Protective Effect of Geranylgeranylacetone on Cisplatin Ototoxicity

Yin, Hai Ying; Xiu, Fang; Liu, Fang; Xia, Ming; Xu, An Ting

doi:10.1159/000166382

Cited by 14 publications

(9 citation statements)

References 62 publications

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“…With higher doses of CDDP, additional damage occurs in the auditory neurons, stria vascularis and supporting cells [27]. Various methods have been studied in order to prevent these side effects of CDDP [7,8,9,11]. New experimental studies should be done in order to explain the mechanisms of CDDP-induced toxicity to limit them [8,9,11].…”

Section: Discussionmentioning

confidence: 99%

“…Various methods have been studied in order to prevent these side effects of CDDP [7,8,9,11]. New experimental studies should be done in order to explain the mechanisms of CDDP-induced toxicity to limit them [8,9,11]. CDDP causes cell damage by interacting with the DNA chain and triggers some mechanisms that result in apoptosis [26,28].…”

Section: Discussionmentioning

confidence: 99%

“…Antioxidants, particularly thiol-based antioxidants, have been used to prevent CDDP ototoxicity [8,9]. Recently, it was shown that geranylgeranylacetone had a protective effect on CDDP ototoxicity due to the induction of heat shock protein 70 and the inhibition of inflammation [11]. However, all of these agents may interfere with the antitumor effects of CDDP.…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of the Effect of Acetyl L-Carnitine on Experimental Cisplatin Ototoxicity and Neurotoxicity

Güneş

Kırkım²,

Kolatan³

et al. 2011

Chemotherapy

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Introduction: Cisplatin (CDDP) is an effective and widely used chemotherapeutic agent for pediatric tumors, and ototoxicity is one of the dose-limiting side effects. Objective: It was the aim of our study to investigate the effect of acetyl L-carnitine (ALCAR) on experimental CDDP ototoxicity by audiologic tests, histomorphologic, immunohistochemical and ultrastructural examinations and to investigate the apoptotic pathways. Materials and Methods: Wistar albino rats (n = 28) were studied. Baseline audiological tests were performed in 4 groups: group 1, control; group 2, ALCAR; group 3, CDDP; group 4, CDDP + ALCAR-administered rats. Control audiological tests were performed on the 3rd day, and then the rats were sacrificed. Ear and brain specimens were examined by transmission electron microscopy, and caspase 3, 8 and 9 activities were investigated. Results: The CDDP-administered rats showed significant auditory brainstem response threshold shifts using all stimuli (clicks, 6-kHz and 8-kHz tone burst) compared with the control groups. The CDDP + ALCAR-administered rats showed significant auditory brainstem response threshold shifts by only click stimuli compared with the control groups. In the brain, spiral ganglion and organ of Corti, ultrastructural damage was prominent in group 3; the number of TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling)-positive cells and caspase 3, 8 and 9 immunostaining cells was significantly high in group 3. Conclusion: ALCAR improves CDDP-induced auditory impairment, and also antioxidative and antiapoptotic properties of ALCAR on CDDP ototoxicity were supported by the findings.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evaluation of the Effect of Acetyl L-Carnitine on Experimental Cisplatin Ototoxicity and Neurotoxicity

Güneş

Kırkım²,

Kolatan³

et al. 2011

Chemotherapy

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“…One example is its protective effect from ototoxicity in cisplatin-treated patients receiving geranylgeranylacetone [7] . Geranylgeranylacetone has the ability to induce HSPs and protect cells from apoptotic procedures.…”

Section: Discussionmentioning

confidence: 99%

Heat Shock Protein 70 Membrane Expression in Oral Cancer: A Possible New Target in Antineoplastic Therapy?

Markopoulos

Deligianni²,

Antoniades³

2009

Chemotherapy

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Background: Heat shock proteins (HSPs) are a group of highly immunogenic proteins with an exceptional degree of conservation. Cells or tissues from a wide range of tumors have been shown to express atypical levels of 1 or more HSPs. Experimental evidence suggests that HSPs may promote tumorigenesis by suppressing apoptosis. Aim: The aim of this investigation was to study the expression and the localization of HSP70 in oral squamous cell carcinoma (OSCC) and to compare HSP70 expression between neoplastic, dysplastic lesions and normal oral tissues. Methods: Immunohistochemistry staining was conducted to study HSP70 expression in 50 paraffinized tissue samples: 30 OSCCs, 10 leukoplakias with dysplasia and 10 samples from normal oral tissue. Results: Our results showed that all slides with OSCC intensely expressed HSP70. Dysplastic lesions were positive to a lesser extent for HSP70. Samples from normal oral tissue were all negative for HSP70. Conclusions: It is concluded that increased HSP70 immunoexpression could be a marker for the presence of epithelial dysplasia or epithelial malignant transformation.

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“…It interacts with both healthy and cancerous tissues and has some side effects [1] . 5-fluorouracil (5-FU), a fluorinated analog of uracil, has frequently been used for the treatment of various tumors, including gastrointestinal and head and neck carcinomas [2] .…”

Section: Introductionmentioning

confidence: 99%

Neem (Azadirachta Indica) Leaf Preparation Prevents Leukocyte Apoptosis Mediated by Cisplatin plus 5-Fluorouracil Treatment in Swiss Mice

et al. 2009

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Background: Neem (Azadirachta indica) is widely regarded as a wonder tree because of its diverse medicinal applications. We investigated the ability of neem leaf preparation (NLP) to protect against apoptosis of circulating blood cells induced by cisplatin and 5-fluorouracil (cis + 5-FU) in carcinoma-bearing mice. Methods: Apoptosis was studied by annexin V-propidium iodide method. Total white blood cell count was performed using 3% glacial acetic acid on hemocytometer. Cytotoxicity was determined by LDH release assay and T/NK cell status was determined by flow cytometry. Results: In comparison to untreated control, during cis + 5-FU therapy, significant down-regulation of leukocyte apoptosis was noted in mice pretreated with NLP or granulocyte colony stimulating factor (GCSF) during cis + 5-FU therapy. This enhanced cytotoxicity may be associated with NLP-induced increase of the cytotoxic T and NK cell pool. Conclusions: Efficacy of NLP is comparable to GCSF in its ability to protect against leukocyte apoptosis induced by cis + 5-FU. NLP would be a better choice of treatment because GCSF is tumor promoting, angiogenic and expensive.

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Protective Effect of Geranylgeranylacetone on Cisplatin Ototoxicity

Cited by 14 publications

References 62 publications

Evaluation of the Effect of Acetyl <i>L</i>-Carnitine on Experimental Cisplatin Ototoxicity and Neurotoxicity

Evaluation of the Effect of Acetyl <i>L</i>-Carnitine on Experimental Cisplatin Ototoxicity and Neurotoxicity

Heat Shock Protein 70 Membrane Expression in Oral Cancer: A Possible New Target in Antineoplastic Therapy?

Neem <i>(Azadirachta Indica)</i> Leaf Preparation Prevents Leukocyte Apoptosis Mediated by Cisplatin plus 5-Fluorouracil Treatment in Swiss Mice

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