Beta-Carotene

The Basics On Beta-Carotene

What is Beta-Carotene?

Member of the carotenoid family.

What are other names for Beta-Carotene?

B,BCAROTENE, B-CAROTENE, BETA CAROTENE, BETA,BETA-CAROTENE, BETA-CAROTENE, FOOD ORANGE 5, and NATURAL YELLOW 26

What is Beta-Carotene used for?

Beta-Carotene (or √ü-Carotene) is an excellent skin care ingredient, serving as an antioxidant and precursor to vitamin A, thus is frequently referred to as provitamin A. It’s a wonderful skin conditioning ingredient and is also used as a cosmetic colorant

How Beta-Carotene is classified

Antioxidants

Recommendations for using Beta-Carotene during pregnancy and breastfeeding

Can you take vitamin A as beta carotene while pregnant? Limited data on taking beta carotene while pregnant suggests no known risk

Beta-Carotene During Pregnancy

What we know about using Beta-Carotene while pregnant or breastfeeding

Is vitamin A as beta carotene safe during pregnancy? Limited information available.

Oral – Animal Retinyl Palmitate The effects of retinyl palmitate ingestion on sexual maturation and mammary gland development were determined in the context of a human food-based diet (whole food diet).32 Female adolescent Sprague-Dawley rats randomized into 3 dietary groups (6 rats per group) were used. At 20 days of age (postnatal day 20 [p20]), female rats received either a wholefood diet with adequate levels of vitamin A, a diet with a 5.5-fold increase in vitamin A from fruits and vegetables (S diet), or a diet with a 6.2-fold increase in vitamin A provided as retinyl palmitate (RP diet). To determine the effect of dietary intervention on pubertal mammary gland development, rats were fed the experimental diets from p21 to p63 and had free access to food and distilled water. All rats were killed at p63. To evaluate the effects of diet on early estrous cycles, defined as cycles within the first 2 weeks of sexual maturation, 12 rats per group received vaginal lavages daily from p43 through p50. To evaluate estrous cycles in more mature rats, 24 rats per dietary group were evaluated from p51 to p58. All rats were killed at p63. The onset of vaginal opening was evaluated as a marker for sexual maturation. The age of vaginal opening onset was significantly delayed in rats fed the S diet (p < 0.001), when compared to those fed the adequate diet and the RP diet. Thus, the S diet suppressed the onset of sexual maturation. The S diet also inhibited markers of mammary alveologenesis more than the RP diet. These data demonstrate that the amount and source of vitamin A consumed by adolescent female rats can influence the onset of puberty and mammary gland alveolar development. Effects on mammary carcinogenesis included in this study are found in the Carcinogenicity section of this report.32 A study was performed to evaluate the effects of defined doses of retinyl palmitate at the critical time of limb morphogenesis limb morphogenesis in Swiss Webster albino mouse embryos.33 Pregnant Swiss albino mice were administered retinyl palmitate (10,000 or 15,000 IU/kg, i.p.) on different days of pregnancy. The higher dose produced malformations in the forelimbs, by day 10, in 28.6% of mice and in the hindlimbs, by day 11, in 20.6% of the mice. Limb abnormalities (at both doses) were as follows: unilateral or bilateral micromelia (abnormally short) in the forelimbs and hindlimbs, shorter unilateral anterior and posterior limbs, limb malrotation, absence or malformation of fingers or toes, and an increased cleft between the metacarpal or metatarsal bones. Furthermore, 2 injections in one day with the lower dose resulted in more teratogenic effects than a single 15,000 IU/kg injection. Two injections of either dose on day 10 caused a greater incidence of embryo absorption. The effects of retinyl palmitate supplementation, during gestation and lactation, on oxidative stress parameters of maternal and offspring tissues of female Wistar rats was studied.34 Each group of pregnant female rats (except for one group of 7 rats), contained 6 animals. The respective groups received retinyl palmitate during pregnancy and lactation (21 days of gestation and 21 days of lactation) at oral (gavage) doses of 2500, 12,500, or 25,000 IU/kg/day. The maximum dose volume was 0.5 ml. The control group was dosed with saline. An increase in oxidative-damage markers in the reproductive tissues Distributed for Comment Only — Do Not Cite or Quote CIR Panel Book Page 18 10 and plasma of dams was observed. In uteri, lipid peroxidation was increased at all doses (p < 0.0001). Also, the liver and kidney had significant alterations in glutathione-S-transferase (GST) activity. It was increased in the liver of dams and decreased in the kidneys of mothers and offspring. In pups, supplementation decreased the total antioxidant potential of the liver, along with decreased superoxide dismutase/catalase activity ratio in the kidney. The levels of lipoperoxidation were increased in male offspring, but decreased in female pups. Collectively, the results suggest that excessive vitamin A intake during gestation and lactation, at oral doses sufficient to produce signs of maternal toxicity, may cause adverse effects in the developing offspring. A study was performed to investigate the effects of vitamin A supplementation in pregnant and nursing rats on maternal and offspring striatum and hippocampus.35 Female Wistar rats (7 per group) were orally supplemented with retinyl palmitate (2500; 12,500; and 25,000 IU/kg/day) or saline (control) throughout pregnancy and nursing. A homing test was performed on offspring on postnatal days (PND) 5 and 10, and an open field test (OFT) was carried out on dams and offspring on PND 19 and 20. Redox parameters were evaluated at PND 21 for both dams and offsprings. Supplementing Vitamin A during pregnancy and nursing increased the ratio of superoxide dismutase/catalase (SOD/CAT) ratio and oxidative damage in maternal and offspring striatum and hippocampus. Additionally, these effects were accompanied by behavioral alterations observed through the homing and OFT tests. Oral – Human Retinol A study examining the effects of vitamin A or beta carotene supplementation on pregnancy-related mortality and infant mortality in rural Bangladesh was performed.36 The study involved pregnant women (13 to 45 years old) and their live-born infants to 12 weeks (84 days) postpartum. Five-hundred ninety-six community clusters (study sectors) were randomized for pregnant women to receive 7000 ¬µg retinol equivalents (as retinyl palmitate), 42 mg of all-trans beta carotene, or placebo from the first trimester through 12 weeks postpartum. Married women (n = 125,257 total; 32,180 to 32,719 per group) underwent surveillance for pregnancy, ascertained by a history of amenorrhea and confirmed by a urine test. Groups were comparable across risk factors. For the maternal mortality, neither of the supplemental groups was significantly different from the placebo groups. The numbers and all-cause, pregnancy-related mortality rates (per 100,000 pregnancies) were: 41 and 206 (95% confidence interval [CI] = 140-273) in the placebo group, 47 and 237 (95% CI = 166- 309) in the vitamin A group, and 50 and 250 (95% CI = 177-323) in the beta carotene group. Relative risks of maternal mortality in the vitamin A and beta carotene groups were not statistically significantly different from controls (1.15; 95% CI = 0.75-1.76 and 1.21; 95% CI = 0.81-1.81 for the vitamin A and beta carotene groups, respectively). There were 703 stillbirths in the placebo group, 665 in the vitamin A group, and 766 in the beta carotene group. Rates of stillbirths per 1000 births were: 47.9 (95% CI = 44.3 -51.5 [placebo]), 45.6 (95% CI = 42.1-49.2) [vitamin A]), and 51.8 (95% CI = 48.0-55.6 [beta carotene]). Relative risks of infants being still born were not statistically significantly different in the supplemented groups, compared to the placebo group (0.95; 95% CI = 0.85 -1.06 for the vitamin A group and 1.08; 95% CI = 0.97 to 1.21 for the beta carotene group). Infant mortality rates per 1000 births were: 68.1 (95% CI = 63.7- 72.5 [placebo]), 65.0 (95% CI = 60.7-69.4 [vitamin A]), and 69.8 (95% CI = 65.4-72.3 [beta carotene]). It was concluded that, compared to the placebo, weekly vitamin A or beta carotene supplementation in pregnant women in Bangladesh did not reduce all-cause maternal, fetal, or infant mortality.36 In Vitro Study Retinol The developmental toxicity of retinol was evaluated in the embryonic stem (ES)-D3 cell differentiation assay of the embryonic stem cell test.37 The murine ES-D3 cell line was used, and this assay was performed to determine the test concentrations affecting ES-D3 cell differentiation into contracting cardiomyocytes. Exposure to the test substance, added from a 400-times concentrated stock solution in DMSO to culture medium, started at day 1 and lasted for 10 days. A test was considered valid when at least 21 out of 24 wells of the blank (non-exposed) cells and the solvent control plate contained contracting cardiomyocytes. Retinol caused a concentration-dependent decrease in ES-D3 cell differentiation in the 102 to 104 nM concentration range.

General safety info about Beta-Carotene from CIR

No report found.

Use this, not that!

Products where you might find Beta-Carotene

Fresh Vitamin Nectar Glow Juice Antioxidant Face Serum Mini, Kiehl’s Since 1851 Mini Creamy Eye Treatment with Avocado, Kiehl’s Since 1851 Creme de Corps Mini