The Role of Antioxidants in Ameliorating Cyclophosphamide-Induced Cardiotoxicity

Ayza, Muluken Altaye; Zewdie, Kaleab Alemayehu; Tesfaye, Bekalu Amare; Wondafrash, Dawit Zewdu; Berhe, Abera Hadgu

doi:10.1155/2020/4965171

Cited by 50 publications

(45 citation statements)

References 90 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For ovaries, this can be averted by modern methods of ovary removal and storage with later reimplantation when therapy has been attenuated [ 128 ]. The cardiotoxic effects can also be muted by antioxidant supplementation [ 129 ].…”

Section: Treatment Optionsmentioning

confidence: 99%

Juvenile Dermatomyositis: New Clues to Diagnosis and Therapy

Pachman

Nolan

DeRanieri

et al. 2021

Curr Treat Options in Rheum

View full text Add to dashboard Cite

Purpose of review To identify clues to disease activity and discuss therapy options. Recent findings The diagnostic evaluation includes documenting symmetrical proximal muscle damage by exam and MRI, as well as elevated muscle enzymes—aldolase, creatine phosphokinase, LDH, and SGOT—which often normalize with a longer duration of untreated disease. Ultrasound identifies persistent, occult muscle inflammation. The myositis-specific antibodies (MSA) and myositis-associated antibodies (MAA) are associated with specific disease course variations. Anti-NXP-2 is found in younger children and is associated with calcinosis; anti-TIF-1γ+ juvenile dermatomyositis has a longer disease course. The diagnostic rash—involving the eyelids, hands, knees, face, and upper chest—is the most persistent symptom and is associated with microvascular compromise, reflected by loss of nailfold (periungual) end row capillaries. This loss is associated with decreased bioavailability of oral prednisone; the bioavailability of other orally administered medications should also be considered. At diagnosis, at least 3 days of intravenous methyl prednisolone may help control the HLA-restricted and type 1/2 interferon–driven inflammatory process. The requirement for avoidance of ultraviolet light exposure mandates vitamin D supplementation. Summary This often chronic illness targets the cardiovascular system; mortality has decreased from 30 to 1–2% with corticosteroids. New serological biomarkers indicate occult inflammation: ↑CXCL-10 predicts a longer disease course. Some biologic therapies appear promising.

show abstract

Section: Treatment Optionsmentioning

confidence: 99%

Juvenile Dermatomyositis: New Clues to Diagnosis and Therapy

Pachman

Nolan

DeRanieri

et al. 2021

Curr Treat Options in Rheum

View full text Add to dashboard Cite

show abstract

“…The hematopoietic system is very susceptible to effects of nitrogen mustards including cyclophosphamide (21). Bone marrow depression is the most important limiting factor for using these agents in cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

Aspirin Protective Effect Against Cyclophosphamide Hematological Toxicity In Experimental Animals

Hashim

Al-Attar

Hamdan

2021

Preprint

View full text Add to dashboard Cite

Bone marrow toxicity is the most important factor limiting the use of cytotoxic drugs like alkylating agents in cancer treatment. Recently PG synthase enzyme inhibitors have been reported to potentiate the cytotoxic effects of these agents on cancer cells but little is known if they can affect the toxicity of these agents on bone marrow or other tissues. Cyclophosphamide is one of the most commonly used alkylating agent. In the present work, the effect of these PG synthase enzyme inhibitors, aspirin on cyclophosphamide myelotoxicity was determined employing the peripheral blood count to reflect bone marrow injury. The effect on body weight changes caused by cyclophosphamide was also determined. 1. Cyclophosphamide in doses of 25, 50 and 75 mg/kg i. v. produced as a dose dependent reduction in total WBC count, granulocyte, non granulocyte, and Hb% which was maximum on second day after injection and still present on 5th day post injection. It also produced a dose dependent reduction in body weight on day 5 after injection. 2. Aspirin in doges of 75, 150 and 300 mg/kg i. m. protected against the reduction in WBC counts 'measured for 5 days after injection of cyclophosphamide (50 mg/kg). This protection was not dose dependent, though it was more optimum with 300 mg/kg and disappeared largely when a dose of 450 mg/kg was used. Aspirin did not prevent the changes in Hb% but retard the reduction in body weight caused by cyclophosphamide. 3. It is concluded that aspirin can help to reduce injury and enhance recovery from bone marrow toxicity caused by cytotoxic agents such as the alkylating drugs cyclophosphamide for which no specific antidote is available. Aspirin produces this effect possibly by eliminating the harmful inhibitory effect of excess PGs or leukotrienes, released by bone marrow injury on growth factors of haemopoietic progenitor cells. The magnitude of this protection on WBC counts does not seem to differ between either PG synthase enzyme inhibitors or steroids when used alone or in combination although a synergistic effect in protecting erythropoiesis is observed.

show abstract

“…Cyclophosphamide is an alkylating anticancer drug with strong cytotoxic and immunosuppressive activity. 11,41 It is used in the treatment of Hodgkin’s and non-Hodgkin’s lymphoma, leukemia, rheumatoid arthritis, and lupus erythematous. 41 Cyclophosphamide cardiotoxicity affects between 7–28% of such patients.…”

Section: Cyclophosphamidementioning

confidence: 99%

“…11,41 It is used in the treatment of Hodgkin’s and non-Hodgkin’s lymphoma, leukemia, rheumatoid arthritis, and lupus erythematous. 41 Cyclophosphamide cardiotoxicity affects between 7–28% of such patients. Cyclophosphamide has been shown to enhance proinflammatory cytokines such as nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β).…”

Section: Cyclophosphamidementioning

confidence: 99%

“…Cyclophosphamide has been shown to enhance proinflammatory cytokines such as nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β). 41 Exposure of animals to cyclophosphamide lead to a decrease of GRx, GPx, and SOD activity. 41 It is known that antioxidants are beneficial in decreasing cyclophosphamide cardiotoxicity by elevation of GSH and SOD levels and reduction in proinflammatory cytokines.…”

Section: Cyclophosphamidementioning

confidence: 99%

See 1 more Smart Citation

Melatonin attenuates chemical-induced cardiotoxicity

et al. 2020

View full text Add to dashboard Cite

Environmental chemicals and drugs can induce cardiotoxicity, mainly by generating free radicals. Reactive oxygen species play a critical role in the pathogenesis of cardiac tissue injury. This highlights a need for prevention of cardiotoxicity by scavenging free radicals. Melatonin has been shown to act as a protector against various conditions in which free radicals cause molecular and tissue injury. Some of the mechanisms by which melatonin operates as a free radical scavenger and antioxidant have been identified. The importance of endogenous melatonin in cardiovascular health and the benefits of melatonin supplementation in different cardiac pathophysiological disorders have been shown in a variety of model systems. Melatonin continues to attract attention for its potential therapeutic value for cardiovascular toxicity. The therapeutic potential of melatonin in treatment of cardiotoxicities caused by various chemicals along with suggested molecular mechanisms of action for melatonin is reviewed.

show abstract

The Role of Antioxidants in Ameliorating Cyclophosphamide-Induced Cardiotoxicity

Cited by 50 publications

References 90 publications

Juvenile Dermatomyositis: New Clues to Diagnosis and Therapy

Juvenile Dermatomyositis: New Clues to Diagnosis and Therapy

Aspirin Protective Effect Against Cyclophosphamide Hematological Toxicity In Experimental Animals

Melatonin attenuates chemical-induced cardiotoxicity

Contact Info

Product

Resources

About