Protective Effect Of Β-carotene Research Articles

Protective effect of β-carotene on OVA-induced food allergy in mice by strengthening intestinal epithelial barrier function and regulating intestinal microflora

β-Carotene is a dietary source of vitamin A, and its physiological functions, such as anti-inflammatory activity, immune regulation, and improvement of intestinal flora, are attracting increasing attention. Recent studies have shown that the development of food allergy is closely related to intestinal dysfunction. Therefore, the present study investigated the potential anti-food allergy activity of β-carotene and its regulatory intestinal homeostasis pathway. The results obtained using an ovalbumin (OVA)-induced food allergy mouse model indicated that the clinical allergic symptoms were alleviated, and the levels of anaphylactic mediators (such as immunoglobulin (Ig) E, IgG, and histamine) were reduced after β-carotene supplementation at 5.00 mg per kg per day. In addition, the expression of tight junction (TJ) proteins (claudin-1, occludin, and ZO-1) increased by 38.58%, 24.39%, and 26.23%, respectively. Additionally, the secretion of secretory IgA (sIgA) and the regeneration of islet-derived protein (Reg) IIIγ were promoted in the intestinal mucous after β-carotene administration. Furthermore, the alpha and beta diversity analysis showed that the composition and diversity of the intestinal flora in the β-carotene group tended to be normalized compared to the model group. Higher levels of beneficial bacteria, such as Clostridiaceae, were evident in the intestinal microflora of the sensitized mice after β-carotene administration, while pathogenic bacteria, such as Streptococcaceae, were reduced. Consequently, β-carotene may protect against food allergy by strengthening intestinal epithelial barrier function and regulating intestinal microflora.

Protective Effects of β-Carotene Against Ammonium Sulfate Toxicity: Biochemical and Histopathological Approach in Mice Model

In this study, the protective role of β-carotene against ammonium sulfate-induced toxicity has been evaluated in Mus musculus var. albino mice, along with biochemical and histopathological parameters. Some biochemical parameters such as aspartate transaminase (AST), alanine transaminase (ALT), blood urea nitrogen (BUN), creatinine and oxidative stress parameters, malondialdehyde (MDA), and glutathione (GSH) levels in kidney and liver tissues were investigated. The mice were randomly divided into six groups. Group I received intraperitoneal injections of 0.9% NaCl; group II received orally administered 250 mg kg-1 bw β-carotene, group III received orally administered 500 mg kg-1 bw β-carotene; group IV received 320 mg kg-1 bw ammonium sulfate; group V was given 250 mg kg-1 bw β-carotene +320 mg kg-1 of bw ammonium sulfate; and group VI received orally administered 500 mg kg-1 of bw β-carotene +320 mg kg-1 of bw ammonium sulfate. As a result, it was determined that the ammonium sulfate treatment causes significant changes in the biochemical and oxidative stress parameters and also in histological examinations. In group IV, significant increases in ALT, AST, BUN, MDA, and creatinine levels, and a significant decrease in GSH levels were observed compared with control group. In histopathological examinations, different pathological findings such as proteinaceous deposits, thickening of basement membrane, hyaline cast in kidney tissue and stellate cell, karyomegaly, and binucleated cells in liver tissue were observed. β-carotene treatment in group V and VI ameliorated the elevated levels of liver enzymes and improved oxidative stress and histopathological findings, and so, it could be concluded that β-carotene offered remarkable protection against ammonium sulfate-induced toxicity.

The cyanobacterium Oscillatoria brevis β-carotene extract modulates alterations of biochemical and hematological circadian patterns in stress-induced rat

Managing stress can prevent serious health problems. The present study aimed to evaluate the possible protective effect of β-carotene (βC), as a natural cyanobacterial product, against stress-induced alterations in biochemical and hematological circadian patterns. Male albino rats were subjected to chronic unpredictable stress (CUS) for 21 days. Rats were randomly divided into four groups (20 rats/group), viz. control, CUS exposed, βC-treated, and βC-treated + CUS-exposed groups. Before CUS exposure, Oscillatoria brevis βC extract was administered (10 mg/kg), intraperitoneally. Blood samples were collected at four Zeitgeber times (ZT: 3, 9, 15 and 21), 5 rats/time point, to monitor circadian profiles of aspartate transferase (AST), alanine transferase (ALT), total protein (TP), glucose (Glu), urea, creatinine, lactate dehydrogenase (LDH), creatinine kinase-MB (CK-MB), hemoglobin (Hb), hematocrite (HCV), red blood cell (RBCs), and white blood cell counts (WBCs). Results revealed that these parameters expressed circadian patterns. CUS exposure significantly (p < 0.05) increased AST, ALT, Glu, urea, creatinine, LDH, CK-MB, and HCV. On the other hand, it significantly decreased Hb, RBCs, and WBCs (p < 0.05). Furthermore, under CUS-exposure the peak time (acrophase) of circadian rhythms of all parameters was variably shifted. On the other hand, βC administration modulated these alternations, where data analysis confirmed a significant decrease in AST, ALT, Glu, urea, creatinine, LDH, CK-MB, and HCV, however, a significant increase in TP, Hb, RBCs, and WBCs (p < 0.05) was observed. Taken together, it can be concluded that βC administration caused restoration of acrophase and level of these parameters thus regulating their circadian rhythms in CUS-induced rats.

β-carotene protects the gastric mucosa against ischemia-reperfusion injury in rats

The aim of the present study was to investigate the protective effect of β-carotene on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rat. Forty male rats were randomly divided into sham, control (I/R injury) and three β-carotene-pretreated groups. To induce the I/R lesions, the celiac artery was clamped for 30 min. The clamp was then removed to allow reperfusion for three hours. Pretreated-rats received β-carotene (15, 30 or 60 mg/kg daily, i.p.) or vehicle for five days before the induction of the I/R injury. Samples of gastric mucosa were collected to measure the mRNA expression of IL-1β, TNF-α and TGF-β by quantitative, real-time PCR. Pretreatment with β-carotene decreased the total area of gastric ulcer and mRNA expression, as well as plasma levels of pro-inflammatory cytokines, IL-1β and TNF-α, in a dose-dependent manner. The gene expression and plasma levels of the anti-inflammatory cytokine, TGF-β, were significantly increased in β-carotene-pretreated groups compared with the control. Our findings showed that the protective effect of β-carotene may be mediated partly by reducing mRNA expression and plasma levels of IL-1β and TNF-α, and concurrently, by increasing gene expression and plasma levels of the anti-inflammatory cytokine TGF-β. These findings suggest that β-carotene has a protective role in gastric mucosa. Further clinical and in vivo studies need to be undertaken to support this hypothesis.

Protective effects of β‐carotene and melanin against protoporphyrine IX‐induced phototoxicity in the photo hen's egg test

The aim of our study was to evaluate the photoprotective potential of melanin and β-carotene against protoporphyrine IX-induced phototoxicity via photo hen's egg test. In three independent test groups, the yolk sac blood vessel system of hen's eggs was exposed to protoporphyrine IX and irradiated with ultraviolet A (UVA). One of the test groups also received melanin to investigate its photoprotective capacity; another test group received β-carotene for the same purpose. Morphological changes and embryo lethality were recorded in these three test groups for a period of 24 h. The same parameters were obtained in five different control groups. The control groups exhibited only minimal morphological changes and no fatalities. In contrast, severe phototoxic damage and a high lethality rate (75%) were observed in the test group exposed to protoporphyrine IX and UVA. Lethality was somewhat lower in the β-carotene test group (58%) and was considerably lower in the melanin test group (17%). The photoprotective potential against protoporphyrine IX-induced phototoxic damage was moderate for β-carotene and was remarkable for melanin. Given that synthetic melanocyte stimulating hormone (MSH) analogues induce a de novo synthesis of melanin without any previous ultraviolet irradiation in human skin, the application of MSH analogues might be conceived of as 'light hardening' without light. Synthetic MSH analogues thus may represent a new promising therapeutic option for photodermatoses especially for erythropoietic protoporphyria.

Protective Effect of β-Carotene on Methotrexate–Induced Oxidative Liver Damage

In this study, the authors aimed to investigate the role of oxidative stress on the hepatic damage caused by methotrexate (MTX) and the possible protective effects of beta-carotene against this damage. The rats were divided into four groups as control, MTX (20 mg/kg ip), beta-carotene (10 mg/kg/day ip) + MTX, and beta-carotene. Histopathologic alterations were evaluated for defining the liver damage. The tissue, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GP-x) contents and serum aspartate aminotransferase (AST) and alanine aminotranferase (ALT) activities were also examined. Histopathologic damage for each group score findings have been determined as control: 0.66 +/- 0.33; MTX: 7.0 +/- 0.68; beta-carotene + MTX: 3.3 +/- 0.42; and beta-carotene: 0.5 +/- 0.3. In the MTX-treated group, MDA, AST, and ALT values were increased, while SOD and GP-x values were decreased compared with the control group. In the beta-carotene + MTX-treated group, AST and ALT values significantly decreased, while all other parameters were similar to the control group. This study shows that beta-carotene has a protective effect on MTX-induced oxidative hepatic damage. Consequently, it seems that an antioxidant agents like beta-carotene may be useful in decreasing the side effects of chemotherapy.

Protective effects of β-carotene against the genotoxicity of doxorubicin in somatic cells of Drosophila melanogaster

beta-carotene (BC), pro-vitamin A, is an efficient antioxidant, effective in the neutralization of oxygen reactive species, which cause serious damage to DNA. Various studies have been conducted on the effectiveness of BC for chemoprevention of cancer and heart disease. Doxorubicin is a chemotherapeutic agent used for cancer treatment that generates free radicals. We examined the effects of BC (1, 2 and 4 mg/mL) on the genotoxicity of doxorubicin (0.125 mg/mL), using the wing spot test in Drosophila melanogaster (somatic mutation and recombination test). The BC alone had no significant effect on the frequency of mutant spots. However, it significantly reduced the number of spots caused by doxorubicin. We concluded that BC is not genotoxic and that it exerts protective effects against the genotoxic action of the chemotherapeutic free-radical generator doxorubicin.

Antibiotic-Induced Alterations in the Osmotic Resistance of Erythrocytes is Modulated by β-Carotene and L –Ascorbic Acid

Ciprofloxacin, Erythromycin and Norfloxacin are potent anti-microbials. These antibiotics, besides affecting bacteria, also exert toxic effects on mammalian cells. The present work was undertaken to study the effect of these antibiotics on the osmotic fragility profile of erythrocytes and the protective role played by vitamin supplementation, which exerts a stabilizing effect on the erythrocytes making them more resistant to lysis under hypotonic stress. The protective effect of β-carotene and L-ascorbic acid was significant (p &lt; 0.01) at 0.1 mM and 0.01 mM concentrations. No significant effect was observed at lower concentrations. The free radical scavenging activity and effect of these vitamins on membrane fluidity and permeability may explain the protective role against the damage induced by the antibiotics on the erythrocytes membrane.

Radioprotection of β-carotene evaluated on mouse somatic and germ cells

In the present paper, the protective effect of β-carotene was evaluated after whole body exposure of mice to 2 Gy of X-rays. Splenocytes, reticulocytes, bone marrow cells and spermatids were evaluated for the frequency of micronuclei (MN) induced by X-rays. Mice were treated (gavage) with β-carotene (10,25 and 50 mg/kg b.w.) for 5 consecutive days and, 4 h after the last treatment, the animals were irradiated. The results obtained showed different frequencies of X-ray-induced-MN between different cell populations analysed and also different response of these cells to the β-carotene treatment. The radioprotective effect of β-carotene was observed in splenocytes, reticulocytes, and spermatids but not in bone marrow cells. No dose-response relationship for β-carotene was detected. The time of sampling, the sensitivity of the cells as well as the antioxidant activity of β-carotene are discussed as important factors for the radioprotective action of this provitamin.

Effects of β-carotene and α-tocopherol on photogenotoxicity induced by 8-methoxypsoralen: The role of oxygen

The protective effect of β-carotene (β-C) and α-tocopherol (α-T), singularly and in equimolar mixtures, toward the photomutagenicity induced by 8-methoxypsoralen (8-MOP), at different oxygen partial pressure (pO 2), was evaluated in two different experimental models: Salmonella typhimurium TA102 and Saccharomyces cerevisiae D7. After phototreatment with 8-MOP, the results show a lethal effect under hypoxic conditions in both experimental model systems, an increase in revertants associated to the pO 2 increase in S. typhimurium TA102, and a decrease in revertants and convertants associated to the pO 2 increase in S. cerevisiae D7. In S. typhimurium TA102, in atmospheric condition, β-C and α-T (1.86 or 18.6 μM) show a protective effect only at the higher dosage. α-T was more protective than β-C. The equimolar mixtures show an antimutagenic effect at both dosage used with a synergistic effect at lower dosage and an additive antimutagenic activity at higher dosage. An inhibition of the spontaneous mutagenicity by mixtures at higher dosage was also observed. The results obtained in S. typhimurium TA102 show an antimutagenic effects of β-C, α-T and their mixture at 190 mmHg pO 2, confirming the data obtained in air condition. At 380 mmHg pO 2, α-T and the mixture show a significant antimutagenic activity; at 570 mmHg pO 2, only α-T is protective. At 760 mmHg pO 2, no protective effect was observed by the two antioxidants, and β-C increases the photomutagenicity induced by 8-MOP. In S. cerevisiae D7 a protective effect was only observed at 380 mmHg pO 2 with the mixture. No antigenotoxic effect was found in the other experimental conditions, even if the uptake of the two antioxidants was confirmed by HPLC. Our results underline the role of oxygen in the photomutagenicity induced by 8-MOP and in the antimutagenic activity of β-C and α-T. This is the first report confirming in a cellular experimental model the data obtained in some chemical systems: the protective effect of β-C only at low pO 2 and the synergistic effect of mixture of β-C and α-T.

β-Carotene inhibition of chemically induced toxicity in vivo and in vitro

In the past several years there has been a great deal of interest in the antioxidant β-carotene and other micronutrients for their protective potential against various toxic insults. Two studies concerning the protective effects of β-carotene, which were conducted in our laboratory, are reported here. The first involved the role of β-carotene in modifying two-stage skin tumorigenesis initiated by 7,12-dimethylbenz[ a]anthracene (DMBA) and promoted by phorbol 12-myristate 13-acetate (PMA, TPA). In this study, the protective effects of two types of dietary β-carotene, a beadlet formulation and crystalline β-carotene, were compared in two strains of mice (Skh:HR-1 and CR:ORL Sencar). Mice were maintained on food fortified with 3% β-carotene or on control diets. Mice receiving the β-carotene-supplemented diets had fewer tumours than mice in the control groups. However, only in the Skh strain of mice was this difference statistically significant. In the second study, an in vitro experiment, BALBc 3T3 mouse fibroblasts were used to determine β-carotene's accumulation in cells and the ability of these cells to metabolize β-carotene to vitamin A. This in vitro model was also used to show a β-carotene protective effect towards 8-MOP phototoxicity. These studies contributed to the increasing evidence of in vivo and in vitro protection by β-carotene against chemically induced toxicity.

Aging and carotene nutriture

There is a growing interest in carotenes, particularly β-carotene, because of the inverse relationship between the incidence of cancer and the consumption of β-carotene and serum levels of β-carotene, which has been seen in specific animal model systems (1–3) and several epidemiologic studies (4–7). The protective effect of β-carotene may be particularly important in the elderly population given that cancer is a major cause of death in this age group. Other age related diseases, such as atrophic gastritis, Alzheimer’s disease, cardiovascular disease, and cataract which are common to the elderly, may also be related to carotene status. The protective effect of β-carotene may not be through β-carotene conversion to vitamin A. β-carotene may also be biologically important as a potent singlet oxygen scavenger and as an antioxidant (8). Antioxidants have substantial potential to inhibit carcinogenesis and other adverse processes related to oxidative events. Therefore, β-carotene is considered to be a biologically important nutrient.

Wavelength Effect on Light-Induced Decomposition of Vitamin A and β-Carotene in Solutions and Milk Fat

The influence of fluorescent light on vitamin A in chloroform and β-carotene in hexane at 15°C and 25°C was investigated. The protective effect of β-carotene at different levels on light-induced destruction of vitamin A in chloroform was also determined. The effect of different wavelengths of fluorescent light on vitamin A and β-carotene contents of milkfat at 25°C was studied using several sharp-cut filters transmitting exactly defined wavelength intervals over a range of 350-750nm. A linear relation was found between the losses in vitamin A as well as β-carotene and time at both 15°C and 25°C. The rate of vitamin destruction tended to increase with increasing temperature; however, the temperature effect was not statistically significant (p≤0.05). β-carotene at concentrations ≤1.0μg/ml had no effect on photolysis of vitamin A; concentrations of 2.5-7.5μg/ml significantly protected vitamin A. The loss of β-carotene in milkfat was caused by wavelengths <465nm; longer wavelengths (465-750nm) had little or no effect. Vitamin A in milkfat was primarily destroyed by wavelengths ≤415nm and only slightly by the wavelengths between 415 and 455nm. It is concluded that vitamin A and β-carotene loss can be markedly reduced in foods by blocking light wavelengths below 465nm.

Letter: Limited usefulness of artificial light sources.

To the Editor.— A recent report 1 on ultraviolet light sources showed that the ultraviolet output of a solar simulator was similar to the natural spectrum of sunlight. For this reason, investigators are using this artificial light source to evaluate the effectiveness of sun-protective agents prior to sunlight performance tests. Implicit in this method is the assumption that the data obtained with such artificial light sources can be used to predict the results in sunlight tests. A recent study 2 with patients having erythropoietic protoporphyria (EPP) compared the ultraviolet protective qualities of orally administered β-carotene in tests using sunlightand a solar simulator. The authors reported that the results showed the qualitative protective effect of β-carotene with either light conditions, but they were concerned about "a lack of more quantitative correlation." We compared their data 2 obtained with sunlight and xenon-arc light in the 21 patients who had both tests by comparing the protective factors obtained with each light source (Table). The correlation coefficient for this comparison was