β‐carotene treatment alters the cellular death process in oxidative stress‐induced K562 cells

Abstract

Oxidizing agents (e.g., H O ) cause structural and functional disruptions of molecules by affecting lipids, proteins, and nucleic acids. As a result, cellular mechanisms related to disrupted macro molecules are affected and cell death is induced. Oxidative damage can be prevented at a certain point by antioxidants or the damage can be reversed. In this work, we studied the cellular response against oxidative stress induced by H O and antioxidant-oxidant (β-carotene-H O ) interactions in terms of time, concentration, and treatment method (pre-, co-, and post) in K562 cells. We showed that co- or post-treatment with β-carotene did not protect cells from the damage of oxidative stress furthermore co- and post-β-carotene-treated oxidative stress induced cells showed similar results with only H O treated cells. However, β-carotene pre-treatment prevented oxidative damage induced by H O at concentrations lower than 1,000 μM compared with only H O -treated and co- and post-β-carotene-treated oxidative stress-induced cells in terms of studied cellular parameters (mitochondrial membrane potential [Δψ ], cell cycle and apoptosis). Prevention effect of β-carotene pre-treatment was lost at concentrations higher than 1,000 μM H O (2-10 mM). These findings suggest that β-carotene pre-treatment alters the effects of oxidative damage induced by H O and cell death processes in K562 cells.

Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents

“…β-Carotene is a chemical compound of the family of terpenes; β-carotene is the most abundant carotenoid in nature, and it is the most important pro-vitamin in the human diet [ 154 ]. The mucosa of the small intestine transforms it into vitamin A, and it is then stored in the liver as a retinol ester [ 155 ]. As a lipo-soluble antioxidant, it reduces the chances of heart attacks and increases the efficiency of the immune system [ 155 ].…”

“…The mucosa of the small intestine transforms it into vitamin A, and it is then stored in the liver as a retinol ester [ 155 ]. As a lipo-soluble antioxidant, it reduces the chances of heart attacks and increases the efficiency of the immune system [ 155 ]. Low β-carotene consumption rates enhance systemic OS in MS patients [ 156 ].…”

Designing a whole cell bioreporter to show antioxidant activities of agents that work by promotion of the KEAP1–NRF2 signaling pathway

“…It benefits from an important component, NRF2 (Nuclear Factor Erythroid 2-Related Factor 2), which is a transcription factor and a member of the cap ‘n’ collar (CNC) subfamily of basic region leucine zipper (bZip) transcription factors. The key role of NRF2 in controlling cellular defense against environmental oxidant agents has been revealed by studies in which NRF2-knocked-out mice have been shown to exhibit sensitivity to hyperoxia-induced injury, as well as increased susceptibility to toxic xenobiotic, including carcinogens 4,5 .…”

Carotenoids in Cancer Apoptosis—The Road from Bench to Bedside and Back

“…Also, β-carotene induced increase in ROS and caspase-3 activity that may reduce the level of DNA repair Ku proteins resulting in the apoptosis of AGS gastric cancer cells [ 128 ]. On the contrary, β-carotene pre-treatment exerted antioxidant effects against oxidative stress in K562 human erythromyeloblastoid leukemia cells protecting them against the damage by oxidative stress [ 129 ].…”