Amelioration of adriamycin-induced cardiotoxicity in rabbits by prenylamine and vitamins A and E☆
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2021, PharmaNutritionCitation Excerpt :The association of numerous antioxidant agents, such as transferrin, metallothionein, desferrioxamine, or proteins that oxidize ferrous ions have been widely studied in reducing the toxic effects of doxorubicin. Certain studies, specifically those related to vitamin antioxidants, report the benefits of these vitamins on the toxic effects of doxorubicin [72–76], while other studies note that vitamins, specifically vitamin E, potentiate doxorubicin toxicity [77–79]. Several studies seek to study the benefits of antioxidant vitamins in reducing doxorubicin toxicity, with vitamin E being the most studied, present in 60 % of published articles (Fig. 5).
An update on the mechanisms related to cell death and toxicity of doxorubicin and the protective role of nutrients
2019, Food and Chemical ToxicologyCitation Excerpt :This property was taken into account for many researchers to carry out investigations on vitamin E potential for preventing DOX-based chemotherapy side effects. Despite an old study reported that vitamin E potentiated DOX toxicity (Alberts et al., 1978), most of earlier preclinical studies in rodents have shown that oral vitamin E tends to protects against acute and chronic toxic effects of DOX, specially at heart, without interfering with its effectiveness as chemotherapeutic agent (Geetha et al., 1990; Herman and Ferrans, 1983; Krivit, 1979; Milei et al., 1986; Myers et al., 1976). Additionally, some old preclinical studies have also observed that oral vitamin E even tended to increase anti-tumor actions (Quiles et al., 2006; Ripoll et al., 1986; Tanigawa et al., 1986).
Cardiovascular effects of systemic cancer treatment
2011, Cancer Treatment ReviewsCitation Excerpt :In particularly sensitive cases this toxicity may occur even after a single drug dose.7 The suggested principal mechanism of anthracycline damage is via generation of reactive oxygen species by iron-anthracycline complexes, leading to lipid peroxidation and membrane damage.1,10,11,14,30–32 Oxidative stress causes activation of kinase pathways (mitogen-activated protein kinase – MAPK, stress-activated protein kinase – SAPK) modulating response to anthracyclines and linking to apoptotic pathway.16
Adriamycin-induced myocardial toxicity: New solutions for an old problem?
2007, International Journal of CardiologyCitation Excerpt :This may be the result of post-receptor abnormalities, including alterations of guanine nucleotide-binding proteins or the catalytic unit of adenylate cyclase [19]. Besides all these mechanisms, adriamycin-generated free radicals would lead to lipid peroxidation and membrane damage [20]. This appears to be the most important mechanism and will be developed in the next topic [21].
Vitamin E: Biological Activity and Health Benefits: Overview
2023, Vitamin E in Health and Disease
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Supported by the National Research Council of Argentina and Fundación H. Pombo de Rodríguez.