Cisplatin Binding and Inactivation of Mitochondrial Glutamate Oxaloacetate Transaminase in Cisplatin-Induced Rat Nephrotoxicity

Ozaki, Taku; Ishiguro, Sei-ichi; Itoh, Hideaki; Furuhama, Kazuhisa; Nakazawa, Makoto; Yamashita, Tetsuro

doi:10.1271/bbb.130172

Cited by 15 publications

(13 citation statements)

References 40 publications

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“…Moreover, it is known that CP-induced nephrotoxicity is characterized mitochondrial dysfunction [16,19,[42][43][44] and that this may be an early event in the CP-induced acute renal failure [19,25,45]. CP-induced mitochondrial damage is characterized alterations in the activity of respiratory complexes (I-IV) and in mitochondrial membrane potential in renal cells in culture [43,46], mitochondrial energy failure [24], ultrastructural increase in respiration after ADP addition and state 4 (S4) was evident by a decrease in oxygen consumption when all ADP added was phosphorylated into ATP. Measurements were conducted in a waterjacketed chamber (37°C) connected to an oxymeter interfaced to a computer.…”

Section: Discussionmentioning

confidence: 99%

“…Several lines of research have proved that CP accumulates in kidney mitochondria decreasing ATP synthesis and increasing ROS production that finally leads to cell damage [22,23]. In fact, mitochondria are both a target and an early event in CP-induced nephrotoxicity [19,24,25]. Several studies have shown the prevention of CP-induced mitochondrial dysfunction by the use of synthetic or natural antioxidants such as carvedilol [26], sulforaphane [27], and 5-aminolevulinic acid [28].…”

Section: Introductionmentioning

confidence: 99%

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C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

et al. 2015

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The potential of C-phycocyanin (C-PC) to prevent cisplatin (CP)-induced kidney mitochondrial dysfunction was determined in CD-1 male mice. The CP-induced mitochondrial dysfunction was characterized by ultrastructural abnormalities and by decrease in the following parameters in isolated kidney mitochondria: adenosine diphosphate (ADP)-induced oxygen consumption (state 3), respiratory control ratio, ADP/oxygen (ADP/O) ratio, adenosine triphosphate synthesis, membrane potential, calcium retention, glutathione (GSH) content, and activity of respiratory complex I, aconitase, catalase, and GSH peroxidase. These mitochondria also showed increase in hydrogen peroxide production, malondialdehyde, and 3-nitrotyrosine protein adducts content. The above-described changes, as well as CP-induced nephrotoxicity, were attenuated in mice pretreated with a single injection of C-PC. Our data suggest that the attenuation of mitochondrial abnormalities is involved in the protective effect of C-PC against CP-induced nephrotoxicity. This is the first demonstration that C-PC pretreatment prevents CP-induced mitochondrial dysfunction in mice.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

et al. 2015

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“…The activity of malate dehydrogenase (MDH), an important enzyme in the mitochondrial tricarboxylic acid cycle, decreased after CP (7.5 mg/kg) intraperitoneal injection as a result of cellular mitochondrial dysfunction in the kidneys of rats (Ozaki et al, 2013). Additionally, the activity of succinate dehydrogenase (SDH), a pivotal mitochondrial enzyme in oxidative phosphorylation, also decreased after CP treatment, and this response combined with an increased level of lipid peroxidation in kidney mitochondria could play an important role in CP-induced nephrotoxicity in mice (Martha et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Effects of cisplatin on testicular enzymes and Sertoli cell function in rats

Liu

Sun

et al. 2015

Fundam. Toxicol. Sci.

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-Cisplatin (CP) is one of important tumour chemotherapeutic agents in humans. Previous reports claim that CP can cause testicular toxicity. The aim of this study was to evaluate the potential effects of CP in the testes of rats. Male Wistar rats were intraperitoneally administered CP at 1.0, 2.5, and 5.0 mg/kg for three consecutive days. After exposure, CP significantly inhibited the testicular activities of succinate dehydrogenase (SDH) and malate dehydrogenase (MDH), but it significantly elevated the activities of acid phosphatase (ACP), alkaline phosphatase (AKP), and lactate dehydrogenase (LDH) in the 5.0 mg/kg group. The decreased levels of superoxide dismutase (SOD), total antioxidant capacity (T-AOC), and metallothionein-1 (MT-1) mRNA as well as the increased levels of malondialdehyde (MDA) and haemoxygenase-1 (HO-1) mRNA showed that CP could increase oxidative stress in rat testes. Western blot analysis showed that the levels of transferrin, vimentin, androgen binding protein (ABP) and inhibinβ-B decreased significantly in the CP 2.5 and 5.0 mg/kg groups compared with the control group. These findings indicated that the inhibited enzymes, oxidative stress, and the down-regulation of Sertoli cell function-related proteins play pivotal roles in CP-induced testicular damage.

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“…Many effective anticancer compounds can induce apoptosis of malignant tumor cells, such as camptothecin, cisplatin, gemcitabine and curcumin [28–30]. However, one of the most important issues for anticancer agents is safety.…”

Section: Resultsmentioning

confidence: 99%

Hispolon Decreases Melanin Production and Induces Apoptosis in Melanoma Cells through the Downregulation of Tyrosinase and Microphthalmia-Associated Transcription Factor (MITF) Expressions and the Activation of Caspase-3, -8 and -9

Chen

Lee

Lin

et al. 2014

IJMS

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Hispolon is one of the most important functional compounds that forms Phellinus linteus (Berkeley & Curtis) Teng. Hispolon has antioxidant, anti-inflammatory, antiproliferative and anticancer effects. In this study, we analyzed the functions of hispolon on melanogenesis and apoptosis in B16-F10 melanoma cells. The results demonstrated that hispolon is not an enzymatic inhibitor for tyrosinase; rather, it represses the expression of tyrosinase and the microphthalmia-associated transcription factor (MITF) to reduce the production of melanin in α-melanocyte-stimulating hormone (α-MSH)-stimulated B16-F10 cells at lower concentrations (less than 2 μM). In contrast, at higher concentration (greater than 10 μM), hispolon can induce activity of caspase-3, -8 and -9 to trigger apoptosis of B16-F10 cells but not of Detroit 551 normal fibroblast cells. Therefore, we suggest that hispolon has the potential to treat hyperpigmentation diseases and melanoma skin cancer in the future.

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Cisplatin Binding and Inactivation of Mitochondrial Glutamate Oxaloacetate Transaminase in Cisplatin-Induced Rat Nephrotoxicity

Cited by 15 publications

References 40 publications

C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

Effects of cisplatin on testicular enzymes and Sertoli cell function in rats

Hispolon Decreases Melanin Production and Induces Apoptosis in Melanoma Cells through the Downregulation of Tyrosinase and Microphthalmia-Associated Transcription Factor (MITF) Expressions and the Activation of Caspase-3, -8 and -9

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