Abstract

The antioxidant activity of food compounds is one of the properties generating the most interest, due to its health benefits and correlation with the prevention of chronic disease. This activity is usually measured using in vitro assays, which cannot predict in vivo effects or mechanisms of action. The objective of this study was to evaluate the in vivo protective effects of six phenolic compounds (naringenin, apigenin, rutin, oleuropein, chlorogenic acid, and curcumin) and three carotenoids (lycopene B, β-carotene, and astaxanthin) naturally present in foods using a zebrafish embryo model. The zebrafish embryo was pretreated with each of the nine antioxidant compounds and then exposed to tert-butyl hydroperoxide (tBOOH), a known inducer of oxidative stress in zebrafish. Significant differences were determined by comparing the concentration-response of the tBOOH induced lethality and dysmorphogenesis against the pretreated embryos with the antioxidant compounds. A protective effect of each compound, except β-carotene, against oxidative-stress-induced lethality was found. Furthermore, apigenin, rutin, and curcumin also showed protective effects against dysmorphogenesis. On the other hand, β-carotene exhibited increased lethality and dysmorphogenesis compared to the tBOOH treatment alone.

Highlights

  • Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are originated during cell metabolism

  • Oxygen is essential for human life; at the same time, it produces toxic substances, such as free radicals and reactive oxygen species (ROS); these substances are oxidizing, unstable, and reactive

  • They can react with any macromolecule and cause cell damage [24]. To counteract these oxidizing substances, the body employs antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase, and antioxidant compounds derived from the diet

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Summary

Introduction

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are originated during cell metabolism They are essential to a normal physiological state, but they participate in pathological processes when in excess [1]. Aerobic organisms have defenses to prevent ROS-induced oxidative damage, involving antioxidant enzymes and/or nonenzymatic mechanisms, including endogenously produced antioxidant compounds or the ingestion of antioxidants in the diet [2]. The consequences of OS include macrophage recruitment; the inhibition of the normal functioning of lipids and proteins; and mitochondrial, membrane, and DNA damage [4,5,6,7] These alterations have been correlated with several pathologies, such as cancer, aging, diabetes, rheumatoid arthritis, and cardiovascular and neurodegenerative diseases, among others [8,9,10,11]

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