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Biofortification of cassava with the provitamin A carotenoid β-carotene is a potential mechanism for alleviating vitamin A deficiency. Cassava is a staple food in the African diet, but data regarding the human bioavailability of β-carotene from this food are scarce. The objective of the present study was to evaluate provitamin A-enhanced cassava as a source of β-carotene and vitamin A for healthy adult women. The study was a randomised, cross-over trial of ten American women. The subjects consumed three different porridges separated by 2 week washout periods. Treatment meals (containing 100 g cassava) included: biofortified cassava (2 mg β-carotene) porridge with added oil (15 ml peanut or rapeseed oil, 20 g total fat); biofortified cassava porridge without added oil (6 g total fat); unfortified white cassava porridge with a 0·3 mg retinyl palmitate reference dose and added oil (20 g total fat). Blood was collected six times from − 0·5 to 9·5 h post-feeding. TAG-rich lipoprotein (TRL) plasma was separated by ultracentrifugation and analysed using HPLC with coulometric array electrochemical detection. The AUC for retinyl palmitate increased after the biofortified cassava meals were fed (P< 0·05). Vitamin A conversion was 4·2 (sd 3·1) and 4·5 (sd 3·1) μg β-carotene:1 μg retinol, with and without added oil, respectively. These results show that biofortified cassava increases β-carotene and retinyl palmitate TRL plasma concentrations in healthy well-nourished adult women, suggesting that it is a viable intervention food for preventing vitamin A deficiency.

B1a lymphocytes—which constitutively produce most natural antibodies (NAb)—arise from an early wave of progenitors unique to fetal life. Vitamin A regulates early lymphopoiesis. In animals, deficiency during this critical period compromises B1 cell populations. The aim of this study was to investigate the effect of maternal supplementation with vitamin A or β-carotene from preconception through lactation on NAb concentrations of offspring. Participants (N = 290) were born to participants of a cluster-randomized, placebo-controlled trial of weekly maternal vitamin A or β-carotene supplementation (7000 μg retinol equivalents) conducted in Sarlahi, Nepal (1994–1997) and assessed at ages 9 to 13 y (2006–2008). Serum retinol was measured by reversed-phase high-performance liquid chromatography at mid-pregnancy and 3 mo of age. Enzyme-linked immunosorbent assay (ELISA) was used to measure children's plasma NAb concentrations at 9 to 13 y. Unadjusted geometric mean concentrations were 20.08 U/mL (95% confidence interval [CI], 17.82–22.64) in the vitamin A group compared with 17.64 U/mL (95% CI, 15.70–19.81) and 15.96 U/mL (95% CI, 13.43–18.96) in the β-carotene and placebo groups (P = 0.07), respectively. After adjustment, maternal vitamin A supplementation was associated with a 0.39 SD increase in NAb concentrations (P = 0.02). The effect was mediated by infant serum retinol in our statistical models. Although girls had 1.4-fold higher NAb concentrations (P < 0.001), sex did not modify the vitamin A effect. In an undernourished population, maternal vitamin A supplementation enhanced NAb concentrations of preadolescent children. We posit that this was due to a greater allotment of B1a precursors during fetal life and a sustained higher count of NAb-secreting B1a cells. •Undernourished women in Nepal were supplemented throughout pregnancy.•Preadolescent children were screened to assess long-term effects of supplementation.•Fetal exposure to vitamin A increased children's natural antibodies (NAb).•NAb are unique products of B1a cells, which arise solely from fetal progenitors.•Inadequate vitamin A nutriture may impair fetal lymphopoiesis.

An adequate immune system is required to prevent diarrhoea in neonates, and IgA provides protection against microbial antigens on mucosal surfaces. Although β-carotene supplementation has been expected to enhance the retinoic acid (RA)-mediated immune response in neonates, the exact mechanism of the enhancement of mucosal IgA production in the small intestine by β-carotene is still unclear. In the present study, we investigated the effect of supplemental β-carotene on the concentrations of IgA, the numbers of IgA antibody-secreting cells (ASC) and the mRNA expressions of IgA C-region, CCL25, retinoid X receptor (RXR) α, retinoic acid receptor (RAR) α and RARγ in the jejunum and ileum of weanling mice. Weanling mice were fed rodent feed or 50 mg/kg β-carotene-supplemented rodent feed for 7, 14 or 21 d. The concentrations of IgA and the numbers of IgA ASC in the jejunum and ileum of mice increased markedly with age, and supplemental β-carotene increased the concentrations of IgA, the numbers of IgA ASC and the mRNA expressions of IgA C-region, CCL25 and RARγ in the jejunum after 14 and 21 d of treatment. Supplemental β-carotene increased the numbers of IgA ASC in the ileum after 14 and 21 d of treatment, but the concentrations of IgA in the ileum were not affected by β-carotene supplementation. The mRNA expressions of RXRα and RARα in the jejunum and those of RXRα and RARγ in the ileum after 21 d of treatment were enhanced by β-carotene supplementation. These results indicate that β-carotene supplementation in weanling mice is effective to enhance mucosal IgA induction in the jejunum or ileum and that the effects are mainly due to the RA-mediated immune response.

Mortality of neonates continues to be a major problem in humans and animals. IgA provides protection against microbial antigens at mucosal surfaces. Although β-carotene supplementation has been expected to enhance retinoic acid-mediated immune response in neonates, the exact mechanism by which β-carotene enhances IgA production is still unclear. We investigated the effect of supplemental β-carotene for maternal mice during pregnancy and lactation on IgA antibody-secreting cells (ASC) in mammary gland and guts and on IgA transfer from milk to neonatal mice. Pregnant mice were fed untreated or 50 mg/kg β-carotene-supplemented diets from 6·5 d postcoitus (dpc) to 14 d postpartum (dpp). Supplemental β-carotene increased the numbers of IgA ASC in mammary gland (P < 0·05) and ileum (P < 0·001), and also mRNA expression of IgA C-region in ileum (P < 0·05) of maternal mice at 14 dpp, but few IgA ASC were detected in mammary gland at 17·5 dpc. IgA concentration in stomach contents, which represents milk IgA level, was significantly higher (P < 0·01) in neonatal mice born to β-carotene-supplemented mothers at 7 and 14 dpp, and IgA concentration in serum, stomach contents and faeces increased (P < 0·001) drastically with age. These results suggest that β-carotene supplementation for maternal mice during pregnancy and lactation is useful for enhancing IgA transfer from maternal milk to neonates owing to the increase in IgA ASC in mammary gland and ileum during lactation.

Data on the vitamin A equivalency of β-carotene in food are inconsistent. We quantified the vitamin A equivalency (μg) of β-carotene in two diets using the dual-isotope dilution technique and the oral–faecal balance technique. A diet-controlled, cross-over intervention study was conducted in twenty-four healthy adults. Each subject followed two diets for 3 weeks each: a diet containing vegetables low in β-carotene with supplemental β-carotene in salad dressing oil (‘oil diet’) and a diet containing vegetables and fruits high in β-carotene (‘mixed diet’). During all 6 weeks, each subject daily consumed a mean of 55 (sd 0·5) μg [13C10]β-carotene and 55 (sd 0·5) μg [13C10]retinyl palmitate in oil capsules. The vitamin A equivalency of β-carotene was calculated as the dose-corrected ratio of [13C5]retinol to [13C10]retinol in serum and from apparent absorption by oral–faecal balance. Isotopic data quantified a vitamin A equivalency of [13C10]β-carotene in oil of 3·4 μg (95 % CI 2·8, 3·9), thus the bio-efficacy of the β-carotene in oil was 28 % in the presence of both diets. However, data from oral–faecal balance estimated vitamin A equivalency as 6:1 μg (95 % CI 4, 7) for β-carotene in the ‘oil diet’. β-Carotene in the ‘oil diet’ had 2·9-fold higher vitamin A equivalency than β-carotene in the ‘mixed diet’. In conclusion, this extrinsic labelling technique cannot measure effects of mixed vegetables and fruits matrices, but can measure precisely the vitamin A equivalency of the β-carotene in oil capsules.

Reports on the effects of carotenoids are conflicting. The present paper examines similarities and differences from contiguous studies in vitro and in vivo. Single-cell gel electrophoresis was used to measure the frequency of single-strand breaks (SSB) in the cell line MOLT-17 (as a model system) and human peripheral blood lymphocytes (PBL). MOLT-17 cells were supplemented with β-carotene, lutein or lycopene at a range of concentrations (0·00–8·00 μmol/l) using a liposome delivery method. Uptake was dose-dependent. β-Carotene concentration in the media had no effect on SSB in control cells, but incubation with lycopene or lutein (>2·00 μmol/l) increased the numbers of SSB in control cells. MOLT-17 DNA was less susceptible to oxidative damage (100 μmol H2O2/l, 5 min, 4 °C) following incubation with carotenoids between 0·50 and 1·00 μmol/l; at >1·00 μmol/l the effects were ambiguous. Apparently healthy male volunteers supplemented their habitual diets with lutein, β-carotene or lycopene (natural isolate capsules, 15 mg/d, 4 weeks) in three independent studies, raising plasma concentrations to different extents. Lycopene and lutein had no effect on SSB in control PBL or following oxidative challenge. However, increased plasma β-carotene was associated with more SSB in control cells whilst PBL DNA resistance to oxidative damage ex vivo was unaffected. These results suggest that the carotenoids are capable of exerting two overlapping but distinct effects: antioxidant protection by scavenging DNA-damaging free radicals and modulation of DNA repair mechanisms.

Purpose Cardiovascular risk factors such as elevated levels of asymmetric dimethylarginine (ADMA)/C-reactive protein (CRP) and homocysteine are potentially related to essential micronutrients such as certain B vitamins and antioxidant vitamins. The aim of the present study was to investigate whether supplementation with moderate doses of B vitamins and/or antioxidants could alter either ADMA and/or CRP concentrations in middle-aged, apparently healthy men with mildly elevated homocysteine levels. Methods A randomised, double-blind, factorial design, intervention study was carried out on 132 men with mildly elevated homocysteine levels, allocated to four groups (a) B vitamins alone—1 mg folic acid, 7.2 mg pyridoxine, 0.02 mg cyanocobalamin daily, (b) antioxidants alone—150 mg ascorbic acid, 67 mg vitamin E, 9 mg β-carotene daily, (c) B vitamins with antioxidant vitamins, or (d) placebo. A total of 101 men completed the study to 8 weeks. Results When the percentage of baseline ADMA and CRP was examined at 8 weeks, no statistically significant differences were observed between the four groups (p = 0.21 and p = 0.90, respectively). Similar non-significant results were observed when analysis was stratified based on baseline CRP levels (<1.0 mg/L, p = 0.10; ≥1.0 mg/L, p = 0.64) and smoking status (all p ≥ 0.05). Conclusions Supplementation with moderate doses of B vitamins and/or antioxidants did not alter either ADMA or CRP concentrations in these middle-aged, apparently healthy men with mildly elevated homocysteine levels.

Endogenous antioxidants are decreased in skin and blood during UV exposure. Combined supplementation of beta-carotene, alpha-tocopherol and ascorbic acid in addition to topical sunscreens may help to lower the risk of sunburning. Acute UV erythema with sunburn reaction are the most important factors in conjunction with the cumulative life-long UV dose for inducing skin damage resulting in photoageing and precancerous and cancerous lesions. Therefore, a clinical, randomized, double-blind, parallel group, placebo-controlled study was conducted in healthy young female volunteers (skin type II) investigating the preventive, photoprotective effect of supplementation with Seresis, an antioxidative combination containing both lipid and water-soluble compounds: carotenoids (beta-carotene and lycopene), vitamins C and E, selenium and proanthocyanidins. In this study, the oral administration of Seresis appeared to be well tolerated. The preparation contains antioxidant compounds in quantities occurring at physiological levels and can therefore be used safely over a long period of time. Despite the fact that the assessment of the light sensitivity (minimal erythemal dose, chromametry) of the skin did not show any statistically significant differences between the Seresis and the placebo group, a clear statistical trend, however, could be demonstrated, i.e. Seresis was able to slow down the time of the development and grade of UVB-induced erythema. The primary efficacy parameter matrix metalloproteinases 1 (MMP-1) between treatment and placebo group following UV irradiation showed a significant difference (p < 0.05), which occurred due to the fact that after a 2-week UV irradiation, MMP-1 slightly increased (p < 0.03) in the placebo group and decreased (p < 0.044) in the treated group. The MMP-9 changes showed a clear tendency of decrease in the Seresis group (p < 1.393) and increase (p < 0.048) in the placebo group. These data emphasise that supplementation with Seresis decreases the UV-induced expression of MMP-1 and 9, which might be important in photoprotective processes. From our data, we thus finally draw the conclusion that by the combination of antioxidants, such as in the formulation of Seresis, a selective protection of the skin against irradiation can be achieved. This might be important for future recommendations for immediate suppression of the early phase of UV-induced erythema, that means pharmacological prevention of sunburn reaction as well as subsequent chronic skin damage.

Enzymes are essential catalysts in biological systems. Substrate inhibition, once dismissed, is now observed in 20% of enzymes 1 and is attributed to the formation of an unproductive enzyme-substrate complex, with no structural evidence of unproductivity provided to date 1 , 2 , 3 , 4 , 5 – 6 . This study uncovers the molecular mechanism of substrate inhibition in tobacco glucosyltransferase Nb UGT72AY1, which transfers glucose to phenols for plant protection. The peculiarity that β-carotene strongly attenuates the substrate inhibition of Nb UGT72AY1, despite being a competitive inhibitor, allows to determine the conformational changes that occur during substrate binding in both active and substrate-inhibited complexes. Crystallography reveals structurally different ternary enzyme-substrate complexes that do not conform to classical mechanisms. An alternative pathway suggests substrates bind randomly, but the reaction occurs only if a specific order is followed (asymmetric cooperativity). This unreported paradigm explains substrate inhibition and reactivation by competitive inhibitors, opening new research avenues in metabolic regulation and industrial applications. This study proposes an unreported molecular mechanism of substrate inhibition in enzymes. It shows that a competitive inhibitor reduces substrate inhibition and identifies unique enzyme-substrate complexes, suggesting an unreported paradigm for enzyme regulation.

β-carotene (β-C) is a hydrophobic compound, easily degradable by light and oxygen and with low solubility, limiting its applications. β-cyclodextrin (β-CD) can encapsulate β-C, protecting it from degradation and maintaining its bioactivity. Therefore, this research aimed to characterize and determine the antioxidant and erythroprotective activity of β-C/β-CD inclusion complexes. The co-precipitation technique was used to elaborate β-C/β-CD in a 40:60 ratio, obtaining a high yield (94.10%), an entrapment efficiency of 82.47%, and a loading efficiency of 11.92%. The moisture of β-C/β-CD was 2.93%. β-C release increased over the time of 216 h (80.8%, 92.8%, and 97.4% at 8 °C, 25 °C, and 37 °C, respectively). A UV–visible analysis confirmed the presence of β-carotene in the inclusion complex, indicating successful encapsulation without significant structural changes. According to the adsorption–desorption isotherms, the complexes showed a type II isotherm. The FT-IR and Raman spectroscopy confirmed the formation of the inclusion complex, which interacted by hydrogen bonds, hydrophobic interactions, or van der Waals forces. The DSC showed an endothermic peak at 118 °C in the β-C/β:CD. The TGA revealed reduced water loss in the β-carotene/β-cyclodextrin complex, indicating limited water binding due to encapsulation. The microscopic surface morphologies observed by the SEM of β-C/β-CD were irregular-shaped clumps in the surface with a particle average size of 8.09 µm. The X-ray diffraction showed a crystalline structure of the complex. The zeta potential determination indicated a negative charge (−23 and −32 mV). The ABTS, DPPH, and FRAP demonstrated the antioxidant activity of β-C/β:CD (34.09%, 21.73%, and 8.85. mM ET/g, respectively), similar to pure β-C (34.64%, 22.63%, and 9.12 μM ET/g, respectively). The complexes showed an erythroprotective effect inhibiting hemolysis (64.09%). Therefore, with these characteristics, β-CD is a good encapsulant for β-C, and this complex could be applied in the food and pharmaceutical industries.