Cardiotoxic and Dyslipidemic Effects of Doxorubicin and Betulinic Acid Amide

Клинникова, М. Г.; Лушникова, Е. Л.; Koldysheva, E. V.; Толстикова, Т. Г.; Сорокина, И. В.; Yuzhik, E. I.; Mzhelskaya, M. M.

doi:10.1007/s10517-016-3594-9

Cited by 12 publications

(4 citation statements)

References 12 publications

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“…On the other hand, the enhancements of plasma levels of total cholesterol and non-HDL-c in both control and F-overloaded rats, after DOX injection are consistent with the dyslipidemic effects of this compound in rodents 44–46 and humans. 47 It has been shown that chronic or subchronic treatments with DOX decreases HDL-c plasma levels, 47–49 and it is believed that this effect contributes to the deleterious action of the drug because there is evidence that HDL-c attenuates the cardiotoxic effects of DOX by protecting cardiomyocytes from apoptosis in vitro 48 and by maintaining cardiac function in vivo.…”

Section: Discussionsupporting

confidence: 71%

Cardiotoxic Effects of the Antineoplastic Doxorubicin in a Model of Metabolic Syndrome: Oxidative Stress and Transporter Expression in the Heart

Ogonowski

Mikusic

Kouyoumdzian

et al. 2021

Journal of Cardiovascular Pharmacology

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The aim of the present work was to examine whether metabolic syndrome–like conditions in rats with fructose (F) overload modify the cardiotoxic effects induced by doxorubicin (DOX) and whether the treatment altered the expression of P-gp, breast cancer resistance protein, and organic cation/carnitine transporters in the heart. Male Sprague–Dawley rats received either tap water (control group [C]; n = 16) or water with F 10% wt/vol (n = 16) during 8 weeks. Three days before being killed, the animals received a single dose of DOX (6 mg/kg, ip, md) (C-DOX and F-DOX groups) or vehicle (VEH; ISS 1 mL/kg BW; ip) (C-VEH and F-VEH groups) (n = 8 per group). F overload enhanced thiobarbituric acid–reactive substance levels in the left ventricle, and DOX injection further increased those values. DOX did not alter thiobarbituric acid–reactive substance production in C animals. DOX caused a decrease of 30% in the ejection fraction and a nearly 40% reduction in the fractional shortening in F animals, but not in C rats. Cardiac tissue levels of P-gp decreased by about 30% in F rats compared with the C groups. DOX did not modify cardiac P-gp expression. Breast cancer resistance protein and organic cation/carnitine transporter (OCTN 1/2/3) protein levels did not change with either F or DOX. It is suggested that DOX could cause greater cardiotoxicity in rats receiving F, probably due to enhanced cardiac lipid peroxidation and lower expression of cardiac P-gp. These results support the hypothesis that the cardiotoxicity of DOX could be increased under metabolic syndrome–like conditions or in other health disorders that involve cardiovascular risk factors.

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Section: Discussionsupporting

confidence: 71%

Cardiotoxic Effects of the Antineoplastic Doxorubicin in a Model of Metabolic Syndrome: Oxidative Stress and Transporter Expression in the Heart

Ogonowski

Mikusic

Kouyoumdzian

et al. 2021

Journal of Cardiovascular Pharmacology

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“…Instead, even though evidence is limited, anthracyclines have shown to be potentially detrimental for lipid metabolism. This association was initially observed in animal studies, where doxorubicin induced a three-fold increase in LDL levels 14 days after injection [50,51]. Anthracyclines have also appeared to be independently associated with higher levels of triglycerides in a retrospective analysis conducted on 1934 patients undergoing adjuvant chemotherapy [52].…”

Section: Lipid Metabolism and Dyslipidemiamentioning

confidence: 75%

Combined Therapy with Anthracyclines and GnRH Analogues for Breast Cancer: Impact on Ischemic Heart Disease

Bergami,

Manfrini,

Cenko

et al. 2023

JCM

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The combination of classic chemotherapy agents like anthracyclines with novel targeted medications has had a positive impact on women’s survival from breast cancer. GnRH analogues are primarily employed to temporarily suppress ovarian function in premenopausal women with hormone-receptor-positive (HR+) breast cancer. Despite their benefits, the true degree of their collateral effects has been widely understudied, especially when it comes to ischemic heart disease. This review aims at summarizing the current state of the art on this issue, with particular focus on the risk for cardiotoxicity associated with the combined use of GnRH analogues and anthracyclines.

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“…In the evaluation there was no statistical difference in the density of cardiac fibers, contrary to what was described in a study conducted with rats evaluating doxorubin carditoxicity. However, changes in the evaluated parameter were evident only after days of chemotherapy administration, showing a late marker for myocardial toxicity (Klinnikova et al 2016).…”

Section: Discussionmentioning

confidence: 97%

Effects of omega 3 on doxorubicin-induced cardiotoxicity in an experimental rabbit model

Barros¹,

Pereira²,

Aldrovani³

et al. 2021

RSD

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To evaluate the effects of the use of omega 3 at different doses, following the response through stereological and morphometric evaluations in doxorubicin-induced acute cardiotoxicity in an experimental rabbit model. Thirty healthy adult New Zealand rabbits were divided into six groups with different doses of omega 3 treatment, GT125, GT500 and GT 2000, receiving doses of 125mg / kg, 500mg / kg and 2000mg / kg, respectively. The induction of acute cardiotoxicity with doxorubicin was treated for six days prior to intravenous administration of 10mg / kg single dose. Then, the animals were euthanized and myocardial samples were collected for stereological and morphometric evaluations. The stereological evaluation showed an increase in the transverse area of cardiomocytes between the SHAM and GT2000 groups and an increase in the interstitial collagen volume density between the SHAM and GT500 and SHAM and GT2000 groups. The omega 3 500mg/kg dose has the potential to attenuate the fibrotic effects of doxorubicin use and the use of a single dose of 10mg/kg doxorubicin can be used as an acute dilated cardiomyopathy induction protocol in an experimental model using rabbits.

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Cardiotoxic and Dyslipidemic Effects of Doxorubicin and Betulinic Acid Amide

Cited by 12 publications

References 12 publications

Cardiotoxic Effects of the Antineoplastic Doxorubicin in a Model of Metabolic Syndrome: Oxidative Stress and Transporter Expression in the Heart

Cardiotoxic Effects of the Antineoplastic Doxorubicin in a Model of Metabolic Syndrome: Oxidative Stress and Transporter Expression in the Heart

Combined Therapy with Anthracyclines and GnRH Analogues for Breast Cancer: Impact on Ischemic Heart Disease

Effects of omega 3 on doxorubicin-induced cardiotoxicity in an experimental rabbit model

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