Identification of β-carotene oxidation products produced by bleaching clay using UPLC-ESI-MS/MS

The influence of 11 kinds of oxygen-containing sulfur flavor molecules was examined on β-carotene stability under UVA irradiation in ethanol system. Both the effects of sulfides on dynamic degradation of β-carotene and the relation between structure and effect were investigated. The oxidation products of β-carotene accelerated by sulfides under UVA irradiation were also identified. The results indicated that the disulfides had more obvious accelerative effects on the photodegradation of β-carotene than mono sulfides. The degradation of β-carotene after methyl (2-methyl-3-furyl) disulfide (MMFDS), methyl furfuryl disulfide (MFDS) and bis(2-methyl-3-furyl) disulfide (BMFDS) exposure followed first-order kinetics. Furan-containing sulfides such as MMFDS and BMFDS showed more pronounced accelerative effects than their corresponding isomers. The oxidation products were identified as 13-cis-β-carotene, 9,13-di-cis-β-carotene and all-trans-5,6-epoxy-β-carotene. These results suggest that both the sulfur atom numbers and the furan group in oxygen-containing sulfides play a critical role in the photooxidation of β-carotene.

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Isolation and Structure Determination of Echinochrome A Oxidative Degradation Products

Molecules ◽

10.3390/molecules25204778 ◽

2020 ◽

Vol 25 (20) ◽

pp. 4778

Author(s):

Natalia P. Mishchenko ◽

Elena A. Vasileva ◽

Andrey V. Gerasimenko ◽

Valeriya P. Grigorchuk ◽

Pavel S. Dmitrenok ◽

...

Keyword(s):

Mass Spectrometry ◽

Degradation Products ◽

Lethal Dose ◽

Oxidative Degradation ◽

Degradation Process ◽

Oxidation Products ◽

Chemical Mechanism ◽

Ionization Mass ◽

Echinochrome A ◽

Esi Ms

Echinochrome A (Ech A, 1) is one of the main pigments of several sea urchin species and is registered in the Russian pharmacopeia as an active drug substance (Histochrome®), used in the fields of cardiology and ophthalmology. In this study, Ech A degradation products formed during oxidation by O2 in air-equilibrated aqueous solutions were identified, isolated, and structurally characterized. An HPLC method coupled with diode-array detection (DAD) and mass spectrometry (MS) was developed and validated to monitor the Ech A degradation process and identify the appearing compounds. Five primary oxidation products were detected and their structures were proposed on the basis of high-resolution electrospray ionization mass spectrometry (HR-ESI-MS) as 7-ethyl-2,2,3,3,5,7,8-heptahydroxy-2,3-dihydro-1,4-naphthoquinone (2), 6-ethyl-5,7,8-trihydroxy-1,2,3,4-tetrahydronaphthalene-1,2,3,4-tetraone (3), 2,3-epoxy-7-ethyl-2,3-dihydro-2,3,5,6,8-pentahydroxy-1,4-naphthoquinone (4), 2,3,4,5,7-pentahydroxy-6-ethylinden-1-one (5), and 2,2,4,5,7-pentahydroxy-6-ethylindane-1,3-dione (6). Three novel oxidation products were isolated, and NMR and HR-ESI-MS methods were used to establish their structures as 4-ethyl-3,5,6-trihydroxy-2-oxalobenzoic acid (7), 4-ethyl-2-formyl-3,5,6-trihydroxybenzoic acid (8), and 4-ethyl-2,3,5-trihydroxybenzoic acid (9). The known compound 3-ethyl-2,5-dihydroxy-1,4-benzoquinone (10) was isolated along with products 7–9. Compound 7 turned out to be unstable; its anhydro derivative 11 was obtained in two crystal forms, the structure of which was elucidated using X-ray crystallography as 7-ethyl-5,6-dihydroxy-2,3-dioxo-2,3-dihydrobenzofuran-4-carboxylic acid and named echinolactone. The chemical mechanism of Ech A oxidative degradation is proposed. The in silico toxicity of Ech A and its degradation products 2 and 7–10 were predicted using the ProTox-II webserver. The predicted median lethal dose (LD50) value for product 2 was 221 mg/kg, and, for products 7–10, it appeared to be much lower (≥2000 mg/kg). For Ech A, the predicted toxicity and mutagenicity differed from our experimental data.

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Qualitative and quantitative comparison of the cytotoxic and apoptotic potential of phytosterol oxidation products with their corresponding cholesterol oxidation products

British Journal Of Nutrition ◽

10.1079/bjn20051500 ◽

2005 ◽

Vol 94 (3) ◽

pp. 443-451 ◽

Cited By ~ 79

Author(s):

Eileen Ryan ◽

Jay Chopra ◽

Florence McCarthy ◽

Anita R. Maguire ◽

Nora M. O'Brien

Keyword(s):

Cell Line ◽

Biological Effects ◽

Oxidation Products ◽

Cholesterol Oxidation ◽

Monocytic Cell ◽

Monocytic Cell Line ◽

Cholesterol Oxidation Products ◽

Phytosterol Oxidation Products ◽

Induced Apoptosis ◽

Β Carotene

Phytosterols contain an unsaturated ring structure and therefore are susceptible to oxidation under certain conditions. Whilst the cytotoxicity of the analogous cholesterol oxidation products (COP) has been well documented, the biological effects of phytosterol oxidation products (POP)have not yet been fully ascertained. The objective of the present study was to examine the cytotoxicity of β-sitosterol oxides and their corresponding COP in a human monocytic cell line (U937), a colonic adenocarcinoma cell line (CaCo-2) and a hepatoma liver cell line (HepG2). 7β-Hydroxysitosterol, 7-ketositosterol, sitosterol-3β,5α,6β-triol and a sitosterol-5α,6α-epoxide–sitosterol-5β,6β-epoxide (6:1) mixture were found to be cytotoxic to all three cell lines employed; the mode of cell death was by apoptosis in the U937 cell line and necrosis in the CaCo-2 and HepG2 cells. 7β-Hydroxysitosterol was the only β-sitosterol oxide to cause depletion in glutathione, indicating that POP-induced apoptosis may not be dependent on the generation of an oxidative stress. A further objective of this study was to assess the ability of the antioxidants α-tocopherol, γ-tocopherol and β-carotene to modulate POP-induced cytotoxicity in U937 cells. Whilst α/γ-tocopherol protected against 7β-hydroxycholesterol-induced apoptosis, they did not confer protection against 7β-hydroxysitosterol-or 7-ketositosterol-induced toxicity, indicating that perhaps COP provoke different apoptotic pathways than POP. β-Carotene did not protect against COP- or POP-induced toxicity. In general, results indicate that POP have qualitatively similar toxic effects to COP. However, higher concentrations of POP are required to elicit comparable levels of toxicity.

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