Adverse effects of anti-tumor drug, cisplatin, on rat kidney mitochondria: Disturbances in glutathione peroxidase activity

Sugiyama, Satoru; Hayakawa, Mika; Kato, Tomoko S.; Hanaki, Yoshihiro; Shimizu, Kazuyuki; Ozawa, Takayuki

doi:10.1016/0006-291x(89)92225-0

Cited by 107 publications

(52 citation statements)

References 12 publications

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“…A number of studies have demonstrated the direct cytotoxic mechanisms of cisplatin including DNA damage (Leibbrandt et al 1995;Ries et al 1986), mitochondrial dysfunction (Sugiyama et al 1989), formation of reactive oxygen species (ROS) (Matsushima et al 1998), and caspase activation (Kaushal et al 2001). In particular, cisplatin ototoxicity occurs primarily in the cochleae, especially in the outer hair cells (OHCs) of the organ of Corti.…”

Section: Introductionmentioning

confidence: 99%

Cisplatin Cytotoxicity of Auditory Cells Requires Secretions of Proinflammatory Cytokines via Activation of ERK and NF-κB

Kim

Lee

et al. 2007

JARO

210

211

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The ototoxicity of cisplatin, a widely used chemotherapeutic agent, involves a number of mechanisms, including perturbation of redox status, increase in lipid peroxidation, and formation of DNA adducts. In this study, we demonstrate that cisplatin increased the early immediate release and de novo synthesis of proinflammatory cytokines, including TNF-a, IL-1b, and IL-6, through the activation of ERK and NF-kB in HEI-OC1 cells, which are conditionally immortalized cochlear cells that express hair cell markers. Both neutralization of proinflammatory cytokines and pharmacologic inhibition of ERK significantly attenuated the death of HEI-OC1 auditory cells caused by cisplatin and proinflammatory cytokines. We also observed a significant increase in the protein and mRNA levels of proinflammatory cytokines in both serum and cochleae of cisplatin-injected rats, which was suppressed by intraperitoneal injection of etanercept, an inhibitor of TNF-a. Immunohistochemical studies revealed that TNF-a expression was mainly located in the spiral ligament, spiral limbus, and the organ of Corti in the cochleae of cisplatin-injected rats. NF-kB protein expression, which overlapped with terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling-positive signal, was very strong in specific regions of the cochleae, including the organ of Corti, spiral ligament, and stria vascularis. These results indicate that proinflammatory cytokines, especially TNF-a, play a central role in the pathophysiology of sensory hair cell damage caused by cisplatin.

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Section: Introductionmentioning

confidence: 99%

Cisplatin Cytotoxicity of Auditory Cells Requires Secretions of Proinflammatory Cytokines via Activation of ERK and NF-κB

Kim

Lee

et al. 2007

JARO

210

211

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show abstract

“…Many studies have demonstrated the direct cytotoxic mechanisms of cisplatin including DNA damage (Ries and Klastersky, 1986), mitochondrial dysfunction (Sugiyama et al, 1989), formation of reactive oxygen species (ROS) (Matsushima et al, 1998;Rybak et al, 1999), and inflammatory cytokines (Previati et al, 2007;So et al, 2007). A subset of cell signaling proteins appear to be involved in cisplatin ototoxicity, including the tumor suppressor p53 (Devarajan et al, 2002;Zhang et al, 2003), the MAP kinase protein ERK (So et al, 2007), caspases, and cytochrome c (Devarajan et al, 2002;Kaushal et al, 2001;Liu et al, 1998;Wang et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Epicatechin protects the auditory organ by attenuating cisplatin-induced ototoxicity through inhibition of ERK

et al. 2010

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“…Superoxide dismutase plays an important role in the dismutation of superoxide anions by catalyzing their conversion to hydrogen peroxide and singlet oxygen. Glutathione peroxidase activity was decreased in the rat renal mitochondria incubated with cisplatin and has been correlated to disturbances in GSH metabolism (Sugiyama et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

“…Quercetin, a common antioxidant bioflavonoid in fruits and vegetables, has potent cytoprotective effects against cisplatin-induced nephrotoxicity in cultured renal proximal tubular epithelial cells (Kaushal et al, 2001). Sugiyama et al (1989) reported that green tea tannin plays a major role as an antioxidant that scavenges the reactive radicals generated from cisplatin in experimental animals.…”

Section: Introductionmentioning

confidence: 99%

Amelioration of cisplatin-induced nephrotoxicity by extracts ofHemidesmus indicusandAcorus calamus

Sandeep¹,

Nair²

2010

Pharmaceutical Biology

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Adverse effects of anti-tumor drug, cisplatin, on rat kidney mitochondria: Disturbances in glutathione peroxidase activity

Cited by 107 publications

References 12 publications

Cisplatin Cytotoxicity of Auditory Cells Requires Secretions of Proinflammatory Cytokines via Activation of ERK and NF-κB

Cisplatin Cytotoxicity of Auditory Cells Requires Secretions of Proinflammatory Cytokines via Activation of ERK and NF-κB

Epicatechin protects the auditory organ by attenuating cisplatin-induced ototoxicity through inhibition of ERK

Amelioration of cisplatin-induced nephrotoxicity by extracts ofHemidesmus indicusandAcorus calamus

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