The Iron Chelator Deferoxamine Prevents Cisplatin-Induced Lipid Peroxidation in Rat Kidney Cortical Slices

Kameyama, Yoshiko; Gemba, Munekazu

doi:10.1254/jjp.57.259

Cited by 23 publications

(13 citation statements)

References 15 publications

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“…First, salicylate is a radical scavenger (Dinis et al, 1994), and there is compelling evidence that the formation of free radicals by CDDP contributes to its toxicity (Appenroth et al, , 1995Clerici et al, 1996;Freeman and Crapo, 1982;Hannemann and Baumann, 1988;Kameyama and Gemba, 1991;Kopke et al, 1997;Ravi et al, 1995;Rybak et al, 1999;Sugihara and Gemba, 1986;Sugihara et al, 1987;Zhang and Lindup, 1994). Such a mechanism would be akin to the protection by salicylate against MPTP-induced dopamine depletion in mice (Aubin et al, 1998), and the prevention of aminoglycoside-induced ototoxicity (Sha and Schacht, 1999a).…”

Section: Et Almentioning

confidence: 99%

“…Evidence has been accumulating that CDDP exerts its renal and cochlear toxicity at least in part through oxidative stress, generating reactive oxygen species (ROS; free radicals) and interfering with the antioxidant defense systems of these organs (Appenroth et al, , 1995Clerici et al, 1996;Gabaizadeh et al, 1997;Hannemann and Baumann, 1988;Kameyama and Gemba, 1991;Kopke et al, 1997;Ravi et al, 1995aRavi et al, , 1995bSugihara et al, 1987;Sugihara and Gemba, 1986;Zhang and Lindup, 1994). This notion is supported by successful attempts at ameliorating the nephrotoxic or ototoxic side effects in experimental animals in vivo by antioxidant therapy with D-methionine (Campbell et al, 1996(Campbell et al, , 1999Li et al, 2001;Reser et al, 1999), diethyldithiocarbamate acid (Rybak et al, 1995), and sodium thiosulfate (Iwamato et al, 1984;Saito et al, 1997).…”

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confidence: 99%

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Salicylate Protects Hearing and Kidney Function from Cisplatin Toxicity without Compromising its Oncolytic Action

Sha

Zotova

et al. 2002

Laboratory Investigation

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SUMMARY:Salicylate has recently been demonstrated to protect against the auditory and vestibular side effects of aminoglycoside antibiotics. Similarities in the toxic mechanisms suggest salicylate as a treatment strategy to prevent the ototoxic side effects of cisplatin (CDDP). We first tested protection of the inner ear in Wistar rats receiving a single infusion of 16 mg CDDP/kg body weight with or without treatment with 100 mg/kg salicylate (bid) for 5 days beginning one day before the CDDP infusion. Cisplatin induced a threshold shift of more than 30 dB (at 14 kHz; measured by auditory evoked brain stem response) that was significantly reduced by salicylate. We then examined the protective potential of salicylate on the cochlea, peripheral nerves, and kidney in a rat model of breast cancer-Fisher344 rats implanted with highly metastatic MTLn3 breast cancer cells. Animals received 3 ϫ 5 mg CDDP/kg (given every third day), and salicylate was administered at 100 mg/kg (bid) from 2 days before to 3 days after CDDP treatment. Salicylate significantly attenuated the CDDP-induced threshold shift from approximately 20 dB (at 16 and 24 kHz) to approximately 5 dB, and drastically reduced the loss of cochlear outer hair cells. Likewise, salicylate protected kidney function (measured as plasma blood urea nitrogen and creatinine levels) from CDDP toxicity. Protection of nerve conduction velocities of both sensory and motor nerves was minimal. The chemotherapeutic efficacy of CDDP on suppression of tumor mass and cancer cell metastasis remained unaffected by salicylate. The results suggest that administration of salicylate may become the basis of an effective therapeutic intervention against the ototoxic and nephrotoxic side effects associated with CDDP chemotherapy. (Lab Invest 2002, 82:585-596).

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Section: Et Almentioning

confidence: 99%

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confidence: 99%

Salicylate Protects Hearing and Kidney Function from Cisplatin Toxicity without Compromising its Oncolytic Action

Sha

Zotova

et al. 2002

Laboratory Investigation

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“…This reaction has been proposed to be the basis of the antineoplastic activity of Adriamycin and mitomycin [14]. Concerning iron in cisplatininduced nephrotoxicity, it was shown that the iron chela tor deferoxamine prevents cisplatin-induced lipid peroxi dation in renal cortical cells [ 15]. Beside radical formation participating in cisplatin-induced nephrotoxicity it has been shown that the xanthine derivate aminophylline pro tects kidney function from cisplatin-induced toxicity, most probably by adenosine receptor antagonism [ 16].…”

Section: Introductionmentioning

confidence: 99%

Modification of Cisplatin-Induced Renal <i>p</i>-Aminohippurate Uptake Alteration and Lipid Peroxidation by Thiols, <i>Ginkgo biloba</i> Extract, Deferoxamine and Torbafylline

Inselmann¹,

Blöhmer²,

Kottny³

et al. 1995

Nephron

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To determine whether inhibition of lipid peroxidation modifies cisplatin-induced changes of renal p-aminohippurate (PAH) uptake, we examined the effects of various radical scavengers and torbafylline on cisplatin-induced lipid peroxidation and PAH accumulation changes in rat renal cortical slices. Renal cortical slices were incubated with different cisplatin concentrations (0.3, 0.6, 1.0 mg/ml) in the presence of either glutathione, N-acetylcysteine, the iron chelator deferoxamine, Ginkgo biloba extract or the xanthine derivate torbafylline. Lipid peroxidation monitored as the production of malondialdehyde (MDA) was stimulated by increasing cisplatin concentrations in a dose-related manner. At a cisplatin concentration of 1.0 mg/ml, MDA production was twofold compared to controls (0.69 ± 0.06 vs. 1.36 ± 0.07 nmol/mg; p < 0.05). In turn, cisplatin decreased PAH uptake of kidney slices dose-dependently from 13.3 ± 1.3 to 2.6 ± 0.2 (p < 0.01). All agents tested inhibited cisplatin-induced lipid peroxidation; however, at a cisplatin concentration of 1.0 mg/ml, none of them prevented the decline of cisplatin-induced PAH uptake. Of the agents tested, deferoxamine proved to be the most effective antioxidant, completely inhibiting cisplatin-induced lipid peroxidation but in contrast preventing the decrease in PAH uptake only at a cisplatin concentration of 0.3 mg/ml. No strict association between lipid peroxidation and decline of PAH uptake was found, suggesting that lipid peroxidation may only in part participate in cisplatin-induced alterations of PAH uptake.

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“…Although the precise mechanism of CDDP-induced ROS production remains unclear, mounting evidence has indicated that antioxidant enzymes or sulfhydryl compounds are able to reduce the toxicity of CDDP. 11,43,44) We also have reported that combined expression of SOD and GSHPx by gene transfer caused resistance to CDDPin HeLa cells. 10) Therefore the utilization of MT null cells for developing CDDP-resistant cells may permit the detection of other important antioxidants associated with the acquisition of CDDP resistance.…”

Section: Discussionmentioning

confidence: 91%

Characterization of cis-Diamminedichloroplatinum (II)-Resistant Murine Cell Lines Derived from Metallothionein Null Cells.

Yamabe

Kondo

Endo

et al. 2001

JOURNAL OF HEALTH SCIENCE

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Metallothionein (MT) is known to play an important role in the resistance of tumor cells to cisdiamminedichloroplatinum (II) (CDDP, cisplatin). To identify non-MT factors that play important roles in CDDP resistance, we established CDDP-resistant cell lines from simian virus 40-transformed MT null cells. Subclones of CDDP-resistant MT null cells, designated as MKCr-3, -12, and -18, exhibited 24-to 62-fold resistance to CDDP compared with parental cells. The contents of glutathione (GSH) and the activities of GSH-related enzymes and antioxidant enzymes in MKCr-12 and -18 were higher than those in parental cells. However, MKCr-3 cells did not show any significant increase in the levels of GSH nor in enzyme activities except for superoxide dismutase. Accumulation of platinum in CDDP-resistant subclones was 15-26% of that in parental cells 24 h after administration of CDDP. Eleven other subclones of CDDP-resistant MT null cells also exhibited low accumulation of platinum. These results suggest that the decreased accumulation of CDDP may be a predominant factor in the resistance to CDDP in the absence of MT, an intracellular metal-and free radical-scavenger.

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The Iron Chelator Deferoxamine Prevents Cisplatin-Induced Lipid Peroxidation in Rat Kidney Cortical Slices

Cited by 23 publications

References 15 publications

Salicylate Protects Hearing and Kidney Function from Cisplatin Toxicity without Compromising its Oncolytic Action

Salicylate Protects Hearing and Kidney Function from Cisplatin Toxicity without Compromising its Oncolytic Action

Modification of Cisplatin-Induced Renal <i>p</i>-Aminohippurate Uptake Alteration and Lipid Peroxidation by Thiols, <i>Ginkgo biloba</i> Extract, Deferoxamine and Torbafylline

Characterization of cis-Diamminedichloroplatinum (II)-Resistant Murine Cell Lines Derived from Metallothionein Null Cells.

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