve as a beneficial supplement during cisplatin chemotherapy. We found that the administration of ISL alone significantly reduced the size of the solid tumors in CT-26 cell-inoculated BALB / c mice, without any detectable induction of nephrotoxicity, hepatotoxicity, and oxidative stress, and ISL reduced the viability and DNA synthesis of CT-26 murine colon cancer cells in a dose-dependent manner. ISL did not affect the therapeutic efficacy of cisplatin. Furthermore, ISL suppressed cisplatin-induced kidney damage characterized by increases in serum creatinine and blood urea nitrogen, as well as cisplatin-induced liver damage characterized by increases in serum alanine aminotransferase and aspartate aminotransferase. The repeated oral administration of ISL prior to cisplatin treatment exerted a preventive effect on cisplatin-mediated increases in serum nitric oxide and tissue lipid peroxidation levels, and it recovered depleted GSH levels in the tissues. Therefore, supplementation with ISL may be an effective approach to counteracting the side effects of cisplatin therapy in cancer patients.

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Section: Discussionmentioning

confidence: 99%

Isoliquiritigenin Inhibits Tumor Growth and Protects the Kidney and Liver Against Chemotherapy-Induced Toxicity in a Mouse Xenograft Model of Colon Carcinoma

et al. 2008

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“…Although the molecular composition and regulation of MPT pores are being debated, it is thought that the MPT occurs after the opening of a channel, which is termed the permeability transition (PT) pore. This classically defined MPT pore putatively consists of the voltage-dependent anion channel, the adenine nucleotide translocator, CypD, and possibly other molecules (Baek et al, 2003). Cyclosporin A (CsA) binds to CypD and blocks MPT under many conditions; however, numerous reports show that MPT or the loss of MMP can occur in a CsA-insensitive manner (Kushnareva et al, 2001;Kinsey et al, 2007a).…”

mentioning

confidence: 99%

Extracellular Signal-Regulated Kinase Activation Mediates Mitochondrial Dysfunction and Necrosis Induced by Hydrogen Peroxide in Renal Proximal Tubular Cells

Zhuang

Kinsey²,

Yan³

et al. 2008

J Pharmacol Exp Ther

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Although tubular necrosis in acute renal failure is associated with excessive production of reactive oxygen species (ROS), such as hydrogen peroxide (H 2 O 2 ), the mechanism of ROSinduced cell necrosis remains poorly understood. In this study, we examined the role of the extracellular signaling-regulated kinase (ERK) pathway in H 2 O 2 -induced necrosis of renal proximal tubular cells (RPTC) in primary culture. Exposure of 60 to 70% confluent RPTC to 1 mM H 2 O 2 for 3 h resulted in 44% necrotic cell death, as measured by trypan blue uptake, and inactivation of mitogen-activated protein kinase kinase (MEK), the upstream activator of ERK, by either 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene (U0126) or 2-(2Ј-amino-3Ј-methoxyphenyl)-oxanaphthalen-4-one (PD98059) or overexpression of dominant-negative mutant of MEK1, inhibited cell death. In contrast, overexpression of active MEK1 enhanced H 2 O 2 -induced cell death. H 2 O 2 treatment led to the loss of mitochondrial membrane potential (MMP) in RPTC, which was decreased by U0126 and PD98059. Furthermore, inhibition of the MEK/ERK pathway decreased oxidant-mediated ERK1/2 activation and mitochondrial swelling in isolated renal cortex mitochondria. However, treatment with cyclosporin A (CsA), a mitochondrial permeability transition blocker, did not suppress RPTC necrotic cell death, loss of MMP, and mitochondrial swelling. We suggest that ERK is a critical mediator of mitochondrial dysfunction and necrotic cell death of renal epithelial cells following oxidant injury. Oxidant-induced necrotic cell death was mediated by a CsA-insensitive loss of MMP that is regulated by the ERK pathway.

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“…Cisplatin (cis-diamminedichloroplatinum II) (CP), a most effective chemotherapeutic agent, has been successfully used in treatment of a variety of solid tumors, including ovary, testis, bladder, head and neck, lung, cervix, and endometrium (Baek et al, 2003;Hadjzadeh et al, 2012). It is an efficient platinum-derived alkylating agent that acts in unspecific phases of the cellular cycle against proliferating and resting cells (Lirdi et al, 2008) However, the use of dose intensification CP is limited by major side effects such as nephrotoxicity, peripheral neuropathy, ototoxicity, azoospermia, sperm morphology and motility alterations in normal tissues (Lirdi et al;Pabla & Dong, 2008).…”

Section: Introductionmentioning

confidence: 99%

Tribulus terrestris Hydroalcoholic Extract Effect on Cisplatin-Induced Apoptosis in Mice Kidney

et al. 2016

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ZARE, F.; KHAZAEI, M.; MORADI, M. & RAOOFI, A.Tribulus terrestris hydroalcoholic extract effect on cisplatininduced apoptosis in mice kidney. Int. J. Morphol., 34(2):713-718, 2016. SUMMARY:Cisplatin (EBEWE Pharma, Unterach, Austria) is an anti-cancer drug used in chemotherapy. One of the limiting major side effects of cisplatin is nephrotoxicity. Tribulus terrestris (TT) has been used as an synthetic or herbal protective agents for kidney disorders. The present study amid to investigate the Tribulus terrestris Hydroalcoholic extract effect on cisplatin-induced apoptosis in mice kidney. Male adult mice (n= 30) were divided into control group and 4 experimental groups (n= 6). Control group received saline, the first experimental group received cisplatin (5.5 mg/kg) and other three experimental groups received cisplatin (5.5 mg/kg) and different doses of hydroalcoholic extact of TT (100, 300 and 500 mg/kg i.p) respectively. The kidneys were removed after 4 days of injections, and TUNEL assay on mice's kidneys were performed. Weights of body and kidneys and apoptotic index were assessed. Data analysis was performed using one-way ANOVA followed by Tukey's post hoc test. The results showed that cisplatin lead to a reduction in the weight of body and kidney (P <0.01), and increased apoptotic index significantly compared to the control group (P <0.001), while in treated groups with TT, the weights of body and kidney were significantly higher compared with cisplatin group, but apoptotic index did not show significant differences. These parameters reached normal range after administration of fruit extracts of TT for 4 days. The study demonstrates that extract of TT could have protective effect on cisplatin-induced apoptosis of kidney. This may be related to the presence of antioxidant components acting via a multitude of central and peripheral mechanisms.

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Differential roles of hydrogen peroxide and hydroxyl radical in cisplatin-induced cell death in renal proximal tubular epithelial cells

Cited by 152 publications

References 38 publications

Isoliquiritigenin Inhibits Tumor Growth and Protects the Kidney and Liver Against Chemotherapy-Induced Toxicity in a Mouse Xenograft Model of Colon Carcinoma

Isoliquiritigenin Inhibits Tumor Growth and Protects the Kidney and Liver Against Chemotherapy-Induced Toxicity in a Mouse Xenograft Model of Colon Carcinoma

Extracellular Signal-Regulated Kinase Activation Mediates Mitochondrial Dysfunction and Necrosis Induced by Hydrogen Peroxide in Renal Proximal Tubular Cells

Tribulus terrestris Hydroalcoholic Extract Effect on Cisplatin-Induced Apoptosis in Mice Kidney

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