Drug-Induced Oxidative Stress and Toxicity

Deavall, Damian G.; Martin, Elizabeth A.; Horner, Judith; Roberts, Ruth

doi:10.1155/2012/645460

Cited by 544 publications

(445 citation statements)

References 115 publications

(116 reference statements)

Supporting

Mentioning

396

Contrasting

Unclassified

Order By: Relevance

“…The DOX induced ROS may interact with membrane lipid producing their peroxides. 15 The increased lipid peroxidation by DOX in a concentration dependent manner is due to this activity of DOX. The administration of naringin before and after DOX treatment led to a significant decline in the lipid peroxidation and both treatments were equally effective.…”

Section: Discussionmentioning

confidence: 99%

“…13,14 Reductive conversion of doxorubicin is characterized by the one-electron reduction of the quinone moiety of doxorubicin, via NADPH and the cytochrome P450 reductase into a semiquinone radical, which exerts the toxic effect or it can oxidized back to the quinine form. 15 The ability of doxorubicin to undergo the reductive conversion depends on the availability of molecular oxygen and NADPH, and the activities of several intracellular enzymes such as superoxide dismutase (SOD), glutathione peroxidase, NADPH oxidases (NOXs) and thioredoxin. 16 The antineoplastic drugs are not specifically selective to neoplastic cells and they are also assimilated by normal healthy cells, especially the proliferating ones.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

Ch¹,

Jagetia²,

Lalrinengi³

2017

MOJAP

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

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

View full text Add to dashboard Cite

show abstract

“…Some of them, such as doxorubicin, cisplatin and the anti-tumor peptide actinomycin, are also known to trigger cell death by increasing the reactive oxygen species (ROS) levels through various mechanisms. 16 Although increasing oxidative stress is considered as a valuable strategy for overcoming primary tumors and metastasis, 17 the Darwinian selection of oxidatively stressed cancer cells can allow the survival of clonal cells that expressing supraphysiological levels of detoxifying enzymes, such as the mitochondria-located manganese superoxide dismutase (MnSOD or SOD2) 18 and gluthatione synthetase, 19 can be responsible of collapse and chemoresistance.…”

mentioning

confidence: 99%

Uncovering metabolism in rhabdomyosarcoma

Monti

Fanzani

2016

Cell Cycle

View full text Add to dashboard Cite

Rhabdomyosarcoma (RMS) is a myogenic tumor classified as the most frequent soft tissue sarcoma affecting children and adolescents. The histopathological classification includes five different histotypes, with two most predominant referred as to embryonal and alveolar, the latter being characterized by adverse outcome. The current molecular classification identifies two major subsets, those harboring the fused Pax3-Foxo1 transcription factor generating from a recurrent specific translocation (fusion-positive RMS), and those lacking this signature but harboring mutations in the RAS/PI3K/AKT signalling axis (fusion-negative RMS). Since little attention has been devoted to RMS metabolism until now, in this review we summarize the “state of art” of metabolism and discuss how some of the molecular signatures found in this cancer, as observed in other more common tumors, can predict important metabolic challenges underlying continuous cell growth, oxidative stress resistance and metastasis, which could be the subject of future targeted therapies

show abstract

“…Free radicals react with Polyunsaturated Fatty Acids (PUFA) of lipid membrane and cause lipid peroxidation (Barrera, 2012). Oxidative stress generates Reactive Oxygen Species (ROS), which produces toxic effect on cell development, growth and survival (Deavall et al, 2012). In hyperglycemia, oxidative stress is produced with the formation of Advanced Glycation End (AGE) product which has a strong association with the diabetic complications such as nephropathy, neuropathy, retinopathy and cardiovascular diseases (Villeneuve and Natarajan, 2010).…”

Section: Science Publicationsmentioning

confidence: 99%

Apigenin Causes Biochemical Modulation, Glut4 and Cd38 Alterations to Improve Diabetes and to Protect Damages of Some Vital Organs in Experimental Diabetes

Hossain

Ghosh

Satapathy

et al. 2014

American Journal of Pharmacology and Toxicology

View full text Add to dashboard Cite

Diabetes mellitus gradually leads to dysfunction and failure of some vital organs specially the eyes, kidneys, pancreas, brain, heart, liver and lungs. The study was aimed to evaluate the antidiabetic potential of apigenin and its mechanistic role in controlling damages of vital tissues in streptozotocin-induced diabetic rats. Streptozotocin-induced diabetic rats were treated with apigenin and glipizide. Various biochemical changes, GLUT4 and CD38 protein expression patterns and histopathological alterations in some vital organs such as liver, kidneys and pancreas were investigated to compare the antidiabetic potentials of those two chemicals and to understand their capability to control the damages of the vital organs during diabetes. Effective control of blood glucose level along with the alteration of hepatic phase I and phase II drug metabolizing enzymes, antioxidant defense enzyme activities and lipid peroxidation level towards their normal values and enhanced GLUT4 translocation and downregulated CD38 expression by apigenin were observed. Apigenin was also found to prevent the deterioration of vital organs during diabetes. In conclusion, apigenin has predominant role in controlling blood glucose level along with the protection of vital organs eventually damaged during diabetes, by minimizing toxicities and associated diabetic complications in streptozotocin-induced diabetic rats and may explore as a potential antidiabetic agent in near future.

show abstract

Drug-Induced Oxidative Stress and Toxicity

Cited by 544 publications

References 115 publications

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

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

Uncovering metabolism in rhabdomyosarcoma

Apigenin Causes Biochemical Modulation, Glut4 and Cd38 Alterations to Improve Diabetes and to Protect Damages of Some Vital Organs in Experimental Diabetes

Contact Info

Product

Resources

About