Abstract
Carotenoids are well known for their potent antioxidant function in the cellular system. However, in cancer cells with an innately high level of intracellular reactive oxygen species (ROS), carotenoids may act as potent pro-oxidant molecules and trigger ROS-mediated apoptosis. In recent years, the pro-oxidant function of several common dietary carotenoids, including astaxanthin, β-carotene, fucoxanthin, and lycopene, has been investigated for their effective killing effects on various cancer cell lines. Besides, when carotenoids are delivered with ROS-inducing cytotoxic drugs (e.g., anthracyclines), they can minimize the adverse effects of these drugs on normal cells by acting as antioxidants without interfering with their cytotoxic effects on cancer cells as pro-oxidants. These dynamic actions of carotenoids can optimize oxidative stress in normal cells while enhancing oxidative stress in cancer cells. This review discusses possible mechanisms of carotenoid-triggered ROS production in cancer cells, the activation of pro-apoptotic signaling by ROS, and apoptotic cell death. Moreover, synergistic actions of carotenoids with ROS-inducing anti-cancer drugs are discussed, and research gaps are suggested.
Highlights
IntroductionA range of short-lived reactive oxygen species (ROS), including superoxide radical/anion (O2 − ), hydroxyl radical ( OH), and hydrogen peroxide H2 O2 are endogenously produced by mitochondria (electron transport chain), NADPH oxidase, peroxisomes, and endoplasmic reticulum (as byproducts during the cellular metabolic process) [1]
In the human body, a range of short-lived reactive oxygen species (ROS), including superoxide radical/anion (O2 − ), hydroxyl radical ( OH), and hydrogen peroxide H2 O2 are endogenously produced by mitochondria, NADPH oxidase, peroxisomes, and endoplasmic reticulum [1]
MCF-7 cellscompared and this effect is synergistically enhanced cells areand treated with ais mixture of enhanced when cells are treated with a mixture of astaxanthin, β-carotene, and lutein increase astaxanthin, β-carotene, and lutein (68.1% increase in ROS) [22]
Summary
A range of short-lived reactive oxygen species (ROS), including superoxide radical/anion (O2 − ), hydroxyl radical ( OH), and hydrogen peroxide H2 O2 are endogenously produced by mitochondria (electron transport chain), NADPH oxidase, peroxisomes, and endoplasmic reticulum (as byproducts during the cellular metabolic process) [1]. Vitamin A (retinol, retinal, and retinoic acid) is an essential nutrient for humans, converted synthesize vitamin A from carotenoid with a non-substituted beta-ionone ring, such as α-carotene, mostly from the retinyl palmitate found in animal-derived food. Herbivores/omnivores can synthesize vitamin A from carotenoid with a non-substituted beta-ionone for vegetarians, fruits, vegetables, and algae are the major dietary sources of pro-vitamin A carotenoids. For vegetarians, fruits, vegetables, and algae are the major dietary sources of proavailable carotenoid DRI is for vitamin A, expressed as the retinol activity equivalent (RAE), which vitamin A carotenoids. In cancer cells with innately high intracellular ROS levels, carotenoids may act as pro-oxidants and trigger ROS-mediated apoptosis of cancer cells. Several dietary carotenoids, including astaxanthin, β-carotene, and lycopene have shown pro-oxidant actions that can mediate apoptosis of cancer cells. A synergistic action of carotenoids with ROS-inducing anti-cancer drugs is discussed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
