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Fig. 1 · Structure
Cat. No.
A10128
CAS No.
7235-40-7
Formula
C40H56
Mol. Weight
536.87

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Beta Carotene

Cat. No. A10128 CAS 7235-40-7
Beta Carotene is a strongly-coloured red-orange pigment abundant in plants and fruits. It is a precursor (inactive form) of vitamin A.

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Biological Activity

Bioactivity / Mechanism

Beta-carotene is a substrate for human BCO1-mediated cleavage to retinal. Reciprocal oxygen-isotope experiments with purified enzyme support a dioxygenase mechanism: the product oxygen originates from molecular oxygen. Retinal-water exchange controls were essential to this interpretation. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
Human Endogenous Metabolite  
apoptosis  

Cellular Effect

Cell Line Activity Value Description Reference
Raji IC50 12.7 nM Inhibition of TPA-induced Epstein-Barr virus early antigen activation in Raji cells after 48 hrs [PMID: 17503850]

In Vitro Studies

In mature mouse NIH 3T3-L1 adipocytes, beta-carotene (2 μM, 24 h) reduced triglyceride content, whereas all-trans-retinol did not reproduce the response. Fenretinide co-treatment largely prevented the decrease. Chromatography and mass spectrometry identified retinoic acid in beta-carotene-treated cells, supporting a metabolic contribution to the response. [2]

Oxygen-isotope tracing of human BCO1 cleavage

Biochemical assay · Purified recombinant human BCO1; reciprocal oxygen-isotope reaction media with retinal exchange controls [1]

The retinal isotope pattern followed molecular oxygen. Parallel retinal incubations accounted for exchange with water, supporting a dioxygenase mechanism for central beta-carotene cleavage.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Percentage of 18O-retinal in reciprocal isotope media18O-retinal fraction 16O2/H2-18O: 3, 6, 10%; 18O2/H2-16O: 79, 85%[1]
Retinal-water isotope exchange in active-enzyme control mixturesreported result 16O-retinal in H2-18O: 5, 7, 13% 18O-retinal; initially 91% 18O-retinal in H2-16O: 67, 84% 18O-retinal[1]
Effect of prolonged incubation on retinal labelingreported result 7.5 h in 16O2/H2-18O yielded 50% 18O-retinal[1]

Literature-Reported Treatment Conditions

Treatment concentration
20 μM beta-carotene; purified human BCO1 10 μg/200 μL
Exposure duration
15 min at 37 °C; a separate 7.5 h incubation tested exchange artifact
Method
Cell-free enzyme reaction followed by LC-MS/MS isotope quantification
Vehicle
Aqueous Tricine-KOH reaction buffer with sodium cholate; beta-carotene substrate solution contained Tween 40 and alpha-tocopherol
Co-treatment
Alpha-tocopherol present in substrate preparation; not a standalone antioxidant assay
Reported limits
Isomer-resolved beta-carotene purity was not specified in Chemicals; no Adooq material was tested.
Methods and source locations

Compound reported in the paper: Beta Carotene; Compound label in the paper: Sigma-Aldrich beta-carotene (≥97%)

Evidence concerns the reported beta-carotene material and model. Isomer-resolved purity and equivalence to an Adooq lot are not established.

Experimental Procedures: Chemicals, In Vitro BCO1 Activity Assays and Control Experiments; Results; Figure 1C and Figure 2 caption

Percentage of 18O-retinal in reciprocal isotope media: LC-MS/MS; individual experiments performed on different days, not means ± error. Three reactions in 16O2/H2-18O and two in 18O2/H2-16O (limited 18O2 supply). — Figure 1C; Results paragraphs 1–4; Figure 2 caption

Retinal-water isotope exchange in active-enzyme control mixtures: Matched retinal incubations; individual experiments, not means ± error. These controls explain minority isotope labeling. — Figure 1C; Results; Experimental Procedures: Control Experiments

Effect of prolonged incubation on retinal labeling: LC-MS/MS; text-reported value. This demonstrates a labeling artifact from exchange; it is not evidence for a second enzyme mechanism. — Results paragraph beginning We also performed the BCO1-β-carotene incubation

Beta-carotene treatment of mature adipocytes with metabolic controls

Cell-based study · Differentiated mouse NIH 3T3-L1 adipocytes treated on day 5 [2]

Beta-carotene lowered cellular triglyceride content relative to vehicle and all-trans-retinol controls. Fenretinide co-treatment largely prevented this response. Retinoic acid was identified in beta-carotene-treated cells by chromatography and tandem mass spectrometry; retinol-treated cells instead accumulated retinol/retinyl esters.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cellular triglyceride content after beta-carotene versus vehicle or retinol treatmentfold reduction Reported 2.7-fold reduction after beta-carotene; retinol did not reproduce the decrease[2]
Effect of fenretinide co-treatment on beta-carotene-induced lipid reductionreported result Largely prevented by fenretinide; fenretinide alone did not lower triglyceride content[2]
Identity and differential production of retinoic acidreported result Retinoic acid detected after beta-carotene; reduced with fenretinide; below detection after retinol treatment[2]

Literature-Reported Treatment Conditions

Treatment concentration
2 μM beta-carotene; comparator all-trans-retinol 2 μM; beta-carotene plus fenretinide 2 μM each, with fenretinide-only control
Exposure duration
24 h
Method
Treatment of differentiated cells, followed by triglyceride assay, Oil Red-O imaging and retinoid HPLC/LC-MS analysis
Vehicle
Tetrahydrofuran; final solvent concentration 0.1% (v/v), with vehicle-matched control
Co-treatment
Single beta-carotene exposure distinguished from beta-carotene + fenretinide mechanistic co-treatment
Reported limits
Beta-carotene isomer-resolved composition and purity were not specified. Replicate descriptions in lipid-assay methods and figure legends are not fully reconciled.
Methods and source locations

Compound reported in the paper: Beta Carotene; Compound label in the paper: Beta,beta-carotene supplied by Wild (Germany)

Evidence concerns the reported beta-carotene material and model. Isomer-resolved purity and equivalence to an Adooq lot are not established.

Experimental Procedures: Cell Culture, Triacylglycerol Accumulation Assay and Extraction of BC and Retinoids; Results: BC but Not ROL Decreases Lipid Content, Fenretinide Selectively Inhibits BC Effects, BC but Not ROL Is Converted to RA; Figures 1C–D, 2C–D and 3

Cellular triglyceride content after beta-carotene versus vehicle or retinol treatment: Triglyceride assay; Figure 1D reports SD and n=3 per condition, with *p<0.001 by two-tailed Student t test. Methods separately describe two repeats with at least four replicates per condition; biological versus technical allocation is not fully specified. — Results: BC but Not ROL Decreases Lipid Content; Figure 1C–D and caption

Effect of fenretinide co-treatment on beta-carotene-induced lipid reduction: Oil Red-O imaging and triglyceride assay; Figure 2D reports SD, n=3 per condition. Qualitative result; no bar-derived decimals. — Results: Fenretinide Selectively Inhibits BC Effects; Figure 2C–D and caption

Identity and differential production of retinoic acid: HPLC/spectral comparison and LC-MS/MS: RA [MH]+ at m/z=301 with fragmentation consistent with standard. Below detection is not zero. No concentration/error estimate extracted. — Results: BC but Not ROL Is Converted to RA; Figure 3A–D and caption

In Vivo Studies

Dietary beta-carotene (150 mg/kg diet for 14 weeks) reduced the dissected-fat-pad adiposity index by a reported 28% in female wild-type mice. The response was absent in Bcmo1-null mice, and supplementation did not change final body weight. The study used formulated beadlets with matched excipient controls and does not establish an equivalent effect for an Adooq lot. [3]

Dietary beta-carotene and Bcmo1-dependent adiposity

Animal study · Female wild-type and Bcmo1-null mice on C57BL/6;129Svj backgrounds; n=6/group [3]

A diet containing beta-carotene reduced the dissected-white-adipose-tissue adiposity index in wild-type mice by a reported 28%; the response was absent in Bcmo1-null mice. Final body weight was not changed by supplementation. This supports a requirement for Bcmo1 in this dietary model, rather than universal weight loss.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Adiposity index: combined inguinal, gonadal and retroperitoneal WAT mass as percentage of body weightrelative reduction 28% reduction in supplemented WT mice (text: p<0.01); no corresponding reduction in Bcmo1-null mice[3]
Final body weight, energy intake and energy efficiencyreported result Final body weight comparable among groups (reported data not shown); cumulative energy intake higher with BC diet; energy efficiency similar[3]

Conditions shared by the study groups

Route
Oral, incorporated in diet
Frequency
Ad libitum dietary access
Treatment course
14 weeks, beginning at 5 weeks of age
Vehicle
Water-soluble beadlets incorporated by cold extrusion into defined pelletized diet
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Wild-type beta-carotene versus matched diet
150 mg beta-carotene/kg diet		Wild-type mice receiving otherwise matched diet with beta-carotene-free beadletsAdiposity index reduced by reported 28%; inguinal adipocyte area lower; final body weight not changed.[3]
Bcmo1-null beta-carotene versus matched diet
150 mg beta-carotene/kg diet		Bcmo1-null mice receiving otherwise matched diet with beta-carotene-free beadletsNo adiposity-index reduction corresponding to the wild-type response; no final-body-weight effect.[3]
Wild-type beta-carotene versus matched diet
Model: 5-week-old female wild-type C57BL/6;129Svj mice; n=6/group
Reported limits: Isomer-resolved purity and actual daily beta-carotene intake per animal not established; 150 mg/kg is feed concentration, not mg/kg body weight.
Bcmo1-null beta-carotene versus matched diet
Model: 5-week-old female C57BL/6;129Svj-Bcmo1tm1Dnp mice; n=6/group
Reported limits: Isomer-resolved purity and actual daily beta-carotene intake per animal not established; 150 mg/kg is feed concentration, not mg/kg body weight.
Methods and source locations

Compound reported in the paper: Beta Carotene; Compound label in the paper: DSM beta-carotene beadlet formulation

Evidence concerns the reported beta-carotene material and model. Isomer-resolved purity and equivalence to an Adooq lot are not established.

Materials and Methods: Animals and diets; Results: Dietary BC reduces adiposity in WT mice; Figure 3A–G and caption

Adiposity index: combined inguinal, gonadal and retroperitoneal WAT mass as percentage of body weight: Dissected fat-pad mass; Figure 3A–E: mean ± SEM, n=6/group. The legend defines its star at p<0.05; p<0.01 is the Results prose, not a value inferred from the plot. — Results: Dietary BC reduces adiposity in WT mice; Figure 3D–G and caption

Final body weight, energy intake and energy efficiency: Body weight and per-cage food intake monitored twice weekly. Figure 3A–C shows mean ± SEM, n=6 animals/group; cage clustering limits interpretation of intake replication. — Results: Dietary BC reduces adiposity in WT mice; Figure 3A–C and caption

Wild-type beta-carotene versus matched diet · Materials and Methods: Animals and diets; Results: Dietary BC reduces adiposity in WT mice; Figure 3A–G and caption

Bcmo1-null beta-carotene versus matched diet · Materials and Methods: Animals and diets; Results: Dietary BC reduces adiposity in WT mice; Figure 3A–G and caption

Specifications

Manufacturer Adooq Bioscience
CAS Number 7235-40-7
Formula C40H56
Molecular Weight 536.87
SMILES
CC1=C(C(CCC1)(C)C)/C=C/C(=C/C=C/C(=C/C=C/C=C(/C=C/C=C(/C=C/C2=C(CCCC2(C)C)C)\C)\C)/C)/C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Warmed: 4 mg/mL (7.45 mM)
Water Insoluble
Ethanol Warmed: 5 mg/mL (9.31 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Carlo dela Seña, Kenneth M Riedl, Sureshbabu Narayanasamy, et al. The Human Enzyme That Converts Dietary Provitamin A Carotenoids to Vitamin A Is a Dioxygenase Journal of Biological Chemistry (2014). PMID: 24668807 DOI: 10.1074/jbc.M114.557710 Source material
  2. [2] Glenn P Lobo, Jaume Amengual, Hua Nan M Li, et al. β,β-Carotene Decreases Peroxisome Proliferator Receptor γ Activity and Reduces Lipid Storage Capacity of Adipocytes in a β,β-Carotene Oxygenase 1-dependent Manner Journal of Biological Chemistry (2010). PMID: 20573961 DOI: 10.1074/jbc.M110.132571 Source material
  3. [3] Jaume Amengual, Erwan Gouranton, Yvonne G. J. van Helden, et al. Beta-Carotene Reduces Body Adiposity of Mice via BCMO1 PLOS ONE (2011). PMID: 21673813 DOI: 10.1371/journal.pone.0020644 Source material

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