Abstract

Nutraceutical antioxidant supplementation in cancer is a controversial and questionable subject, as potential drug-nutrient interactions can affect cancer treatment. Between 13% and 87% of patients with cancer uses antioxidant supplements, often at higher doses compared to those recommended [1,2].

Highlights

  • Nutraceutical antioxidant supplementation in cancer is a controversial and questionable subject, as potential drug-nutrient interactions can affect cancer treatment

  • For pediatric cancer the debate remains open: should paediatric oncologists provide adequate antioxidant intake, which is essential for normal cellular homeostasis and growth, thereby risking a potential reduction of the effectiveness of anti-cancer therapy, or should not? In this review we evaluate the possible antioxidant supplementations in patients with Ewing Sarcoma (ES)

  • In vitro and in vivo data suggest that many nutraceutical antioxidants can enhance or reduce the effects of cytotoxic therapy by differentially altering the intracellular redox state and can promote cells proliferation and malignant progression

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Summary

Introduction

Nutraceutical antioxidant supplementation in cancer is a controversial and questionable subject, as potential drug-nutrient interactions can affect cancer treatment. In non-small-cell lung cancer Vitamin C treatment exert anti-cancer effects via increasing redox-active labile iron [37] Vitamin E induce apoptosis in tumour cell lines, increases the efficacy of chemotherapy and reduces drug toxicity [38]. N-Acetylcysteine (NAC), a medication that works by increasing the glutathione levels and vitamin E, was shown to accelerate the tumor progression in a B-RAF and K-RAS induced lung cancer in murine models These antioxidants promote tumour progression by reducing ROS levels and in turn reduce p53 expression levels that could have induced apoptosis leading to the cell death [58]. It could be possible that this activity is linked to mitochondria bioenergetics function

Materials and Methods
Conclusion
Findings
Conklin
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