Coenzyme Q10 treatment ameliorates acute cisplatin nephrotoxicity in mice

Fouad, Amr A.; Al-Sultan, Ali Ibrahim; Refaie, Shereen M.; Yacoubi, Mohamed Tahar

doi:10.1016/j.tox.2010.05.007

Cited by 76 publications

(68 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Also our results and several studies have shown that coenzyme Q10 is able to reduce nephropathy without any side effects or additional burden on kidney (Fouad, Al-Sultan, Refaie, & Yacoubi, 2010;Persson et al, 2012).…”

Section: In Vitro Antioxidant Activity Of Coenzyme Q10supporting

confidence: 77%

Amelioration of altered antioxidant enzymes activity and glomerulosclerosis by coenzyme Q10 in alloxan-induced diabetic rats

Ahmadvand

Tavafi

Khosrowbeygi

2012

Journal of Diabetes and its Complications

View full text Add to dashboard Cite

Section: In Vitro Antioxidant Activity Of Coenzyme Q10supporting

confidence: 77%

Amelioration of altered antioxidant enzymes activity and glomerulosclerosis by coenzyme Q10 in alloxan-induced diabetic rats

Ahmadvand

Tavafi

Khosrowbeygi

2012

Journal of Diabetes and its Complications

View full text Add to dashboard Cite

“…57,58) In our previous studies, we have also described the anti-inflammatory activity of 23-HTA 21,22) ; however, further study is needed to determine whether the protective effect of 23-HTA against cisplatin is due to its ability to inhibit the activation of the NF-kB signaling pathway, which promotes the transcriptions of NADPH oxidase, TNF-a, and iNOS. 59) The results of the present study indicate that 23-HTA effectively protects rat kidney tissues against cisplatin-induced acute nephrotoxicity, which suggests that the antioxidant activities of 23-HTA are primarily responsible for the nephroprotective effect of 23-HTA. The findings of the present study indicate that 23-HTA is potential therapeutic candidate for the prevention of renal injury and dysfunction which is a major and dose-limiting problem during cisplatin therapy.…”

Section: Discussionsupporting

confidence: 56%

The Ameliorative Effect of 23-Hydroxytormentic Acid Isolated from Rubus coreanus on Cisplatin-Induced Nephrotoxicity in Rats

Sohn

Rim

Kim

et al. 2011

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Cisplatin (cis-diaminedichloroplatinum II) is a highly effective antineoplastic DNA alkylating agent that is widely used to treat many cancers, such as, head and neck, ovarian, testicular, mammalian, and cervical cancer.1) However, although higher doses of cisplatin are more effective, many reversible and irreversible side effects including nephrotoxicity, neurotoxicity, bone marrow toxicity, gastrointestinal toxicity, and ototoxicity limit its therapeutic profile.2) The primary targets of cisplatin in the kidney are the proximal straight and distal convoluted tubules, in which it accumulates and promotes cellular damage via multiple mechanisms, such as, oxidative stress, DNA damage, and apoptosis. [3][4][5] Cisplatin nephrotoxicity can present as Fanconi-like syndrome, distal renal tubular acidosis, hypocalcemia, and acute kidney injury, the latter of which occurs in 20-30% of patients undergoing cisplatin treatment. 6) It has been demonstrated that cisplatin induces cell death of renal tubules, which is characterized by reduced glutathione (GSH) levels, and higher blood urea nitrogen (BUN), serum creatinine, and malondialdehyde (MDA) levels, which are suggestive of accelerated peroxidative processes. Furthermore, reactive oxygen species (ROS) are known to cause tissue damage by interacting with various macromolecules, such as, polyunsaturated fatty acids, in the cellular membrane. ROS are generated endogenously in renal cells, and are directly removed by endogenous antioxidants, such as, GSH and superoxide dismutase (SOD). It has been suggested that ROS upregulation is associated with an impaired glomerular filtration rate (GFR).7) On the other hand, antioxidants maintain intracellular reduced GSH concentrations, restore cellular defense mechanisms, block lipid peroxidation, and thus, protect real cells against the noxious effects of a wide variety of nephrotoxic agents. 8,9) Several studies have suggested that cisplatin induces ROS and reactive nitrogen species (RNS), which both deplete GSH and cause lipid peroxidation. [10][11][12] In particular, the hydroxyl radical is generated by the interaction between DNA and cisplatin, and attacks renal microsomal membranes and causes lipid peroxidation.13) Furthermore, the depletion of renal GSH may also increase MDA levels and the formations of stable proteincisplatin adducts, and decrease the activities of antioxidant enzymes, such as, SOD, catalase (CAT), glutathione reductase (GR), and glutathione peroxidase (GPx).14,15) Cisplatin is also known to increase the activities of the oxidant enzymes, such as aldehyde oxidase (AO) and xanthine oxidase (XO), which are major contributors to oxidant load in renal tissues. 16,17) Rubus coreanus (Rosaceae) is a perennial shrub found in southern part of Korea, and its dried unripe fruits have been used for centuries as an herbal medicine, particularly to improve libido.11) In one study undertaken to compare of antioxidant activities of seventy herbs used in Korean traditional medicine, Rubus coreanus demonstrated potent antiox...

show abstract

“…In Langendorff preparations of isolated heart, pretreatment with CoQ protected coronary vascular reactivity after isquemia/reperfusion radical scavenger activity (Whitman et al, 1997). CoQ was also able to ameliorate cisplatin-induced acute renal injury in mice (Fouad et al, 2010). Many in vitro and in vivo studies showed that CoQ, mainly in its reduced state, may act as an antioxidant protecting membranes from oxidative damage (Beyer, 1990).…”

Section: Wwwintechopencommentioning

confidence: 99%