PPARγ; PPARα; UCP1; SOD; iNOS; Caspase 3/8/9;ERK2

This study explored the antitubercular properties of Fucoxanthin, a marine carotenoid, against clinical isolates of Mycobacterium tuberculosis (Mtb). Two vital enzymes involved in Mtb cell wall biosynthesis, UDP-galactopyranose mutase (UGM) and arylamine-N-acetyltransferase (TBNAT), were selected as drug targets to reveal the mechanism underlying the antitubercular effect of fucoxanthin. The obtained results showed that fucoxanthin showed a clear bacteriostatic action against the all Mtb strains tested, with minimum inhibitory concentrations (MIC) ranging from 2.8 to 4.1 µM, along with a good degree of selectivity index (ranging from 6.1 to 8.9) based on cellular toxicity evaluation compared with standard drug isoniazid (INH). The potent inhibitory actions of fucoxanthin and standard uridine-5'-diphosphate against UGM were recorded to be 98.2% and 99.2%, respectively. TBNAT was potently inactivated by fucoxanthin (half maximal inhibitory concentration (IC50) = 4.8 µM; 99.1% inhibition) as compared to INH (IC50 = 5.9 µM; 97.4% inhibition). Further, molecular docking approaches were achieved to endorse and rationalize the biological findings along with envisaging structure-activity relationships. Since the clinical evidence of the last decade has confirmed the correlation between bacterial infections and autoimmune diseases, in this study we have discussed the linkage between infection with Mtb and autoimmune diseases based on previous clinical observations and animal studies. In conclusion, we propose that fucoxanthin could demonstrate great therapeutic value for the treatment of tuberculosis by acting on multiple targets through a bacteriostatic effect as well as by inhibiting UGM and TBNAT. Such outcomes may lead to avoiding or decreasing the susceptibility to autoimmune diseases associated with Mtb infection in a genetically susceptible host.[1]

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The fFucoxanthin IC50 was 1 445 and 1 641 µM (Hela and SiHa cells, respectively). Chip results revealed 2 255 DEGs, including 943 upregulated and 1 312 downregulated genes, in fucoxanthin-treated versus untreated SiHa cells. Disease and function analysis indicated that these DEGs are primarily associated with cancer and organismal injuries and abnormalities, and online integrated pathway analysis showed that the DEGs were mainly enriched in p53 signalling. HIST1H3D was significantly downregulated in response to fucoxanthin. Inhibition of HIST1H3D mRNA significantly reduced cell proliferation and colony formation, significantly augmented the percentage of apoptotic HeLa and SiHa cells, and cells were arrested in G0/G1 cell cycle phase. Conclusion: The results suggest that HIST1H3D may be an oncogene in cervical carcinogenesis and a potential fucoxanthin target in treating cervical cancer.[2]

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Fucoxanthin, a natural carotenoid prepared from brown algae, inhibited the growth of GOTO cells, a human neuroblastoma cell line. Fucoxanthin at 10 micrograms/ml reduced the growth rate of GOTO cells to 38% of the control at day 3 after drug treatment. Flowcytometric analysis revealed that fucoxanthin caused the arrest in the G0-G1 phase of cell cycle. Expression of N-myc gene was proved to be decreased by fucoxanthin as early as 4 h after treatment at 10 micrograms/ml and that may be important for the mechanism of anti-proliferative action of the carotenoid [3].

The aim of the present study was to investigate the efficacy of Fucoxanthin on endotoxin-induced uveitis (EIU) in rats. The effects of fucoxanthin on endotoxin-induced leucocyte and protein infiltration, nitric oxide (NO), prostaglandin (PG)-E2 and tumour necrosis factor (TNF)-alpha concentrations in rat aqueous humour, as well as on the cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) protein expression in a mouse macrophage cell line (RAW 264.7 cells) were studied. EIU was induced in male Lewis rats by a footpad injection of lipopolysaccharide (LPS). Immediately after the LPS injection, either 0.1, 1 or 10mgkg(-1) of fucoxanthin was injected intravenously. The aqueous humour was collected 24hr later from both eyes, and both the number of cells infiltrating into the aqueous humour and the aqueous humour protein concentration were measured. The levels of PGE2, NO and TNF-alpha were determined by enzyme-linked immunosorbent assay. The RAW 264.7 cells were pretreated with various concentrations of fucoxanthin for 24hr and subsequently incubated with LPS for 24hr. COX-2 and iNOS protein expression was analysed by the Western blotting method. Levels of PGE2, NO and TNF-alpha production were determined. Fucoxanthin suppressed the development of EIU in a dose-dependent fashion. Treatment with fucoxanthin resulted in a reduction in PGE2, NO and TNF-alpha concentrations in the aqueous humour. The expression of COX and iNOS protein in the fucoxanthin treated RAW264.7 cells decreased significantly compared to that the LPS group. It also significantly reduced the concentration of PGE2, NO and TNF-alpha production in the medium of cells. The present result indicate fucoxanthin suppresses the inflammation of EIU by blocking the iNOS and COX-2 protein expression and its anti-inflammatory effect on eye is comparable with the effect of predinisolone used in similar doses. [8]

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Renal Cadmium Levels Changes in the Kidney [9]
To assess the impacts of cadmium exposure in renal functions, we first detected the basic cadmium level in the kidney of the control group without CdCl2 administration. The results were observed to be only 5.28 ± 0.45 ng/mL in the control group (revised Table 2). The CdCl2 treatment, but no Fucoxanthin as a negative control group (NCG), significantly increased renal cadmium levels (P < 0.05). Treatment with Shenfukang tablets as a positive control greatly decreased the renal cadmium level compared with those in the NCG and 10 (F1) mg/kg bw/day fucoxanthin treatment group (P < 0.05). In contrast, treatments with 25 (F2) and 50 (F3) mg/kg bw/day fucoxanthin blocked the Cd-induced increase in the cadmium level (P < 0.05, compared with the NCG), whereas the renal cadmium levels in the F2 and F3 groups were significantly lower than that of the PCG (P < 0.05). These results indicated that the supplementation with fucoxanthin at 25 or 50 mg/kg bw/day promoted the renal cadmium metabolism, with better amelioration against Cd accumulation than that of the Shenfukang tablets.

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Changes in Levels of Kidney Injury Markersy [9]
To explore the molecular mechanisms of these physiological changes, we investigated kidney injury relevant biomarkers (revised Table 3). The result showed that the plasma BUN, KIM-1, and NGAL levels of in the CdCl2 treated group (NCG) were significantly increased than that in no CdCl2 treated control group (P < 0.05). Shenfukang tablets (PCG), 25 (F2) and 50 (F3) mg/kg bw/day of Fucoxanthin significantly decreased the BUN levels in comparison with that in the NCG (P < 0.05). BUN levels in F2 group, F3 group and PCG group were not significantly different from those in the control group (P > 0.05). Shenfukang tablets and fucoxanthin treatments significantly decreased the KIM-1 level in comparison to the NCG (P < 0.05). The KIM-1 level in the F2 group was not significantly different from that in the control group (P > 0.05), indicating that the 25 mg/kg bw/day of fucoxanthin supplementation could decrease the KIM-1 level toward normal value. Shenfukang tablets and fucoxanthin treatments significantly decreased the NGAL levels in comparison with those in the NCG (P < 0.05). The NGAL level in the PCG group was not significantly different from that in the control group (P > 0.05), indicating that the Shenfukang tablets supplementation could decrease the NGAL level toward normal value.

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Effects of Fucoxanthin on Antioxidant in CdCl2-treated Micey [9]
To assess the roles of Fucoxanthin in anti-oxidative stress, we detected a few key enzyme levels in lipid peroxidation pathways. Activities of renal POD, SOD, CAT, and APX in the NCG mice were significantly decreased, compared with those in the control group (P < 0.05). Fucoxanthin and Shenfukang tablets treatments significantly improved redox states compared with that in mice of the NCG. Mice treated with middle (F2) and high (F3) concentrations of fucoxanthin administration showed significant improvement in POD, SOD, CAT and APX activities compared to the control group. There were no significant differences in renal CAT and APX activities between the PCG and NCG (P > 0.05). In the F2 and F3 groups, the renal CAT activity was significantly higher than that of NCG (P < 0.05), and there was no significant difference compared with the control group (P > 0.05). The renal APX activity in the F2 and F3 groups was significantly higher than that of NCG (P < 0.05), but in F3, there was no significant difference compared with the control group (P > 0.05), indicating that 25 and 50 mg/kg bw/day of fucoxanthin treatment exerted a better effect in increasing CAT and APX activities than Shenfukang tablets (Figure 6).

UGM Activity [4]
UGM activity was accomplished as previously specified. Fucoxanthin and the standard UGM inhibitor uridine-5’-diphosphate were prepared in DMSO (DMSO 2% (v/v) was used in all performed reactions). Concisely, UGM (25 µg/mL) prepared in a buffer (100 mM of 3-(N-morpholino) propanesulfonic acid (MOPS); pH = 8.0) was pre-incubated with Na2S2O3 (20 mM) on ice for 1 min. Further, the solution mixture was incubated with the test inhibitors (20 mM) followed by adding the substrate UDP-Galf (60 µM) at 25 °C. Subsequently, the reactions were stopped at various times by adding ice-cold HCl and directly subjected to quick freezing in liquid nitrogen. The activity of UGM in the presence of 2% (v/v) DMSO was considered a control. A high performance liquid chromatography (HPLC) system was applied to monitor UGM activity, where all instrumental setup and operational requirements were tracked according to the detailed procedures. The degree of conversion was measured throughout the comparison of the integration of substrate and product peaks.

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TBNAT Activity [4]
Microplate photometer-based assay was subjected to determine TBNAT-catalyzed reaction with slight refinement. TBNAT activity was detected by monitoring the rate of hydrolysis of acetyl coenzyme A (AcCoA) through detection with 5,5′-dithio-bis(2-nitrobenzoic acid) (DTNB), and the absorbance was recorded at 405 nm. To sum up, the test molecules (Fucoxanthin and standard INH) were prepared and dissolved in DMSO and all reactions were processed in the presence of DMSO (2%; v/v). TBNAT (170 ng; prepared in 20 mM Tris-HCl (pH = 8) mixed with dithiothreitol (1 mM) and 5% glycerol) was incubated with test compounds (5 µL at final concentrations ranging from 10 to 20 µM) for 15 min at 25 °C. Further, 15 µL of a substrate hydralazine (30 µM) and 12 µL of acetyl CoA (30 µM) were blended with the obtained mixture solution. Subsequently, the reaction was stopped by utilizing 25 µL of DTNB (processed in guanidine-HCl (6.4 M) and Tris-HCl (100 mM) with pH = 7.3) after 10 min at 25 °C and the enzyme activity was achieved as an end-point readout analysis. The TBNAT-catalyzed reaction (no inhibition) was assigned as a control. The % inhibition was ascertained as the ratio of enzyme activity (expressed as the rate of CoA formation with test molecules) to the activity of the control without inhibition. The inhibitory curves which were obtained by non-linear fitting of the % inhibition and the logarithmic concentration of the inhibitor versus the response were used to assess IC50 values.

Assessment of Minimum Inhibitory Concentration (MIC) [4]
Minimum inhibitory concentration of Fucoxanthin and INH was assessed by microdilution assay as previously described in CLSI guideline. The negative controls were assigned to be dimethyl sulfoxide (DMSO) and the broth. Here, 1% DMSO was employed to dissolve and dilute the test compounds and further mixed with broth (25 µL of DMSO solution in 5 mL of broth). The used 1% of DMSO had no effect on the growth of Mtb. Final concentrations of test substances in wells ranged from 2.8 to 6.2 µM. After 24 h of incubation, the results were registered and represented as minimal inhibitory concentration (MIC) at a micromolar scale that impeded the blue to pink color change.

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Cellular Toxicity Analysis [4]
Cell Lines and Culture Requirements [4]
Normal human fetal lung fibroblast cells were cultured in Minimum Essential Eagle Medium MEM supplemented with 10% fetal bovine serum, 2 mM L-glutamine solution, and 1% non-essential amino acid solution, in a humidified state with 5% CO2 at 37 °C. Subsequently, for subculture the cells were collected after treatment with trypsin/EDTA at 37 °C.

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Cytotoxicity Assessment [4]
The potential cytotoxicity of Fucoxanthin and INH was assessed using a CellTiter‒96 assay. This assay is based on the reduction of tetrazolium dye MTS in living cells to formazan, which is then ascertained colorimetrically following the hitherto reported procedure. The MRC-5 cells treated with the test compounds were applied as investigational groups, whereas untreated MRC-5 cells acted as control groups. The absorbance of test samples was detected at 490 nm and the inhibitory curves were assembled for each compound, using incubation concentrations vs. percentage of absorbance relative to untreated control. The half maximal inhibitory concentration (IC50) was ascertained by a nonlinear regression analysis of the inhibitory curves. The statistical analyses were aided by PRISM software.

Animals groups and EIU [8]
Eight-week-old male Lewis rats were used. The rats weighed about 250 g. EIU was induced by injection into one footpad of 200 μg of LPS from Salmonella typhimurium that had been diluted in 0.2 ml of saline. The rats were injected intravenously with 0.1, 1 or 10 mg kg−1 Fucoxanthin or 10 mg kg−1 prednisolone in a 0.1% dimethyl sulfoxide solution (Sigma, St. Louis, MO) mixed with 0.1 ml phosphate-buffered saline (PBS). Fucoxanthin was isolated from brown algae using a previously published method (Britton, 1995). Fucoxanthin was administered three times; simultaneously and 30 min before and after the LPS injection. For the LPS group, 0.1% dimethyl sulfoxide of PBS was administered intravenously using the same schedule for the fucoxanthin-administered group. In the control group, neither LPS nor fucoxanthin was injected into the rats.

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Experimental Design [9]
Total animals (N = 120) were randomly divided into two groups of equal average body weight. The mice of the control group (N = 20) were given pure water only, whereas the animals of the cadmium exposure group (N = 100) were given CdCl2 orally at a dose of 30 milligram (mg)/kilogram (kg) body weight (bw)/day for 30 days. In this study, Fucoxanthin was administered at 10, 25 and 50 mg/kg bw/day. To evaluate ameliorative effects of fucoxanthin on the kidney, the cadmium exposure group was divided into the following five subgroups: without fucoxanthin treatment as a negative control group (NCG, N = 20); positive control group (PCG, N = 20) was mice received Shenfukang tablets orally at a dose of 50 mg/kg bw/day for 14 days; low (F1), medium (F2), and high (F3) fucoxanthin concentration treated mice (N = 20 mice at each group) were received fucoxanthin orally at a dose of 10, 25, and 50 mg/kg bw/day for 14 days, respectively.

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Animal Sacrifice and Sample Collection [9]
After the 14-day Fucoxanthin treatment, mice were sacrificed. Kidney tissues and peripheral blood samples were collected directly. In each group, kidney samples of 14 mice were subsequently kept at −80°C in ultra cold storage freezer for analyses of cadmium concentration, antioxidant activity and relative gene expression; 3 mice were kept at 4°C in 10% neutral-buffered formalin for microscopic observation; and 3 mice were kept at 4°C in 2.5% neutral-buffered glutaraldehyde for electron microscope observation. As for the blood samples, they were added to the test tubes with anticoagulant, centrifuged for 5 minutes at a speed of 1372 g, and the upper plasma was collected for analysis of kidney damage.

[1]. Anti-obesity activity of the marine carotenoid fucoxanthin. Mar Drugs. 2015 Apr 13;13(4):2196-214.

[2]. Fucoxanthin, a Marine-Derived Carotenoid from Brown Seaweeds and Microalgae: A Promising Bioactive Compound for Cancer Therapy. Int J Mol Sci. 2020;21(23):9273.

[3]. In Vivo and in Vitro Toxicity Studies of Fucoxanthin, a Marine Carotenoid. null. 2011;0 (0):319-328.

[4]. A Microbiological, Toxicological, and Biochemical Study of the Effects of Fucoxanthin, a Marine Carotenoid, on Mycobacterium tuberculosis and the Enzymes Implicated in Its Cell Wall: A Link Between Mycobacterial Infection and Autoimmune Diseases. Mar Drugs. 2019 Nov 14;17(11):641.

[5]. Fucoxanthin may inhibit cervical cancer cell proliferation via downregulation of HIST1H3D. J Int Med Res. 2020 Oct;48(10):300060520964011.

[6]. Inhibitory effects of fucoxanthin, a natural carotenoid, on N-myc expression and cell cycle progression in human malignant tumor cells. Cancer Lett. 1990 Nov 19;55(1):75-81.

[7]. Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol. Int J Cancer. 2008 Dec 1;123(11):2702-12.

[8]. Effects of fucoxanthin on lipopolysaccharide-induced inflammation in vitro and in vivo. Exp Eye Res. 2005 Oct;81(4):422-8.

[9]. Role of Fucoxanthin towards Cadmium-induced renal impairment with the antioxidant and anti-lipid peroxide activities. Bioengineered. 2021 Dec;12(1):7235-7247.

Fucoxanthin is an epoxycarotenol that is found in brown seaweed and which exhibits anti-cancer, anti-diabetic, anti-oxidative and neuroprotective properties. It has a role as an algal metabolite, a CFTR potentiator, a food antioxidant, a neuroprotective agent, a hypoglycemic agent, an apoptosis inhibitor, a hepatoprotective agent, a marine metabolite and a plant metabolite. It is an epoxycarotenol, an acetate ester, a secondary alcohol, a tertiary alcohol and a member of allenes.
Fucoxanthin is under investigation in clinical trial NCT03613740 (Effect of Fucoxanthin on the Components of the Metabolic Syndrome, Insulin Sensitivity and Insulin Secretion). Fucoxanthin isis a marine carotenoid mainly found in brown algae, giving them a brown or olive-green color. Fucoxanthin is investigated for its anti-inflammatory, antinociceptive and anti-cancer effects. In vivo studies have demonstrated that oral administration of fucoxanthin inhibited carcinogenesis in an animal model of duodenal, skin, colon and liver cancer. Fucoxanthin causes antitumor and anticarcinogenic effects by inducing G1 cell-cycle arrest and apoptosis by modulating expression of various cellular molecules and cellular signal transduction pathways, but the exact mechanism of anti-cancer action of fucoxanthin is not fully elucidated. Fucoxanthin regulates lipids metabolism, the effect most likely mediated by AMK-activated protein kinase. A clinical trial of fucoxanthin against non-alcoholic fatty liver disease is ongoing.
Fucoxanthin has been reported in Jania, Corbicula sandai, and other organisms with data available.

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Objective: To investigate the role of fucoxanthin, reported to have significant anticancer effects, and histone Cluster 1 H3 Family Member D (HIST1H3D; implicated in tumorigenesis) in cervical cancer. Methods: The half maximal inhibitory concentration (IC50) of fucoxanthin against HeLa and SiHa cervical cancer cells was determined. Differentially expressed genes (DEGs) in SiHa cells treated with IC50 fucoxanthin were screened by high-throughput techniques and subjected to signal enrichment. Following identification of HIST1H3D as a candidate gene, HIST1H3D-knockdown models were created via transfection with a short hairpin HIST1H3D payload. Impacts on cell proliferation, cell-cycle distribution, colony formation, and apoptosis were studied. Results: The fucoxanthin IC50 was 1 445 and 1 641 µM (Hela and SiHa cells, respectively). Chip results revealed 2 255 DEGs, including 943 upregulated and 1 312 downregulated genes, in fucoxanthin-treated versus untreated SiHa cells. Disease and function analysis indicated that these DEGs are primarily associated with cancer and organismal injuries and abnormalities, and online integrated pathway analysis showed that the DEGs were mainly enriched in p53 signalling. HIST1H3D was significantly downregulated in response to fucoxanthin. Inhibition of HIST1H3D mRNA significantly reduced cell proliferation and colony formation, significantly augmented the percentage of apoptotic HeLa and SiHa cells, and cells were arrested in G0/G1 cell cycle phase.[5]

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Fucoxanthin, a natural carotenoid prepared from brown algae, inhibited the growth of GOTO cells, a human neuroblastoma cell line. Fucoxanthin at 10 micrograms/ml reduced the growth rate of GOTO cells to 38% of the control at day 3 after drug treatment. Flowcytometric analysis revealed that fucoxanthin caused the arrest in the G0-G1 phase of cell cycle. Expression of N-myc gene was proved to be decreased by fucoxanthin as early as 4 h after treatment at 10 micrograms/ml and that may be important for the mechanism of anti-proliferative action of the carotenoid. [6]

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Adult T-cell leukemia (ATL) is a fatal malignancy of T lymphocytes caused by human T-cell leukemia virus type 1 (HTLV-1) infection and remains incurable. Carotenoids are a family of natural pigments and have several biological functions. Among carotenoids, fucoxanthin is known to have antitumorigenic activity, but the precise mechanism of action is not elucidated. We evaluated the anti-ATL effects of fucoxanthin and its metabolite, fucoxanthinol. Both carotenoids inhibited cell viability of HTLV-1-infected T-cell lines and ATL cells, and fucoxanthinol was approximately twice more potent than fucoxanthin. In contrast, other carotenoids, beta-carotene and astaxanthin, had mild inhibitory effects on HTLV-1-infected T-cell lines. Importantly, uninfected cell lines and normal peripheral blood mononuclear cells were resistant to fucoxanthin and fucoxanthinol. Both carotenoids induced cell cycle arrest during G(1) phase by reducing the expression of cyclin D1, cyclin D2, CDK4 and CDK6, and inducing the expression of GADD45alpha, and induced apoptosis by reducing the expression of Bcl-2, XIAP, cIAP2 and survivin. The induced apoptosis was associated with activation of caspase-3, -8 and -9. Fucoxanthin and fucoxanthinol also suppressed IkappaBalpha phosphorylation and JunD expression, resulting in inactivation of nuclear factor-kappaB and activator protein-1. Mice with severe combined immunodeficiency harboring tumors induced by inoculation of HTLV-1-infected T cells responded to treatment with fucoxanthinol with suppression of tumor growth, showed extensive tissue distribution of fucoxanthinol, and the presence of therapeutically effective serum concentrations of fucoxanthinol. Our preclinical data suggest that fucoxanthin and fucoxanthinol could be potentially useful therapeutic agents for patients with ATL.[7]

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Kidney damages caused by cadmium are considered to be one of the most dangerous consequences for the human body. This study aimed to investigate the protective effects of fucoxanthin supplementation on mice models subjected to cadmium-induced kidney damage. The mice treated with cadmium chloride (CdCl2) were observed to have significantly reduced the cross-section area of glomeruli. Cadmium exposure has also caused the damage of the structural integrity of mitochondria and increased blood urea nitrogen (BUN), kidney injury molecule 1 (KIM1), and neutrophil gelatinase associated lipocalin (NGAL) levels. Peroxidase (POD), superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) levels in cadmium-exposed mice were markedly declined. Caspase3, caspase8, and caspase9 gene expressions in association with apoptosis were dramatically elevated in renal tissues. The CdCl2 treated mice were orally administered with 50 mg/kg Shenfukang, 10 mg/kg, 25 mg/kg, and 50 mg/kg fucoxanthin for 14 days. The results revealed that high doses of fucoxanthin administration significantly decreased BUN, KIM1, NGAL levels, increasing POD, SOD, CAT, and ascorbate APX levels. Fucoxanthin administration also promoted recovery of the renal functions, micro-structural organization, and ultra-structural organization in the renal cells. In summary, the ameliorative effects of fucoxanthin supplementation against cadmium-induced kidney damage were mediated via inhibiting oxidative stress and apoptosis, promoting the recovery of structural integrity of mitochondria. [9]

C42H58O6

658.92

676.433

C, 76.56; H, 8.87; O, 14.57

3351-86-8

5281239

Pink to red solid powder

1.1±0.1 g/cm3

786.5±60.0 °C at 760 mmHg

166-168ºC

228.5±26.4 °C

0.0±6.2 mmHg at 25°C

1.563

7.7

2

6

12

48

1530

5

O=C(/C(C)=C/C=C/C(C)=C/C=C/C=C(C)/C=C/C=C(C)/C([H])=[C@@]=C([C@@]1(O)C)C(C)(C[C@H](OC(C)=O)C1)C)C[C@]2(C3(C)C)[C@@](C)(C[C@@H](O)C3)O2

InChI=1S/C42H58O6/c1-29(18-14-19-31(3)22-23-37-38(6,7)26-35(47-33(5)43)27-40(37,10)46)16-12-13-17-30(2)20-15-21-32(4)36(45)28-42-39(8,9)24-34(44)25-41(42,11)48-42/h12-22,34-35,44,46H,24-28H2,1-11H3/b13-12+,18-14+,20-15+,29-16+,30-17+,31-19+,32-21+/t23?,34-,35-,40+,41+,42-/m0/s1

InChI=1S/C42H58O6/c1-29(18-14-19-31(3)22-23-37-38(6,7)26-35(47-33(5)43)27-40(37,10)46)16-12-13-17-30(2)20-15-21-32(4)36(45)28-42-39(8,9)24-34(44)25-41(42,11)48-42/h12-22,34-35,44,46H,24-28H2,1-11H3/b13-12+,18-14+,20-15+,29-16+,30-17+,31-19+,32-21+/t23?,34-,35-,40+,41+,42-/m0/s1

C/C(=C\C=C\C=C(/C)\C=C\C=C(/C)\C(=O)C[C@]12[C@](O1)(C[C@H](CC2(C)C)O)C)/C=C/C=C(\C)/C=C=C3[C@](C[C@H](CC3(C)C)OC(=O)C)(C)O

α-Carotene; 3351-86-8; all-trans-Fucoxanthin; CCRIS 4055; Sebatrol; 06O0TC0VSM; BRN 0073179; CHEBI:5186; Fucoxanthin

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~12.5 mg/mL (~18.97 mM)

Solubility in Formulation 1: 1.25 mg/mL (1.90 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)