Administration Of Beta-carotene Research Articles

9-cis beta-carotene-enriched diet significantly improved cognition and decreased Alzheimer’s disease neuropathology and neuroinflammation in Alzheimer’s disease-like mouse models

A significant progressive decline in beta-carotene (βC) levels in the brain is associated with cognitive impairment and a higher prevalence of Alzheimer’s disease (AD). In this study, we investigated whether the administration of 9-cis beta-carotene (9CBC)-rich powder of the alga Dunaliella bardawil, the best-known source of βC in nature, inhibits the development of AD-like neuropathology and cognitive deficits. We demonstrated that in 3 AD mouse models, Tg2576, 5xFAD, and apoE4, 9CBC treatment improved long- and short-term memory, decreased neuroinflammation, and reduced the prevalence of β-amyloid plaques and tau hyperphosphorylation. These findings suggest that 9CBC has the potential to be an effective preventive and symptomatic AD therapy.

Zinc, Beta-Carotene, and Vitamin D<SUB>3</SUB> Supplementation and Placental IL-1β in Spontaneous Preterm Labor

Preterm birth (PTB) is one of the leading causes of neonatal death. Studies have shown that Interleukin-1 (IL-1β) critically contributes to inflammation-induced PTB, and micronutrients deficiencies might influence the inflammatory pathways. Since zinc, vitamin A, and vitamin D deficiencies are common in Indonesia, this study aims to evaluate those nutrients supplementation on placental IL-1β in PTB. A quasi-experimental study was conducted in pregnant women who underwent spontaneous delivery. They were divided into 3 groups; control-term group (n=25), control-preterm group (n=27), and experimental-preterm group (n=26). No intervention was given to the control-term and the control-preterm groups, while the experimental-preterm group was given zinc 50 mg/day, a single dose beta-carotene 25,000 IU, and vitamin D3 50,000 IU/week until delivery. Zinc, all-trans retinoic acid (AtRA) and 25-hydroxyvitamin D (25(OH)D) concentrations in maternal serum were measured before and after intervention, followed by assessment of placental concentration of those nutrients and IL-1β expression after delivery. One-way ANOVA and Kruskal Wallis tests were performed for comparison analysis and using Pearson or Spearman test for correlation analysis correlation test using Statistical Package for Social Sciences (SPSS). No significant difference in zinc, AtRA, and 25(OH)D concentrations was found in maternal serum, before and after the intervention. However, the experimental-preterm group had the lowest IL-1β concentration (7.17 pg/g (0.45–283.29), p=0.009). This study suggests that the administration of zinc, beta-carotene, and vitamin D3 in PTB was associated with lower placental IL-1β expressions, although it did not directly increase those nutrient concentrations in serum and placenta.

Effects of Beta-carotene Administration on Fertility in Lactating Dairy Cows

Background: Beta-(β-) carotene, is the precursor to vitamin A, in particular, has some potential benefits on reproduction. The main objective of this study was to investigate the efficacy of β-carotene administration on fertility following either prostaglandin F2 alpha (PGF) induced estrus or Ovsynch protocol in lactating dairy cows. Methods: Cows with at 47±3 postpartum days were divided into two groups: β-carotene group (βC, n=139) was treated with injectable β-carotene while untreated cows served as control (CON, n=227). In both groups, PGF was administered and heatmount detectors were applied at 54±3 days postpartum. Cows detected in estrus after PGF were inseminated. Cows that had not been detected in estrus were divided into two groups 7 days after PGF administration; βC-OVS (n=137) and CON-OVS (n=89). Ovsynch protocol was initiated 4 days after β-carotene administration. Result: The estrus detection rate was similar between the βC and CON groups (P = 0.19). Pregnancy per AI (P/AI) on d 31 was also similar between groups (P = 0.93). In the Ovsynch protocol, ovulation to the first GnRH and ovulatory follicle diameter at the time of insemination did not differ between groups. No difference was observed in P/AI at d 31 (P = 0.13). The results of this study indicated that β-carotene administration had no effect on fertility either PGF induced estrus or Ovsynch protocol in dairy cows.

Pharmacological Prevention of Noise-induced Hearing Loss: A Systematic Review.

This study aims to explore and determine the effectiveness of current pharmacologic agents for the prevention of noise-induced hearing loss (NIHL) via a systematic review. The PubMed, Scopus, ClinicalTrials.gov, and Cochrane Library databases were searched from inception through February 6, 2020. Full-text, English-language articles detailing prospective randomized and nonrandomized clinical trials with pharmacological interventions administered to prevent NIHL were included in accordance with PRISMA guidelines. The detailed search terms are included in the Appendix, http://links.lww.com/MAO/B67. Eleven articles were included in this review with 701 patients receiving a pharmacologic prevention for various noise exposures. Various regimens included administration of alpha-lipoic acid, ambient oxygen, beta-carotene, carbogen, ebselen, Mg-aspartate, N-acetylcysteine, and vitamins C, E, and B12. A number of studies demonstrated statistically significant amelioration of NIHL with pharmacologic intervention. Two studies demonstrated significantly better hearing outcomes for pharmacological prophylaxis with carbogen or ebselen as compared with placebo for the 4 kHz frequency, where the noise-notch is most likely to be encountered. Given the considerable heterogeneity in agents and methodologies, however, it was not possible to conduct a meta-analysis. While several heterogenous articles demonstrated promising results for Mg-aspartate, carbogen, vitamin B12, and alpha-lipoic acid, the clinical significance of these pharmaceuticals remains unclear. Initial data from this study alongside future clinical trials might potentially contribute to the generation of clinical practice guidelines to prevent NIHL. 2.

Beta Carotene Modulates Nitric Oxide Production in the Renal Ischemia/Reperfusion Injury in Rat

Background: Renal ischemia and subsequent reperfusion injury is a major cause of acute renal failure and transplant rejection. Nitric oxide and its metabolites have important role in renal ischemia/reperfusion injury. Beta carotene as an antioxidant effectively scavenges toxic metabolites of nitric oxide. Our previous study has shown that beta carotene pretreatment protects kidney against ischemia/reperfusion injury. Objectives: In this experimental study we investigated whether effect of beta carotene is causally linked with nitric oxide signal transduction. Methods: In this experimental study, male adult Wistar rats (250 - 300 g) were exposed to 45 minutes of renal ischemia followed by 4 hours of reperfusion. Beta carotene (10, 30 and 100 mg kg-1) or vehicle was administered for 5 days prior to ischemia. Nitrite and nitrate were measured in the urine sample. Blood Flow and blood pressure were monitored during I/R period. Results: I/R decreased (P < 0.001) urinary nitrite - nitrate and renal blood flow. Beta carotene pretreatment increased them (P < 0.05 - P < 0.001), although not by all doses. Blood pressure was not affected by beta carotene. Conclusions: Since beta carotene administration improved renal blood flow and reduced the injury, it seems that beta carotene exerts some of its protective effects, probably by modulating of nitric oxide system.

Sun protection for preventing basal cell and squamous cell skin cancers.

'Keratinocyte cancer' is now the preferred term for the most commonly identified skin cancers basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC), which were previously commonly categorised as non-melanoma skin cancers (NMSC). Keratinocyte cancer (KC) represents about 95% of malignant skin tumours. Lifestyle changes have led to increased exposure to the sun, which has, in turn, led to a significant increase of new cases of KC, with a worldwide annual incidence of between 3% and 8%. The successful use of preventive measures could mean a significant reduction in the resources used by health systems, compared with the high cost of the treatment of these conditions. At present, there is no information about the quality of the evidence for the use of these sun protection strategies with an assessment of their benefits and risks. To assess the effects of sun protection strategies (i.e. sunscreen and barrier methods) for preventing keratinocyte cancer (that is, basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC) of the skin) in the general population. We searched the following databases up to May 2016: the Cochrane Skin Group Specialised Register, CENTRAL, MEDLINE, Embase, and LILACS. We also searched five trial registries and the bibliographies of included studies for further references to relevant trials. We included randomised controlled clinical trials (RCTs) of preventive strategies for keratinocyte cancer, such as physical barriers and sunscreens, in the general population (children and adults), which may provide information about benefits and adverse events related to the use of solar protection measures. We did not include trials focused on educational strategies to prevent KC or preventive strategies in high-risk groups. Our prespecified primary outcomes were BCC or cSCC confirmed clinically or by histopathology at any follow-up and adverse events. Two review authors independently selected studies for eligibility using Early Review Organizing Software (EROS). Similarly, two review authors independently used predesigned data collection forms to extract information from the original study reports about the participants, methods of randomisation, blinding, comparisons of interest, number of participants originally randomised by arm, follow-up losses, and outcomes, and they assessed the risk of bias. We resolved any disagreement by consulting a third author and contacted trial investigators of identified trials to obtain additional information. We used standard methodological procedures expected by Cochrane. We included one RCT (factorial design) that randomised 1621 participants.This study compared the daily application of sunscreen compared with discretionary use of sunscreen, with or without beta-carotene administration, in the general population. The study was undertaken in Australia; 55.2% of participants had fair skin, and they were monitored for 4.5 years for new cases of BCC or cSCC assessed by histopathology. We found this study to be at low risk of bias for domains such as allocation, blinding, and incomplete outcome data. However, we found multiple unclear risks related to other biases, including an unclear assessment of possible interactions between the effects of the different interventions evaluated (that is, sunscreen and beta-carotene). We found no difference in terms of the number of participants developing BCC (n = 1621; risk ratio (RR) 1.03, 95% confidence interval (CI) 0.74 to 1.43) or cSCC (n = 1621; RR 0.88, 95% CI 0.50 to 1.54) when comparing daily application of sunscreen with discretionary use, even when analyses were restricted to groups without beta-carotene supplementation. This evidence was of low quality, which means that there is some certainty that future studies may alter our confidence in this evidence.We reported adverse events in a narrative way and included skin irritation or contact allergy.We identified no studies that evaluated other sun protection measures, such as the use of sun-protective clothing, sunglasses, or hats, or seeking the shade when outdoors. In this review, we assessed the effect of solar protection in preventing the occurrence of new cases of keratinocyte cancer. We only found one study that was suitable for inclusion. This was a study of sunscreens, so we were unable to assess any other forms of sun protection. The study addressed our prespecified primary outcomes, but not most of our secondary outcomes. We were unable to demonstrate from the available evidence whether sunscreen was effective for the prevention of basal cell carcinoma (BCC) or cutaneous squamous cell carcinoma (cSCC).Our certainty in the evidence was low because there was a lack of histopathological confirmation of BCC or cSCC in a significant percentage of cases. Amongst other sources of bias, it was not clear whether the study authors had assessed any interaction effects between the sunscreen and beta-carotene interventions. We think that further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.

ROLE OF DIETARY SUPPLEMENTATION IN PREVENTING PROGRESSION OF AGE-RELATED MACULAR DEGENERATION

Age-related macular degeneration (AMD) is a chronic, progressive, degenerative eye disease affecting the central retina. It is the leading cause of blindness among individuals of 65 years and older. In the early stage patients have drusen and/or alterations of pigmentation in the macular region. This disease can progress to geographic atrophy and/or choroidal neovascularization. It has been shown that oxidative stress and hypoxia are important in the pathogenesis of AMD. Patients may gain some visual improvement with inhibitors of vascular endothelial growth factor, but complete restoration of visual function is achieved only in small cases. No effective therapies are known for atrophic AMD. Many large observational studies have shown that dietary antioxidant supplementation is beneficial in preventing the progression of AMD from early to late stages. The Age-Related Eye Disease Study (AREDS) demonstrated that daily oral supplementation with vitamins C (500 mg) and E (400 IU), beta carotene (15 mg), zinc (80 mg) and copper (2 mg) reduced the risk of progression to advanced AMD by 25% at 5 years. In primary analyses AREDS II failed to show further reduce of this risk by addition of lutein (10 mg) and zeaxanthin (2mg), or/and omega-3 long-chain polyunsaturated fatty acids [docosahexaenoic acid (350 mg DHA) and eicosapentaenoic acid 650 mg (EPA)] to the AREDS formulation. But there was no true placebo group. The simultaneous administration of beta carotene, lutein and zeaxanthin may suppress tissue level of the both laters because of competitive absorption of carotenoids. Subgroup analyses revealed that dietary supplementation with lutein, zeaxanthin and AREDS formulation without beta carotene may reduce the risk of progression to advanced AMD.The LUNA (Lutein nutrition effects measured by autofluorescence) study demonstrated that supplementation with lutein (12 mg), zeaxanthin (1 mg), vitamin C (120 mg), vitamin E (17,6 mg), zinc (10 mg), selenium (40 mg) resulted in a significant augmentation of macular pigment optical density (MPOD). This effect was more prominent in cases with initial low level of MPOD. The CARMA (Carotenoids in Age-Related Maculopathy) Study has shown that lutein (6 mg), zeaxanthin (0,3 mg), vitamin C (75 mg), vitamin E (7,5 mg), zinc (10 mg) and copper (0,2 mg) prevented progression from early to late stages of AMD. Early intervention is more effective in maintaining visual function.

Beta-carotene reduces oxidative stress, improves glutathione metabolism and modifies antioxidant defense systems in lead-exposed workers

The aim of this study was to determine whether beta-carotene administration reduces oxidative stress and influences antioxidant, mainly glutathione-related, defense systems in workers chronically exposed to lead.The population consisted of two randomly divided groups of healthy male volunteers exposed to lead. Workers in the first group (reference group) were not administered any antioxidants, while workers in the second group (CAR group) were treated orally with 10mg of beta-carotene once a day for 12weeks. Biochemical analysis included measuring markers of lead-exposure and oxidative stress in addition to the levels and activities of selected antioxidants.After treatment, levels of malondialdehyde, lipid hydroperoxides and lipofuscin significantly decreased compared with the reference group. However, the level of glutathione significantly increased compared with the baseline. Treatment with beta-carotene also resulted in significantly decreased glutathione peroxidase activity compared with the reference group, while the activities of other glutathione-related enzymes and of superoxide dismutase were not significantly changed. However, the activities of glucose-6-phosphate dehydrogenase and catalase, as well as the level of alpha-tocopherol, were significantly higher after treatment compared with the baseline.Despite controversy over the antioxidant properties of beta-carotene in vivo, our findings showed reduced oxidative stress after beta-carotene supplementation in chronic lead poisoning.

THE INFLUENCE OF β-CAROTENE ON HOMOCYSTEINE LEVEL AND OXIDATIVE STRESS IN LEAD-EXPOSED WORKERS

Oxidative stress is involved in lead toxicity. This suggests that some antioxidants may play a role in the treatment of lead poisoning. In the light of this, the aim of the study was to determine whether beta-carotene administration reduces oxidative stress and homocysteine level in workers chronically exposed to lead. The exposed population included healthy male workers exposed to lead who were randomly divided into 2 groups (mean blood lead level ca. 44 microg/dl). Workers in the 1st group (N = 49, reference group) had no antioxidants, drugs, vitamins or dietary supplements administered, while workers in the 2nd group (N = 33) had beta-carotene administered in a dose of 10 mg per day for 12 weeks. Biochemical analysis included markers of lead-exposure and the level of malondialdehyde (MDA), an oxidative stress biomarker. We also measured the level of homocysteine (Hcy) and thiol groups as well as the activity of superoxide dismutase (SOD) and its isoenzyme EC-SOD in serum. After supplementation, the level of MDA significantly decreased, compared to baseline, by 16%, and to the reference group. When compared to the reference group, Hcy level was also significantly decreased. However, the level of thiol groups was significantly higher after supplementation with beta-carotene compared to the reference group. Analogically, the activity of SOD and EC-SOD was significantly higher compared to the baseline and to the reference group. Despite some controversies over antioxidant properties of beta-carotene, our results indicate that its antioxidant action could provide some beneficial effects in lead poisoning independent of chelation.

Diet supplementation with beta-carotene improves the serum lipid profile in rats fed a cholesterol-enriched diet

The present study investigated the underlying mechanism associated with the hypocholesterolemic activity of beta-carotene by examining its effects on the serum lipid profile, fecal cholesterol excretion, and gene expression of the major receptors, enzymes, and transporters involved in cholesterol metabolism. Female Fischer rats were divided into three groups and were fed either a control or a hypercholesterolemic diet supplemented or not supplemented with 0.2 % beta-carotene. After 6 weeks of feeding, blood, livers, and feces were collected for analysis, and quantitative real-time polymerase chain reaction (qRT-PCR) was performed. Dietary supplementation with 0.2 % beta-carotene decreased serum total cholesterol, non-HDL cholesterol, the atherogenic index, and hepatic total lipid and cholesterol contents. These changes were accompanied by an increase in the total lipid and cholesterol contents excreted in the feces. The qRT-PCR analyses demonstrated that the hypercholesterolemic diet promoted a decrease in the gene expression of sterol regulatory element-binding protein 2, 3-hydroxy-3-methylglutaryl CoA reductase, and low-density lipoprotein receptor and an increase in the gene expression of peroxisome proliferator-activated receptor α and cholesterol-7a-hydroxylase. The expression of these genes and gene expression of ATP-binding cassette subfamily G transporters 5and 8 were unaffected by beta-carotene supplementation. In conclusion, the decrease in serum cholesterol and the elevation of fecal cholesterol obtained following beta-carotene administration indicate that this substance may decrease cholesterol absorption in the intestine and increase cholesterol excretion into the feces without a direct effect on the expression of cholesterol metabolism genes.

Effect of MAO-B Inhibition against Ischemia-induced Oxidative Stress in the Rat Brain

An increasing number of reports suggest the involvement of oxidative stress in neurodegenerative diseases where the increased formation of reactive oxygen species (ROS) leads to neuronal damage and cell death. Dopamine may contribute to neurodegenerative disorders such as Parkinson's disease and ischemia/reperfusion-induced damage. Monoamine oxidase (MAO) enzyme (particularly MAO-B) is responsible for metabolizing dopamine and plays an important role in oxidative stress through altering the redox state of neuronal and glial cells. MAO participates in the generation of hydroxyl radicals during ischemia/reperfusion. This suggests the possible use of MAO inhibitors as neuroprotective agents for treating ischemic injury. The protective effect of deprenyl (N-methyl-N-(1-methyl-2-phenyl-ethyl)-prop-2-yn-1-amine, CAS 14611-51-9) (2 and 10 mg/kg), a MAO-B inhibitor, and beta-carotene (10 and 20 mg/kg), a natural antioxidant, was examined in a rat model of cerebral ischemia. Ischemia was induced in rats by bilateral carotid artery occlusion for 1 h followed by declamping for another hour. The effect of the drugs on the brain activity of lactate dehydrogenase (LDH) and some of the oxidative stress biomarkers such as brain activity of superoxide dismutase (SOD) and catalase (CAT) enzymes and brain malondialdehyde (MDA) content was determined. In addition, the content of catecholamines such as noradrenaline (NA) and dopamine (DA) was determined. Deprenyl decreased the ischemia-induced elevation of LDH activity and MDA content and normalized the SOD activity. In addition, deprenyl increased the CAT activity back to normal, and increased the noradrenaline and dopamine content in the brain of rats. Beta-carotene administration ameliorated the effect of ischemia followed by reperfusion (I/R) demonstrated as decreasing the LDH activity and MDA content and by increasing the SOD activity. The drug also increased CAT activity in the brain of rats. However, beta-carotene did not alter the NA and DA content. These results indicate that deprenyl protected the rat brains against the ischemia-induced oxidative damage, an effect which might be explained through multiple mechanisms, possibly due to reduction of dopamine catabolism with a subsequent increased activity on dopaminergic D2 receptors and suppressing the action of ROS as well.

Effect of beta carotene on lipid peroxidation and antioxidant status following renal ischemia/reperfusion injury in rat

Background. The production of free radicals and reactive oxygen species are important factors contributing to ischemia/reperfusion injury. Thus scavenging of the excess free radicals can be an important therapeutic approach. Beta carotene, a carotenoid pigment has a potent antioxidant property. The present study examined the effect of beta carotene administration on the level of renal content of antioxidants and lipid peroxidation following ischemia/reperfusion injury in the rat kidney. Methods. Male adult Wistar rats (250–300 g) were exposed to 45 min of renal ischemia followed by 4 h of reperfusion. Beta carotene (10, 30 and 100 mg kg−1) or vehicle was administered for 5 days prior to ischemia. Renal content of antioxidants and the level of lipid peroxidation were measured after the reperfusion period. Results. Our results showed that ischemia/reperfusion injury increased lipid peroxidation (p < 0.001) and decreased antioxidant (p < 0.001) in renal tissue. Pre-administration of beta carotene could attenuate these alterations (p < 0.05–p < 0.001), although not at all doses. Since beta carotene administration improved renal lipid peroxidation and antioxidants, it seems that beta carotene protects renal tissue against ischemia/reperfusion-induced oxidative damage.

Protective Effect of Beta Carotene Pretreatment on Renal Ischemia/Reperfusion Injury in Rat

Renal ischemia/reperfusion injury is a major cause of acute renal failure. The production of free radicals and reactive oxygen species are important factors contributing to ischemia/reperfusion injury. Thus, scavenging of the excess free radicals can be an important therapeutic approach. The present study examined the protective effect of beta carotene against renal ischemia/reperfusion injury in rat. Male adult Wistar rats (250-300 g) were exposed to 45 min of renal ischemia followed by 4 h of reperfusion. Beta carotene (10, 30 and 100 mg kg(-1)) or vehicle was administered for 5 days prior to ischemia. Renal function was assessed by plasma and urinary analysis. Present results showed that ischemia/reperfusion injury increased (p < 0.05-p < 0.001) serum urea and creatinine levels, as well as urinary excretion of protein and calcium and fractional excretion of sodium, while decreased glomerular filtration rate and potassium excretion. However, alterations in these biochemical indices due to ischemia/reperfusion injury were attenuated by beta carotene pretreatment (p < 0.05-p < 0.001), although not by all doses. Since, beta carotene administration improved renal function, it seems that beta carotene protects renal tissue against ischemia/reperfusion-induced oxidative damage.

Administration of Lycopene and Beta-Carotene Decreased Risks of Pneumonia among Children

This study aimed to investigate the effect of lycopene and beta-carotene on pneumonia among children. Forty infant and child aged 6 to 36 months suffer from pneumonia and admitted Bab El-Shaareya Hospital for treatment were selected for this study. The children divided into four equal groups; control group (CG), beta carotene group (BCG), lycopene group (LYG) and mixture (lycopene+beta-carotene) group (MG). All subjects were received hospital meal without any modification, while BCG received 15mg/day of beta carotene; LYG received 15 mg/day of lycopene and MG received 7.5 mg/day lycopene +7.5 mg/day beta carotene. All groups received hospital meal in addition to tested carotenoid that dissolved in orange juice. The intervention period continued for 14 consecutive days. The respiratory rate (RR) and temperature were measured daily till recovery. Also, WBCs, IgE and IgG were determined at admission and after intervention period. Results showed that RR of MG and LYG groups returned normal after 21.6±7.2 and 26.4±10.4 hours respectively at P<0.05, while CG recovered after 37.2±13.6 hours. Moreover, administration of lycopene decreased RR significantly (P<0.05) by 37.6%, while administration of beta carotene or the mixture resulted in decrement of RR by 33.4% and 28.4% respectively. Also, the administration of lycopene reduced IgE significantly (P<0.05) by 63.7%, followed by the mixture that reduced it by 40.7% (P<0.05). In conclusion the administration of lycopene alone or mixed with beta carotene had a favorable affect on recovery of pneumonia among children.

Efeito da suplementação de beta-caroteno na pressão arterial de ratos

OBJETIVO: Investigar se a suplementação com doses suprafisiológicas de beta-caroteno exerce efeito positivo no controle da hipertensão arterial, e detectar possíveis efeitos adversos dessa suplementação. MÉTODOS: Ratos espontaneamente hipertensos (n=12) e normotensos (n=12) com 20 semanas, foram submetidos a um período basal de 10 dias, e subdivididos em 4 grupos de 6 animais, suplementados com beta-caroteno em três diferentes doses: 2,5mg, 3,75mg e 5,0mg por animal, via gavagem orogástrica diária, durante 14 dias para cada dose, intercaladas por um período de wash-out de 7 dias; os grupos controle receberam apenas o veículo (óleo de coco). Foram ainda submetidos à avaliação ectoscópica para possível detecção de efeitos tóxicos ou interação entre nutrientes, e à análise dos parâmetros biológicos; a pressão sistólica foi aferida por pletismografia duas vezes na semana, em dias alternados. Após o período de suplementação os animais foram sacrificados, e tiveram o peso do fígado determinado pelo método de Scherle. RESULTADOS: A administração de beta-caroteno não levou a alterações dos parâmetros biológicos dos animais, assim como não foi detectado efeito tóxico. Quanto à pressão arterial sistólica, as duas linhagens apresentaram redução significante (p&lt;0,05), sendo a maior redução observada durante administração da terceira dose. O peso médio do fígado foi de 7,25 (desvio-padrão 3,2) gramas, e a relação média do peso do órgão/média do peso corpóreo igual a 0,0192 para o grupo dos hipertensos. CONCLUSÃO: A suplementação de beta-caroteno tem efeito positivo tanto no controle quanto na prevenção da hipertensão arterial de ratos. A relação peso do fígado/peso corpóreo apresentou-se dentro dos padrões de normalidade.

Effects of Administration of beta-Carotene, Ascorbic Acid, Persimmons, and Pods on Antioxidative Ability in UV-Irradiated ODS Rats

To evaluate the effects of supplementing diets with carotenoid and ascorbic acid (AsA) on the antioxidative ability of Osteogenic Disorder-Shionogi (ODS) rats, we added synthetic beta-carotene (betaC), AsA, and powders of persimmon (Ka) and pods (Po) containing betaC and AsA to the diet and obtained the following results. The urinary 8-hydroxydeoxyguanosine (8-OHdG) concentration was low in the -betaC.AsA and +AsA groups but high in the +betaC.AsA, +Ka, and +Po groups. The thiobarbituric acid-reactive substances (TBARS) in both the liver and skin were higher in the -betaC.AsA group than in the +betaC.AsA group and were low in the +Ka and +Po groups. As antioxidant enzymes, glutathione peroxidase (GSH-Px) activity was high in the +betaC.AsA group, low in the -beta3C.AsA group in both the skin and liver, and also high in the + Ka and +Po group in the liver. Superoxide dismutase (SOD) activity was high in the -betaC.AsA group and low in the +betaC.AsA and +Ka groups in both the skin and liver. Catalase (CAT) activity in the liver was low in the -betaC.AsA, +AsA, and +betaC groups and high in the +betaC.AsA and +Po groups. These results confirmed that the administration of betaC, AsA, and persimmons and pods increases antioxidative ability in the skin and liver of ultraviolet-b(UV-B)-irradiated ODS rats.

Morphology of ferret subcutaneous adipose tissue after 6-month daily supplementation with oral beta-carotene

Adipose tissue is an important retinoid depot and retinoids are known to influence white and brown adipocyte metabolism. Identifying nutrients that can affect the biological activity of the adipose organ would be of great medical interest in the light of the current obesity epidemic and related disorders in developed countries. The vast majority of mammal studies of chronic administration of oral beta-carotene have used murine models, while few have employed mammals exhibiting uptake and processing of intestinal beta-carotene similar to those of humans. While rodents transform practically all ingested beta-carotene into retinol, in ferrets, as in humans, part of the beta-carotene is absorbed and released into the circulation intact. We studied the effects of 6-month daily administration of two doses of oral beta-carotene (0.8 or 3.2 mg/kg/day) on ferret body weight, size of body fat depots, and, using morphological and morphometric methods, on subcutaneous (inguinal) white adipose tissue (WAT). Because of the oral mode of administration, liver, stomach, and small and large intestine were also studied. Control animals received the vehicle. Data show that at the end of treatment the higher dose induced significantly higher body weight compared with controls and significantly higher inguinal fat depot compared with animals treated with the lower dose. In addition, chronic treatment with beta-carotene induced a dose-dependent hypertrophy of white adipocytes and increased neoangiogenesis in subcutaneous WAT in all treated ferrets. Vasculogenesis was independent of adipocyte hypertrophy. We also found focally evident liver steatosis in the ferrets treated with the higher dose of beta-carotene. The other gastrointestinal tract organs studied were not significantly different from those of control animals.

Role of oxidative stress and antioxidants in aetiopathogenesis and management of oral submucous fibrosis

Lipid peroxidation product, malonaldehyde (MDA) and antioxidants were estimated in plasma and erythrocytes of 34 cases of oral submucous fibrosis (OSMF) of different grades with equal number of healthy controls to evaluate the association of reactive oxygen species (ROS) and OSMF. While plasma MDA was found to be significantly higher in patients (3.3±0.4 nmole/ml, P<0.001) as compared to controls (2.4±0.5 nmole/ml), plasma beta carotene and vitamin E levels were found to be decreased significantly in patients (81.7±14.3 μg/100 ml, P<0.001; 9.3±0.9 mg/L, P<0.01 respectively) with respect to healthy controls (110±20.8 μg/100 ml and 10.1±1.2 mg/L). The decrease in beta-carotene and vitamin E was found to be more significant in OSMF grade II and III than in grade I. After 6 weeks of oral administration of beta-carotene and vitamin E, patients showed increase in plasma level of these two antioxidants along with decrease in MDA level associated with clinical improvement.

Administration of beta-carotene suppresses lipid peroxidation in tissues and improves the glucose tolerance ability of streptozotocin-induced diabetic rats.

The present study attempted to examine the antioxidative effect of dietary beta-carotene (BC) on lipid peroxidation (LPO) in the streptozotocin (STZ)-induced diabetic rats. Male Sprague-Dawley (SD) rats were fed on the AIN76 standard diet with or without 0.1% BC. On the 21st day after introduction of these diets, STZ was intraperitoneally injected in half the subjects of both groups. All animals were sacrificed seven days after the STZ injection. Glucose tolerance and thiobarbituric acid reactive substance (TBARS) in the tissues or serum were measured. Body weight gain in the BC + STZ group was significantly higher than that in the STZ group (p < 0.05). Blood glucose and TBARS concentrations of the liver, pancreas, and serum in the BC + STZ group were significantly lower than those in the STZ group. The blood insulin concentration in the BC + STZ group was significantly higher than that in the STZ group. The hepatic and serum beta-carotene concentrations in the BC + STZ group were significantly lower than those in the BC group. Moreover, the synthesis and oxidation of glutathione (GSH) in the BC + STZ group were reduced when compared to the STZ group. These results suggest that the administration of beta-carotene suppresses the elevation of LPO and reduces the symptoms of diabetes mellitus (DM) in the STZ-induced diabetic rats.

β-Carotene beadlets potentiate hepatotoxicity of alcohol

Administration of beta-carotene in beadlets to baboons potentiates alcohol-induced liver injury. To determine whether this also occurs in other species, and whether the beadlet carrier itself contributes to the toxicity, rats were given for 2 mo vitamin A (1.4 U/J), beta-carotene (4.8, 12.0, and 24.0 U/J, with or without beadlets), or corresponding amounts of beadlets without beta-carotene, in diets containing either carbohydrates or equivalent amounts of ethanol. Isoenergetic substitution of ethanol (36% of total energy) for carbohydrates reduced hepatic vitamin A by 80%, and such a depletion was also observed with beta-carotene as vitamin A precursor. By contrast, ethanol raised hepatic beta-carotene, which was further increased by beadlets. Thus, whereas alcohol promoted hepatic depletion of vitamin A, it had the opposite effect on beta-carotene. Ethanol seems to affect the homeostasis of beta-carotene. Furthermore, the ethanol-induced oxidative stress, assessed by an increase in hepatic 4-hydroxynonenal and F2-isoprostanes (measured by gas chromatography-mass spectrometry), was not improved despite a concomitant rise in hepatic antioxidants (beta-carotene and vitamin E). Moreover, beadlets resulted in proliferation of the smooth endoplasmic reticulum and in leakage of the mitochondrial glutamate dehydrogenase into the plasma, reflecting mitochondrial injury (both documented by electron microscopy). Thus, in rats given ethanol, beta-carotene is not an efficient vitamin A precursor. Its bioavailability was improved by beadlets, but the ethanol-induced oxidative stress was not attenuated and there was associated hepatotoxicity that now needs to be assessed in humans.