Administration Of Β-carotene Research Articles

고강도 운동을 통한 Lactate상승에서 경구투여 β-Carotene의 항산화 및 피로도 회복력에 미치는 효과

The purpose of this study is to identify the antioxidant effect of oral administration of β-carotene in order to effectively prevent body acidification of lactate, an oxidizing substance that rapidly increases through high-intensity exercise, and to suggest a method for preventing acidosis in the body. The study subjects were 22 males and females between the ages of 20 and 29 while performing high-intensity CrossFit exercise in common, and 11 each of the G1 group, which performed high-intensity CrossFit exercise and orally administered β-carotene during the study period, and the G2 group, which controlled intake of health supplements. assigned randomly. The study period was 8 weeks in total, and the intensity of HRmax 70 Over % was regularly conducted twice a week for 30 minutes each. As a result 1. Oral administration of β-Carotene to the rapid increase in lactate caused by high-intensity exercise has the effect of preventing body acidification by increasing antioxidant power. 2. Oral administration of β-Carotene to the rapid increase in lactate caused by high-intensity exercise has the effect of recovering from fatigue by suppressing the increase in lactate. 3. There is a significant correlation between the increase in lactate and antioxidant activity.

The investigation of the effects of vitamin A, vitamin E, and β-carotene plus vitamin E on some fertility parameters in ewes.

This study was aimed at investigating the effects of vitamin A (VITA), vitamin E (VITE), and combined β-carotene plus vitamin E (βCAR+VITE) injections on some fertility parameters in ewes. Estrus synchronization was performed by treating the ewes with intravaginal FGA sponges impregnated with 30 mg of fluorogestone acetate. On the days of the insertion and withdrawal of the intravaginal sponges, groups VITA, VITE, and βCAR+VITE were administered with 500 000 IU of vitamin A, 50 mg of vitamin E, and a combination of β-carotene plus vitamin E, respectively. The ewes in the control group (C) were maintained for control purposes. Statistically significant differences were determined between groups VITA and βCAR+VITE, groups VITE and βCAR+VITE, and groups C and βCAR+VITE, as well as groups VITE and C, groups VITA and C for the multiple birth rates. While significant differences were determined between groups VITA and C, groups VITE and C, and groups βCAR+VITE and C for the lambing rates, it was ascertained that the ratio of newborn lambs to delivered ewes (litter size) significantly differed between groups VITA and βCAR+VITE, groups VITA and C, groups VITE and βCAR+VITE, groups VITE and C, and groups βCAR+VITE and C. The highest MDA level and lowest GSH level were determined on day 20 after mating in the control group. In conclusion, it is suggested that both multiple birth rates and litter size can be increased by the combined administration of β-carotene and vitamin E.

Natural β-carotene prevents acute lung injury induced by cyclophosphamide in mice.

IL-17 is associated with varied inflammatory and immune-related diseases. However, the biological function of IL-17 and its expression in acute lung damage are not entirely known. Thanks to the powerful antioxidant properties of β-carotene, we presumed that it would show a potent protecting effect against cyclophosphamide (CP) -induced acute lung injury (ALI) in mice. We studied the mechanisms underlying the effect of β-carotene supplementation against CP-induced ALI in mice. We isolated the β-carotene from Scenedesmus obliquus microalgae n-hexane extract and identified it by HPLC and 1H-NMR analysis. Within the experiments, 40 mice were assigned into five groups randomly: Group 1 (Control): Mice received saline. Group 2 (β-carotene control): Mice were administered β-carotene (40 mg/kg; orally) once daily for 10 sequent days without CP injection. Group 3 (CP): One i.p injection of 200 (mg/kg) of CP was given to mice. Group 4 and 5 (CP + β-carotene): Mice were administered β-carotene (20 and 40 mg/kg; orally) once a day for ten days following the CP injection. Lung samples were collected for lab analysis, after scarifying the animals at the experiment end. Administration of β-carotene orally reduced CP-induced ALI and inflammation. β-carotene significantly decreased wet-to-dry weight ratios (W/D), down-regulated IL-17, NF-κB, and IKBKB, decreased the contents of TNF-α, COX-2, and PKC, and increased the contents of SIRT1 and PPARγ in the lung tissues. β-carotene ameliorated the histopathological changes induced by CP and reduced the scoring number of inflammatory cell infiltration and emphysema when compared to CP. Consequently, we conclude natural β-carotene is a promising anti-inflammatory mediator for different inflammatory-related complications.

β-Carotene enhances the expression of inflammation-related genes and histone H3 K9 acetylation, K4 dimethylation, and K36 trimethylation around these genes in juvenile macrophage-like THP-1 cells

β-Carotene is converted into vitamin A in the body and can remove reactive oxygen species. However, it is still unclear whether β-carotene alters the expression levels of inflammation-related genes in macrophages and how this is regulated. In the present study, we investigated whether the administration of β-carotene under hyperglycemic conditions altered the expression level of inflammation-related genes and whether any observed differences were associated with changes in histone modifications in juvenile macrophage-like THP-1 cells. THP-1 cells (from a human monocytic leukemia cell line) were cultured in low glucose (5 mM), high glucose (25 mM), or high glucose (25 mM) + β-carotene (5 μM) media for 1 day, and mRNA expression levels of genes related to oxidative stress and inflammation, and histone modifications were determined by mRNA microarray and qRT-PCR analyses, and chromatin immunoprecipitation assays, respectively. The expression of inflammation-related genes, such as IL31RA, CD38, and NCF1B, and inflammation-associated signaling pathway genes, such as ITGAL, PRAM1, and CSF3R, were upregulated by β-carotene under high-glucose conditions. Under these conditions, histone H3 lysine 4 (K4) demethylation, H3K36 trimethylation, and H3K9 acetylation around the CD38, NCF1B, and ITGAL genes were higher in β-carotene-treated cells than in untreated cells. Treatment of juvenile macrophage-like THP-1 cells with β-carotene under these high glucose conditions induced the expression of inflammation-related genes, K9 acetylation, and K4 di- and K36 trimethylation of histone H3 around these genes.

Direct Binding to NLRP3 Pyrin Domain as a Novel Strategy to Prevent NLRP3-Driven Inflammation and Gouty Arthritis.

The NLRP3 inflammasome is closely linked to the pathophysiology of a wide range of inflammatory diseases. This study was undertaken to identify small molecules that directly bind to NLRP3 in order to develop pharmacologic interventions for NLRP3-related diseases. A structure-based virtual screening analysis was performed with ~62,800 compounds to select efficient NLRP3 inhibitors. The production of caspase 1-p10 and interleukin-1β (IL-1β) was measured by immunoblotting and enzyme-linked immunosorbent assay to examine NLRP3 inflammasome activation. Two gouty arthritis models and an air pouch inflammation model induced by monosodium urate monohydrate (MSU) crystal injection were used for in vivo experiments. Primary synovial fluid cells from gout patients were used to determine the relevance of NLRP3 inflammasome inhibition in human gout. Beta-carotene (provitamin A) suppressed the NLRP3 inflammasome activation induced by various activators, including MSU crystals, in mouse bone marrow-derived primary macrophages (P < 0.05). Surface plasmon resonance analysis demonstrated the direct binding of β-carotene to the pyrin domain (PYD) of NLRP3 (KD = 3.41 × 10-6 ). Molecular modeling and mutation assays revealed the interaction mode between β-carotene and the NLRP3 PYD. Inflammatory symptoms induced by MSU crystals were attenuated by oral administration of β-carotene in gouty arthritis mouse models (P < 0.05), correlating with its suppressive effects on the NLRP3 inflammasome in inflamed tissues. Furthermore, β-carotene reduced IL-1β secretion from human synovial fluid cells isolated from gout patients (P < 0.05), showing its inhibitory efficacy in human gout. Our results present β-carotene as a selective and direct inhibitor of NLRP3, and the binding of β-carotene to NLRP3 PYD as a novel pharmacologic strategy to combat NLRP3 inflammasome-driven diseases, including gouty arthritis.

β-Carotene: A Natural Compound Improves Cognitive Impairment and Oxidative Stress in a Mouse Model of Streptozotocin-Induced Alzheimer's Disease.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a cascade of changes in cognitive, behavioral, and social activities. Several areas of the brain are involved in the regulation of memory. Of most importance are the amygdala and hippocampus. Antioxidant therapy is used for the palliative treatment of different degenerative diseases like diabetes, cirrhosis, and Parkinson’s, etc. The objective of this study was to assess the effectiveness of exogenous antioxidants, in particular, β carotene (1.02 and 2.05 mg/kg) against intracerebroventricular injected streptozotocin-induced memory impairment in mice. Streptozotocin (3 mg/kg, i.c.v) was administered in two separate doses (on 1st and 3rd days of treatment) for neurodegeneration. Fifty Albino mice (male) were selected in the protocol, and they were classified into five groups (Group I—control, Group II—disease, Group III—standard, Group IV–V—β-carotene-treated) to investigate the cognitive enhancement effect of selected antioxidants. The cognitive performance was observed following the elevated plus-maze, passive avoidance, and open field paradigms. Acetylcholine esterase, β-amyloid protein, and biochemical markers of oxidative stress such as glutathione peroxidase, superoxide dismutase, and catalase were analyzed in brain homogenates. In silico activity against acetylcholinesterase (AChE) was determined by the molecular modeling of β-carotene. β-carotene at a dose of 2.05 mg/kg was found to attenuate the deleterious effects of streptozotocin-induced behavioral and biochemical impairments, including the inhibition of acetylcholinesterase activity. The in silico studies confirmed the binding capacity of β-carotene with the acetylcholinesterase enzyme. The administration of β-carotene attenuated streptozotocin-induced cognitive deficit via its anti-oxidative effects, inhibition of acetylcholinesterase, and the reduction of amyloid β-protein fragments. These results suggest that β-carotene could be useful for the treatment of neurodegenerative diseases such as Alzheimer’s disease.

Effects of β-carotene on oxazolone-induced atopic dermatitis in hairless mice.

Skin acts as a barrier, which protects internal tissues and promotes moisture retention. Atopic dermatitis (AD) is an inflammatory skin disease associated with a variety of genetic and environmental factors that involve helper T cells. β-Carotene (provitamin A) exhibits antioxidant activity and activates the immune system. However, it is not clear whether inflammation in AD skin is improved by posttreatment with β-carotene. In the current study, we investigated the effects of β-carotene on the skin of hairless mice with oxazolone-induced inflammation/oedema (Ox-AD mice). We found that skin inflammation was significantly reduced by oral administration of β-carotene. In addition, treatment with β-carotene suppressed protein levels of TNF-α, IL-1β and MCP-1, as well as mRNA expression associated with IL-1β, IL-6, IL-4 and Par-2 in skin tissues. Furthermore, the mRNA and protein levels of filaggrin, a structural protein in the epidermal stratum corneum, were elevated by β-carotene administration as compared with Ox-AD mice. β-Carotene significantly reduced the activity of proMMP-9, but not proMMP-2. These results suggest that in Ox-AD mice, β-carotene improves skin inflammation by suppressing the expression of inflammatory factors, promoting filaggrin expression and reducing MMP-9 activity. β-Carotene is a potent anti-inflammatory agent that improves the barrier functions of AD skin.

Effects of Post-administration of β-Carotene on Diet-induced Atopic Dermatitis in Hairless Mice.

Atopic dermatitis (AD) is a cutaneous condition characterized by itchy, swollen, and dry skin, which is mediated by T helper cell-related cytokines. β-Carotene, a natural red pigment found in plants, exhibits antioxidant activity that has been shown to promote an inflammatory response. Because it is not clear whether β-carotene suppresses inflammation in AD skin tissues, we examined the effects of oral administration of β-carotene in mice induced by a low zinc/magnesium diet (HR-AD diet). Our studies found that AD-like inflammation was remarkably reduced by β-carotene. In addition, β-carotene significantly suppressed protein expression of TNF-α, IL-1β, and MCP-1 and mRNA expression of TSLP, IL-6, IL-1β, IL-4, IL-5, and Par-2 in AD-like skin tissues. It was also found that mRNA and protein expression of filaggrin (a major structural protein in epidermis) in AD-like skin was significantly elevated by β-carotene administration. Furthermore, β-carotene treatment significantly reduced the activity and/or mRNA expression of matrix metalloproteinases (MMPs), degradation of the extracellular matrix and regulation of chemokines. These results suggest that β-carotene reduces skin inflammation through the suppressed expression of inflammatory factors or the activity of MMPs as well as the promotion of filaggrin expression in AD-like skin. β-Carotene is a potent anti-inflammatory agent, which improves AD-like skin by enhancing the skin barrier function.

Hypocholesterolemic Effect of Oral Administration of β-Carotene and Carrot Juice in Exogenous Hypercholesterolemic Mice

Hypocholesterolemic Effect of Oral Administration of β-Carotene and Carrot Juice in Exogenous Hypercholesterolemic Mice

Oral administration of β-carotene or lycopene prevents atopic dermatitis-like dermatitis in HR-1 mice.

Atopic dermatitis (AD) is a chronic relapsing eczematous skin disease. Certain populations of patients are resistant to standard therapies with topical steroids and/or calcineurin inhibitors, and require systemic medication, such as immunosuppressants. Recently, several reports have shed light on the anti-allergic effects of carotenoids. Therefore, we investigated the effect of p.o. administration of β-carotene or lycopene on AD-like symptoms of HR-1 hairless mice fed with a low zinc/magnesium diet. Mice were divided into four groups: (i) fed with a standard diet (Co group); (ii) low zinc/magnesium diet (HR group); (iii) low zinc/magnesium and β-carotene diet (HR-C group); and (iv) low zinc/magnesium and lycopene diet (HR-L group). They were then fed these diets for 8 weeks. Severities of dermatitis were assessed by their appearance, and histopathological and hematological observations. Mice in the HR group developed AD-like dermatitis both clinically and histologically. HR-C and HR-L group mice also developed xerosis and wrinkle-like skin changes, but they were milder than those of HR group mice. Histological analysis revealed that epidermis thickening and inflammatory cell infiltration in the skin of the HR-C and HR-L groups were both statistically less than those of the HR group. The concentration of thymus and activation regulated chemokine in the skin of the HR-L group and the concentration of CCL27 in the skin of the HR-C group were significantly lower than those of the HR group, respectively. In conclusion, p.o. administration of β-carotene or lycopene prevents AD-like symptoms in association with a suppression of T-helper 2 chemokines in a murine model. Ingestion of carotenoids may be beneficial for patients with AD.

β-Carotene Increases Muscle Mass and Hypertrophy in the Soleus Muscle in Mice.

Supplements and naturally occurring nutraceuticals effective for maintenance or enhancement of skeletal muscle mass are expected to contribute to prevention of decreased mobility and increased risk of developing metabolic diseases. However, information about available food components remains widely unavailable. In the present study, we investigated the effects of dietary β-carotene on the quantity and quality of skeletal muscle under physiological conditions. Male ddY mice (8 wk old) were orally administered β-carotene (0.5 mg once daily) for 14 d. Dietary β-carotene had no influence on body weight, but increased the soleus muscle/body weight ratio. The cross-sectional area (CSA) in muscle fibers of the soleus muscle was increased, indicating that administration of β-carotene induces muscle hypertrophy. In the soleus muscle of the β-carotene-administered mice, twitch force tended to be increased (p=0.06) and tetanic force was significantly increased, whereas specific force (force per CSA) remained unchanged. Dietary β-carotene increased the mRNA level of insulin-like growth factor 1 (Igf-1) as its splicing variant Igf-1ea, but had no influence on the liver Igf-1 mRNA level or serum IGF-1 level. β-Carotene promoted protein synthesis in the soleus muscle and reduced levels of ubiquitin conjugates, but had no influence on the mRNA levels of two atrogenes, Atrogin-1 and Murf1. On the other hand, β-carotene had no influence on the processing of the autophagy marker protein light chain 3. These results indicate that in mice, administration of β-carotene increases mass and induces functional hypertrophy in the soleus muscle, perhaps by promoting IGF-1-mediated protein synthesis and by reducing ubiquitin-mediated protein degradation.

Effect of beta-Carotene from Yellow Ambon Banana Peel on Rat Serum Retinol Level

Vitamin A Deficiency (VAD) is associated with significant morbidity and mortality from common childhood infections and is the world’s leading preventable cause of childhood blindness. Studies showed that carotenoid is one of the promissed vitamin A source. H owever the studies on carotenoid from yellow banana peel and its potential as a natural source of vitamin A has not been widely reported. This study was conducted to measure the blood serum retinol levels of rats after administration of β-carotene from yellow ambon banana peel. This was an experimental study with post test only control group design, with sample size of 18 rats with age 1 month, devided into 3 groups. β-carotene dose administered based on the dose of red capsules vitamin A are (200,000 doses SI) for toddlers aged 12-59 months. Serum retinol levels were measured using a spectrophotometer according metide. This present study showed that the blood serum level in group treated with of β - carotene from yellow ambon banana peel (28.35 ± 1.61 mg/ dL ), was significantly different (p &lt; 0.05) from that of control group ( 22.08 ± 1.35 mg /dL ). β-carotene from yellow ambon banana peel are potential as provitamin A.

Diverse Effects of β-Carotene on Secretion and Expression of VEGF in Human Hepatocarcinoma and Prostate Tumor Cells

Oral administration of β-carotene (BC) was found to exert opposite effects on plasma levels of vascular endothelial growth factor (VEGF) in two animal models. One study in nude mice injected via tail vein with hepatocarcinoma SK-Hep-1 cells showed that BC decreases the plasma VEGF level, whereas the other study in nude mice injected subcutaneously with prostate tumor PC-3 cells showed that BC increases the plasma VEGF level. Herein we investigated whether BC (0.5–20 μM) possesses diverse effects on VEGF secretion in SK-Hep-1, PC-3 and melanoma B16F10 cells. We found that incubation of SK-Hep-1 cells with BC (1–20 μM) for 6 h significantly decreased VEGF secretion, whereas BC (1–10 μM) significantly increased the VEGF secretion in PC-3 cells. However, these effects disappeared at 12 h of incubation. Similar effects occurred in VEGF mRNA and protein expression after treatment of SK-Hep-1 and PC-3 cells with BC for 6 h. In contrast, BC (0.5–20 μM) did not affect mRNA and protein expression and secretion of VEGF in B16F10 cells. We also found that the proliferation of SK-Hep-1 and B16F10 cells was significantly inhibited by 20 μM BC at 6 and 12 h of incubation, whereas the proliferation of PC-3 cells was significantly inhibited by 20 μM BC at 12 h of incubation. In summary, the present study demonstrated the tumor-specific effect of BC on VEGF secretion in different cancer cell lines.

Influence of dietary spices on thein vivoabsorption of ingested β-carotene in experimental rats

Animal studies were conducted to evaluate the influence of dietary spice compounds, piperine, capsaicin and ginger, on the absorption of orally administered β-carotene and its conversion to vitamin A. In rats maintained on these spice-containing diets for 8 weeks, concentrations of β-carotene and retinol were determined in the serum, liver and intestine 4 h after a single oral administration of β-carotene. β-Carotene concentration was significantly increased in the serum, liver and intestine of piperine- and ginger-fed rats, suggesting improved absorption of β-carotene. However, retinol concentration was not significantly changed in these animals, suggesting that the bioconversion of β-carotene to vitamin A was not similarly influenced. Between the two enzymes involved in the bioconversion of β-carotene to vitamin A, the activity of intestinal and hepatic β-carotene 15,15'-dioxygenase was either unaffected or lowered by these spice treatments. The activity of intestinal and hepatic retinal reductase was unaffected by the dietary spices. Activities of these two enzymes involved in the bioconversion of β-carotene to retinal were inhibited by the test spices in vitro, thus corroborating with the in vivo observation. Although the bioconversion of β-carotene was not promoted, increased absorption and tissue levels of β-carotene by the dietary spices may contribute to a higher antioxidant protection.

Regulation of CMO1 and CMO2 expression during mouse embryonic development

β‐carotene‐15, 15′‐oxygenase (CMO1) and β‐carotene‐9,10′‐oxygenase (CMO2) are the only enzymes known to generate vitamin A from β‐carotene. Both are expressed in mouse and human embryonic and extraembryonic tissues, suggesting a role for β‐carotene as a localized source of vitamin A for developing tissues. Studies indicate that β‐carotene cleavage activity is regulated by nutrient availability in adult tissues. Here we investigate whether nutrient availability may regulate the expression of CMO1 and CMO2 during mouse embryogenesis.Wildtype and CMO1−/− pregnant females were administered β‐carotene by IP injection at 13.5 dpc and sacrificed one day later to collect maternal serum and liver, embryos, yolk sac and placenta. This procedure leads to detectable amounts of β‐carotene in these tissues. Real‐time PCR analysis demonstrated that, in maternal liver, CMO1 expression is down‐regulated while CMO2 is up‐regulated with increasing amounts of β‐carotene. Furthermore, HPLC analysis revealed that administration of β‐carotene also altered maternal serum retinol levels, suggesting the existence of highly regulated mechanisms to ensure that adequate amount of vitamin A are available to the embryo. Experiments are ongoing to analyze the changes in CMO1 and CMO2 expression in embryonic tissues in response to maternal β‐carotene availability and vitamin A status.Grant Funding Source: NIH 5R01HD57493.

Enhancement of Antiradiation Potential of Some Aminothiols by Beta-Carotene

In the present study, protection of mice, BALB/c inbred as measured by survival at 30 days against whole-body gamma exposure at two dose levels, namely, 7.60 and 10.12 Gy by prior irradiation treatment with combination of β-carotene, N-(2-mercapto-propionyl)-glycine (MPG) and S-(2-aminoethyl) isothiouroniumbromide hydrobromide (AET), is reported. It was found that administration of β-carotene (1 mg per 20 g body mass) and 24 h before whole-body irradiation (7.60 Gy) had significantly improved the post-irradiation survival. It was also found that administration of a combination of AET (260 mg per kg body mass) and MPG (60 mg per kg body mass) 20 min before exposure to 7.60 Gy gamma irradiation to mice which have been treated with β-carotene (1 mg per 20 g body mass) 24 h before exposure had resulted in 80% survival in comparison to 10% survival recorded for control animals. On the other hand, when the animals were exposed to a higher dose (10.12 Gy) under similar experimental conditions as above, a significant improvement in survival was observed during the first 10 days following the exposure but only a slight effect afterward. On the other hand, the response of male and female mice 10 days after exposure to the above radiation dose indicated that the females were more radioresistant than the males.

Role of beta-carotene in ameliorating the cadmium-induced oxidative stress in rat brain and testis.

The role of oxidative stress in chronic cadmium (Cd) toxicity and its prevention by cotreatment with beta-carotene was investigated. Adult male rats were intragastrically administered 2 mg CdCl2/kg body weight three times a week intragastrically for 3 and 6 weeks. Brain and testicular thiobarbituric acid reactive substances (TBARS) was elevated after 3 and 6 weeks of Cd administration, indicating increased lipid peroxidation (LPO) and oxidative stress. Cellular damage was indicated by inhibition of adenosine triphosphatase (ATPase) activity and increased lactate dehydrogenase (LDH) activity in brain and testicular tissues. Chronic Cd administration resulted in a decline in glutathione (GSH) content and a decrease of superoxide dismutase (SOD) and glutathione S-transferase (GST) activity in both organs. Administration of beta-carotene (250 IU/kg i.g.) concurrent with Cd ameliorated Cd-induced LPO. The brain and testicular antioxidants, SOD, GST, and GSH, decreased by Cd alone, were restored by beta-carotene cotreatment. Concurrent treatment with beta-carotene also ameliorated the decrease in ATPase activity and the increase in LDH activity in brain and testis of Cd-treated rats, indicating a prophylactic action of beta-carotene on Cd toxicity. Therefore, the results indicate that the nutritional antioxidant beta-carotene ameliorated oxidative stress and the loss of cellular antioxidants and suggest that beta-carotene may control Cd-induced brain and testicular toxicity.

Concentration-dependent inversion of antioxidant and prooxidant effects of β-carotene in tissuesin vivo

Low doses (below 20 mg/kg) of oral β-carotene inhibit, while high doses (above 100 mg/kg) activate ascorbate-dependent LPO in rat liver and myocardial cells. Administration of β-carotene in a dose of 20 mg/kg decreased by 34% infarction zone in coronary occlusion, while the dose of 100 mg/kg was ineffective. Anin vivo concentration-dependent inversion of β-carotene from antioxidant to prooxidant in tissues is hypothesized. Pharmacological efficacy of β-carotene is determined by its antioxidant effect, while high doses provoke the prooxidant effect and can lead to negative consequences.

Studies on the bioconversion of β-carotene to active vitamin A in underprivileged Guatemalan children

The mechanism by which the rate of β-carotene conversion to active vitamin A in the enterocyte is poorly understood. It is postulated that body vitamin A status plays a very important role. Unitl recently, it has not been possible to detect and quantify the product of β-carotene bioconversion, i.e., retinal, in the gut, and retinyl ester, in the circulation. This study aimed at confirming that a rise in plasma retinyl palmitate concentration would occur after administration of β-carotene to underprivileged Guatemalan schoolchildren. Twenty rural children, aged 7 to 11 years, received 30 mg of pure, crystalline β-carotene in oral capsules in the fasting state. Thirteen peri-urban poor children participated as controls; each received capsules of cellulose. Standard meals with low vitamin A levels were served during the observation period. Plasma levels of β-carotene, retinol, and retinyl palmitate were determined by HPLC at baseline, 2 hr, and 24 hr after ingestion of capsules. Anthropometric and biochemical characteristics were similar in both groups at baseline. An average increase of 0.15 ± 0.05 μmol/L in retinyl esters was observed in the supplemented group at 2 hr, with a return to baseline levels at 24 hr; whereas in the control group no retinyl esters were detected at all at any time. A tendency of a greater retinyl ester response with a lower baseline circulating retinol level was observed. This is the first instance in which β-carotene bioconversion to retinyl palmitate has been quantified in children. We propose that the rise in retinyl esters after oral administration of β-carotene could be used to examine the factors that influence the rate of bioconversion of β-carotene to active vitamin A.

Effect of β-carotene administration on reproductive function of horse and pony mares

The objective of this study was to determine whether supplemental β-carotene would influence reproductive function in mares maintained on spring and summer pastures and to characterize plasma carotene concentrations during the estrous cycle. Carotene concentrations in plasma did not vary with day of estrous cycle (P = 0.7455). Mares receiving every other day injections of β-carotene (400 mg; n = 4) or saline (10 ml; n = 4) during proestrus/estrus did not differ in plasma estradiol (E 2) concentrations (P = 0.6313), follicle development (P = 0.8068), or plasma progesterone (P 4) concentrations during the following diestrus (P = 0.4954). Moreover, no differences in plasma P 4 concentrations (P = 0.9047) were detected between mares receiving every other day injections of β-carotene (400 mg; n = 4) or saline (10 ml; n = 4) during diestrus. However, administration of β-carotene raised plasma carotene concentrations relative to controls when injected during proestrus/estrus (P = 0.0096) and diestrus (P = 0.0099). Pregnancy rates (P = 0.4900) and number of cycles required for pregnancy (P = 0.2880) were similar for mares administered injections of saline (10 ml; n = 37), β-carotene (400 mg; n = 37), vitamin A (160,000 IU; n = 38), or vitamin A + β-carotene (160,000 IU + 400 mg; n = 43), on the first or second day of estrus and on the day of breeding. Therefore, these results collectively suggest that supplemental β-carotene does not affect the reproductive function of mares fed adequate dietary carotene. Whether supplemental β-carotene would enhance reproductive function in mares on low carotene diets warrants further investigation.