zeaxanthin and Neuroblastoma

Goji berry has recently been introduced in Mediterranean diet and its consumption is increasing. This study aims to determine cytoprotection of lutein (LUT), zeaxanthin (ZEAX) and goji berry extract (GBE) rich in carotenoids against Beauvericin (BEA)-induced cytotoxicity on SH-SY5Y neuroblastoma cells. Both carotenoids and GBE showed cytoprotective effects. Cytoprotection was evaluated by simultaneous combination of the two xanthophylls LUT and ZEAX with BEA, as well as using pre-treatment assays. The highest protective effect occurred in 16%, 24% and 12% respectively for LUT, ZEAX and LUT + ZEAX incubating simultaneously with BEA, while by pre-treatment assay LUT showed a cytoprotection effect over 30% and ZEAX alone or LUT + ZEAX promoted only a slight cytoprotection (<10%). Pre-treatment assays with GBE, showed a cytoprotection, between 3 and 20%, for BEA concentrations ranging from 0.1 to 6.25 μM, whereas no protective effect was observed when the cells were simultaneously incubated with GBE and BEA. Finally, by means of CI-isobologram method, the interaction between LUT, ZEAX and BEA were evaluated, and the results showed an synergism effect for almost all combinations tested. The data presented shows a option of using goji berries to potentially mitigate the toxicity of beauvericin eventually present in foods.

Topics: Carotenoids; Cell Line, Tumor; Cytoprotection; Depsipeptides; Humans; Lutein; Lycium; Neuroblastoma; Plant Extracts; Zeaxanthins

The purpose of this study was to evaluate the ability of the predominant carotenoids (lutein and zeaxanthin) of the macular pigment of the human retina, to protect SK-N-SH human neuroblastoma cells against DNA damage induced by different RNOS donors. Although astaxanthin has never been isolated from the human eye, it was included in this study because its structure is very close to that of lutein and zeaxanthin and because it affords protection from UV-light. DNA damage was induced by GSNO-MEE, a nitric oxide donor, by Na(2)N(2)O(3), a nitroxyl anion donor and by SIN-1, a peroxynitrite-generating agent. DNA damage was assessed using the comet assay, a rapid and sensitive single cell gel electrophoresis technique able to detect primary DNA damage in individual cells. The tail moment parameter was used as an index of DNA damage. The values of tail moment increased in all the samples incubated with the RNOS donors, indicating DNA impairment. Data obtained show that the ability of zeaxanthin, lutein, and astaxanthin to reduce the DNA damage depends on the type of RNOS donor and the carotenoid concentration used. All the carotenoids studied were capable of protecting against DNA damage in neuroblastoma cells when the cells were exposed to GSNO-MEE. However, a different behaviour was present when the other two RNOS donors were used. The presence of a carotenoid alone (without an RNOS donor) did not cause DNA damage. Spectrophotometric studies showed that the order with which tested carotenoids reacted with RNOS was not always in agreement with the DNA protection results. The data from this study provides additional information on the activities of the macular pigment carotenoids of the human retina.

Topics: Comet Assay; DNA Damage; Dose-Response Relationship, Drug; Free Radical Scavengers; Humans; Lutein; Neuroblastoma; Reactive Nitrogen Species; Tumor Cells, Cultured; Xanthophylls; Zeaxanthins

In order to gain more knowledge about the antioxidant role of the predominant carotenoids (lutein and zeaxanthin) of the human retina, this study investigated their antioxidant activity and capacity. Astaxanthin was also studied, because its structure is very close to that of lutein and zeaxanthin. The antioxidant activity of these molecules was evaluated using chemiluminescence techniques, with lucigenin and luminol as chemiluminogenic probes for the superoxide radical and hydrogen peroxide, respectively. It was found that all three carotenoids have similar superoxide-scavenging activity. The effect on the reduction of H(2)O(2)-luminol chemiluminescence was present in the following order, zeaxanthin>astaxanthinlutein. Possible antioxidant capacity of these three compounds was sought using a biological system consisting of SK.N.SH human neuroblastoma and rat trachea epithelial cells subjected to oxidative stress from exposure to UVA radiation. In particular, we determined whether these compounds were capable of minimizing DNA damage and influencing the kinetics of DNA repair. DNA damage was assessed using the Comet assay, a rapid and sensitive single-cell gel electrophoresis technique used to detect primary DNA damage in individual cells. Neuroblastoma cells appeared more resistant to oxidative irradiation insult. The presence of carotenoids reduced DNA damage when rat epithelial cells were exposed to UVA radiation for 2min. A different result was obtained in experiments performed on neuroblastoma cells; in this case, the presence of carotenoid during UVA exposition increased the damage. The addition of carotenoids to epithelial cells after 2min of UVA exposition did not seem to improve the kinetics of DNA repair; on the contrary, zeaxanthin (after 60' incubation) and lutein (after 180' incubation) showed a genotoxic effect. The addition of carotenoids to neuroblastoma cells after 30' UVA exposition positively influences the kinetics of DNA repair in the first 15min of incubation. At longer exposition times, while the behaviour measured was not constant, a genotoxic effect was not observed. The data from this study provide additional information on the antioxidant and pro-oxidant activities of the predominant macular pigment carotenoids of the human retina.

Topics: Animals; Cells, Cultured; Comet Assay; DNA Damage; Dose-Response Relationship, Drug; Epithelial Cells; Female; Humans; Lutein; Male; Neuroblastoma; Rats; Rats, Wistar; Reactive Oxygen Species; Ultraviolet Rays; Xanthophylls; Zeaxanthins