Doxorubicin Induced Nephrotoxicity: Protective Effect of Nicotinamide

Ayla, Şule; Seçkin, İsmail; Tanrıverdi, Gamze; Cengiz, Müjgan; Eser, Mediha; Soner, Burak Cem; Öktem, Gülperi

doi:10.1155/2011/390238

Cited by 128 publications

(88 citation statements)

References 26 publications

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“…Doxorubicin and Cisplatin are widely used anticancer drugs for various cancers including brain cancer. A large number of reports have documented the hepatotoxicity and nephrotoxicity of these drugs (36)(37)(38)(39). Therefore, alternative therapeutic agents that kill cancer cells without or with low hepatotoxicity and nephrotoxicity are highly desirable.…”

Section: Discussionmentioning

confidence: 99%

Alantolactone induces apoptosis in glioblastoma cells via GSH depletion, ROS generation, and mitochondrial dysfunction

et al. 2012

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Glioblastoma multiforme (GBM) is the most malignant and aggressive primary brain tumor in adults. Despite concerted efforts to improve current therapies, the prognosis of glioblastoma remains very poor. Alantolactone, a sesquiterpene lactone compound, has been reported to exhibit antifungal, antibacteria, antihelminthic, and anticancer properties. In this study, we found that alantolactone effectively inhibits growth and triggers apoptosis in glioblastoma cells in a time‐ and dose‐dependent manner. The alantolactone‐induced apoptosis was found to be associated with glutathione (GSH) depletion, reactive oxygen species (ROS) generation, mitochondrial transmembrane potential dissipation, cardiolipin oxidation, upregulation of p53 and Bax, downregulation of Bcl‐2, cytochrome c release, activation of caspases (caspase 9 and 3), and cleavage of poly (ADP‐ribose) polymerase. This alantolactone‐induced apoptosis and GSH depletion were effectively inhibited or abrogated by a thiol antioxidant, N‐acetyl‐L‐cysteine, whereas other antioxidant (polyethylene glycol (PEG)‐catalase and PEG‐superoxide‐dismutase) did not prevent apoptosis and GSH depletion. Alantolactone treatment inhibited the translocation of NF‐κB into nucleus; however, NF‐κB inhibitor, SN50 failed to potentiate alantolactone‐induced apoptosis indicating that alantolactone induces NF‐κB‐independent apoptosis in glioma cells. These findings suggest that the sensitivity of tumor cells to alantolactone appears to results from GSH depletion and ROS production. Furthermore, our in vivo toxicity study demonstrated that alantolactone did not induce significant hepatotoxicity and nephrotoxicity in mice. Therefore, alantolactone may become a potential lead compound for future development of antiglioma therapy. © © 2012 IUBMB Life, 64(9): 783–794, 2012

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Section: Discussionmentioning

confidence: 99%

Alantolactone induces apoptosis in glioblastoma cells via GSH depletion, ROS generation, and mitochondrial dysfunction

et al. 2012

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“…Adriamycin toxicity limits its application in chemical therapy ADR has toxic action on the kidneys, thus causes acute renal failure that is a limiting factor for its beneficial application (Ayla et al, 2011). In this work, ADR significantly increased blood urea and creatinine after treatment for 8 weeks.…”

Section: Discussionmentioning

confidence: 65%

Effect of aqueous extract of basil (ocimum basilicum) leaves on nephrotoxicity induced by adriamycin in male rats: histological and immunohistochemical assessment

2017

IJAPSA

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Adriamycin, isa widely utilized anticancer drug applicable innumber ofhuman malignancies. Adriamycin exerted considerable effectsin many organs that possibly hamper its utilization. The beneficial action of the natural plant basil was proven against many aliments. The present work studied the effect of aqueous extract of basil (ocimumbasilicum) on adriamycin -induced nephrotoxicity in rats.Administration of Adriamycin intra peritoneally resulted innephrotoxicity manifested as enlargement and congestion of blood vessels in the kidney, occurrence of vacuolated cells, shrinkage of glomeruli, edema and leucocytic infiltration and appearance of proteinous casts in kidney tubules. Immuno histochemically, adriamycin caused elevated expression of bax and α-SMA in renal cells. Adriamycin treatment induced serum urea and creatinine increase. Treatment with basil extract with adriamycin lowered the abnormalities decreased the pro-apoptotic protein, bax and fibrosis marker, α-SMA. Again, basil moved the levels of serum urea and creatinine towards normal. In conclusion, basiloffered protectively against nephrotoxicity of adriamycin in male albino rats.

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“…The high levels of NO react with superoxide anions, resulting in the formation of peroxynitrite. Peroxynitrite is a potent and aggressive cellular oxidant [36,37]. The increased NO levels in the DOX group (Group 3) could be explained by this mechanism.…”

Section: Discussionmentioning

confidence: 95%

Protective effects of molsidomine against doxorubicin-induced renal damage in rats

Oğuz¹,

Beytur²,

Sarihan³

et al. 2016

CIM

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Purpose: The purpose of this study was to investigate the therapeutic and protective effects of molsidomine (MLS) against doxorubicin (DOX)-induced renal damage in rats.Methods: Forty rats were randomly divided into five groups (control, MLS, DOX, DOX+MLS and MLS+DOX groups). Thiobarbituric acid reactive substance (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitric oxide (NO) and glutathione peroxidase (GPx) levels were determined from kidney tissues and blood urea nitrogen (BUN), creatinine (Cr) and albumin (Alb) levels also determined.Results: DOX treatment caused a significant increase in TBARS levels and a significant decrease in the GSH and CAT levels compared with the control group. In comparison, MLS administration before DOX injection caused a significant decrease in TBARS levels and also increases in GSH and CAT levels, whereas treatment of MLS after DOX injection did not show any beneficial effect on these parameters. All groups showed a significant increase in NO levels compared to the control group. There were no significant differences among the all groups for BUN and Cr levels. Serum level of Alb decreased in the DOX-treated groups when compared with control and MLS groups. The histopathological findings were in accordance with the biochemical results. MLS treatment reversed the DOX-induced kidney damage in group 4. MLS treatment before DOX injection exerted a protective effect against DOX-induced kidney damage.Conclusions: MLS shows promise as a possible therapeutic intervention for the prevention of kidney injury associated with DOX treatment. Additional studies are warranted.

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Doxorubicin Induced Nephrotoxicity: Protective Effect of Nicotinamide

Cited by 128 publications

References 26 publications

Alantolactone induces apoptosis in glioblastoma cells via GSH depletion, ROS generation, and mitochondrial dysfunction

Alantolactone induces apoptosis in glioblastoma cells via GSH depletion, ROS generation, and mitochondrial dysfunction

Effect of aqueous extract of basil (ocimum basilicum) leaves on nephrotoxicity induced by adriamycin in male rats: histological and immunohistochemical assessment

Protective effects of molsidomine against doxorubicin-induced renal damage in rats

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