Oxidative stress induced in rat liver by anticancer drugs doxorubicin, paclitaxel and docetaxel

Pieniążek, Anna; Czepas, Jan; Piasecka-Zelga, Joanna; Gwoździński, Krzysztof; Koceva‐Chyła, Aneta

doi:10.2478/v10039-012-0063-1

Cited by 74 publications

(38 citation statements)

References 48 publications

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“…The increased lipid peroxidation by doxorubicin may have involved similar mechanism in the present study. This is in good agreement with earlier studies, where DOX has been reported to increase lipid peroxidation in mice and rat heart and liver [18,19,46,47,48,60]. Naringin has been reported to protect against the DOX-induced lipid peroxidation in mouse liver and heart [18].…”

Section: Biochemistry and Molecular Biology Journal Issn 2471-8084supporting

confidence: 92%

The Citrus Flavanone Naringin Enhances Antioxidant Status in the Albino Rat Liver Treated with Doxorubicin

Ch¹,

Jagetia²,

Lalnuntluangi³

2016

Biochem Mol Biol J

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Section: Biochemistry and Molecular Biology Journal Issn 2471-8084supporting

confidence: 92%

The Citrus Flavanone Naringin Enhances Antioxidant Status in the Albino Rat Liver Treated with Doxorubicin

Ch¹,

Jagetia²,

Lalnuntluangi³

2016

Biochem Mol Biol J

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“…DOX treatment has been earlier reported to increase the lipid peroxidation in rat and mice. 32,[61][62][63][64][65]72 Naringin treatment has been found to protect mouse and rat liver and heart against the DOX-induced lipid peroxidation. 32,[63][64][65] Naringin has also been reported to protect against iron and bleomycin-induced lipid peroxidation in earlier studies.…”

Section: Discussionmentioning

confidence: 99%

Treatment of Mice with Naringin Alleviates the Doxorubicin-Induced Oxidative Stress in the Liver of Swiss Albino Mice

Ch¹,

Jagetia²,

Lalrinengi³

2017

MOJAP

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Doxorubicin a photosensitive antibiotic is frequently used to treat various malignancies in clinics; however, doxorubicin is also taken up by the normal cells of the body leading to increased oxidative stress and subsequently DNA damage and dysfunction in the cells. The agents which can reduce the adverse effect of doxorubicin will of great value. The present study has attempted to study the effect of naringin a citrus flavonoid on the doxorubicininduced oxidative stress in mice liver. The mice were administered with 0, 1, 5 or 10mg/ kg body weight of doxorubicin and treated with 10mg/kg body weight of naringin before or after doxorubicin treatment. The glutathione concentration and lipid peroxidation and activities of glutathione-s-transferase, catalase and super oxide dismutase were studied at 0.5, 1, 2 and 4h post-treatment in the mouse liver. The doxorubicin increased the lipid peroxidation in a dose dependent manner at all the post treatment times. Conversely, it attenuated the activities of glutathione-s-transferase, catalase and super oxide dismutase in dose dependent fashion and time dependent manner. A similar effect was observed for glutathione concentration. Treatment of mice with naringin before or after doxorubicin treatment elevated all the antioxidants and reduced the doxorubicin -induced lipid peroxidation. The effect of naringin pretreatment was more effective when compared to its post treatment. The naringin was very effective in reducing the oxidative stress induced by doxorubicin as indicated by the elevated levels of glutathione concentration, glutathiones-transferase, catalase and super oxide dismutase. The pretreatment of naringin was better than its post treatment.

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“…In all groups receiving treatment with MgIG, SOD and GSH-Px levels increased, whereas those of MDA decreased. The results of previous studies indicated that oxidative stress is responsible for the cardiotoxicity and hepatotoxicity induced by DOX and is associated with decreased activity of the antioxidant system (20,38,39). As a consequence, it was hypothesized that MgIG may improve the body's antioxidant capacity, which may be an important mechanism of MgIG in resisting damage to the liver and heart induced by DOX.…”

Section: Discussionmentioning

confidence: 99%

“…It is estimated that ~40% of patients treated with DOX experience liver injury, since large amounts of DOX accumulate and are metabolized in the liver (15,19). Furthermore, the concurrent administration of DOX, paclitaxel and docetaxel enhances oxidative stress in the liver (20).…”

Section: Introductionmentioning

confidence: 99%

Magnesium isoglycyrrhizinate ameliorates doxorubicin‑induced acute cardiac and hepatic toxicity via anti‑oxidant and anti‑apoptotic mechanisms in mice

Zhang

Song

et al. 2017

Exp Ther Med

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Abstract. The present study investigated the effects and potential mechanisms of action of magnesium isoglycyrrhizinate (MgIG) in doxorubicin (DOX)-treated mice. Histopathological analysis and western blot analysis were conducted in the liver and heart tissues and biochemical analysis of the serum was performed. The results revealed that MgIG (10, 20 and 40 mg/kg/day) could protect the structure and functions of the liver and heart by inhibiting the activities of the myocardial enzymes creatine kinase (CK), CK-MB and lactate dehydrogenase and the hepatic-specific enzymes aspirate aminotransferase and alanine aminotransferase, increasing the activities of the antioxidants superoxide dismutase and glutathione peroxidase, and inhibiting cellular apoptosis induced by DOX (30 mg/kg). These results demonstrate that inhibiting lipid peroxidation and reducing myocardial and hepatocyte apoptosis may be one of the mechanisms by which MgIG exhibits hepatoprotective and cardioprotective effects in DOX-treated mice.

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Oxidative stress induced in rat liver by anticancer drugs doxorubicin, paclitaxel and docetaxel

Cited by 74 publications

References 48 publications

The Citrus Flavanone Naringin Enhances Antioxidant Status in the Albino Rat Liver Treated with Doxorubicin

The Citrus Flavanone Naringin Enhances Antioxidant Status in the Albino Rat Liver Treated with Doxorubicin

Treatment of Mice with Naringin Alleviates the Doxorubicin-Induced Oxidative Stress in the Liver of Swiss Albino Mice

Magnesium isoglycyrrhizinate ameliorates doxorubicin‑induced acute cardiac and hepatic toxicity via anti‑oxidant and anti‑apoptotic mechanisms in mice

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