Nitric oxide-mediated tumor cell killing of cisplatin-based interferon-γ gene therapy in murine ovarian carcinoma

Son, Kyonghee; Hall, Kevin J

doi:10.1038/sj.cgt.0235

Cited by 10 publications

(3 citation statements)

References 10 publications

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“…In nephrotoxicity, the increase in NOx production after IFO administration could be a secondary event following the increase in inducible nitric oxide synthase [39, 40]. Our study showed similar correlation in which the increase in NOx production accompanied with iNOS increase expression level after IFO administration.…”

Section: Discussionsupporting

confidence: 77%

Downregulation of Oxidative and Nitrosative Apoptotic Signaling by L-Carnitine in Ifosfamide-Induced Fanconi Syndrome Rat Model

Sayed‐Ahmed

Hafez

Aldelemy

et al. 2012

Oxidative Medicine and Cellular Longevity

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It is well documented that ifosfamide (IFO) therapy is associated with sever nephropathy in the form of Fanconi syndrome. Although oxidative stress has been reported as a major player in IFO-induced Fanconi syndrome, no mechanism for this effect has been ascertained. Therefore, this study has been initiated to investigate, on gene expression level, the mechanism of IFO-induce nephrotoxicity and those whereby carnitine supplementation attenuates this serious side effect of IFO. To achieve the ultimate goals of this study, adult male rats were assigned to one of four treatment groups, namely, control, L-carnitine, IFO, and IFO plus L-carnitine. Administration of IFO for 5 days significantly increased serum creatinine, blood urea nitrogen (BUN), and total nitrate/nitrite (NOx) production in kidney tissues. In addition, IFO significantly increased mRNA expression of inducible nitric oxide synthase (iNOS), caspase-9, and caspase-3 and significantly decreased expression of glutathione peroxides (GPx), catalase (CAT), and Bcl2 in kidney tissues. Administration of L-carnitine to IFO-treated rats resulted in a complete reversal of the all biochemical and gene expression changes, induced by IFO, to the control values. Data from this study suggest that L-carnitine prevents the development of IFO-induced nephrotoxicity via downregulation of oxidative and nitrosative apoptotic signaling in kidney tissues.

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Section: Discussionsupporting

confidence: 77%

Downregulation of Oxidative and Nitrosative Apoptotic Signaling by L-Carnitine in Ifosfamide-Induced Fanconi Syndrome Rat Model

Sayed‐Ahmed

Hafez

Aldelemy

et al. 2012

Oxidative Medicine and Cellular Longevity

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“…Tumor-bearing mice sequentially receiving cisplatin and a liposomal interferonc gene completely killed murine ovarian tumor cells or inhibited tumor growth with long-term survival (Son 1997a). The effectiveness of this combination therapy is largely due to sensitization of tumor cells by cisplatin for the subsequent lipofection (Son and Huang 1994).…”

mentioning

confidence: 99%

Chemical Toxicants Activate Murine Ovarian Ascitic Tumor Cells for In Situ Lipofection

Son

1999

Drug Delivery

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“…It also acts as a preservative of liver GSH content and prevents LPO. This effect may be due to its antioxidant activity [80][81][82].…”

Section: Discussionmentioning

confidence: 99%

Possible Protective Effects of Garlic, Ginkobiloba and Silymarin on Cisplatin Hepatotoxicity in Protein-Malnourished Rats

Ezzeldin

Raslan

El-Nahhas

et al. 2014

BJMMR

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Background: Protein malnutrition (PM) is one of the major public health problems in developing countries. Cisplatin (CDDP) is an effective anticancer drug that elicits many hepatotoxicity. CDDP hepatotoxicity restricts its clinical use under long term treatment. Objectives: The study was carried out to determine the possible protective effects of fresh garlic homogenate (FGH), Ginkobiloba extract (GBE) or silymarin (Sly) on cisplatin hepatotoxicity in protein malnourished rats. Methods: Sprague-Dawley rats were divided into NF set and PM set. Each set divided into control group and seven treated groups received cisplatn and FGH, GBE or Sly and its combinations with cisplatin. Biochemical changes, reactive oxygen species (ROS) and superoxide dismutase (SOD), Malondialdehyde (MDA) and glutathione (GSH) parameters were evaluated. Liver samples were examined for histopathological changes Results: Cisplatin increased ALT and AST, as well as liver body weight ratio. ROS

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Nitric oxide-mediated tumor cell killing of cisplatin-based interferon-γ gene therapy in murine ovarian carcinoma

Cited by 10 publications

References 10 publications

Downregulation of Oxidative and Nitrosative Apoptotic Signaling by L-Carnitine in Ifosfamide-Induced Fanconi Syndrome Rat Model

Downregulation of Oxidative and Nitrosative Apoptotic Signaling by L-Carnitine in Ifosfamide-Induced Fanconi Syndrome Rat Model

Chemical Toxicants Activate Murine Ovarian Ascitic Tumor Cells for In Situ Lipofection

Possible Protective Effects of Garlic, Ginkobiloba and Silymarin on Cisplatin Hepatotoxicity in Protein-Malnourished Rats

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