The effects of supraphysiological supplementation of b-carotene in spontaneously hypertensive rats (SHR and SHR-sp) / Efeitos da suplementação suprafisiológica de b-caroteno em ratos espontaneamente hipertensos (SHR e SHR-sp)

Objective: to investigate the effect of administration of supraphysiological âcaroteno on biological parameters (ectoscopy and blood pressure), laboratory (malondialdehyde) and histological (liver and carotid arteries) of spontaneously hypertensive rats prone to stroke (SHR-sp). Methods: we used 36 male rats were divided into three groups, each containing 12 rats Wistar, SHR and SHR-sp, subdivided into six control animals and six animals treated with supraphysiological doses of âcaroteno for two periods of ten weeks interspersed with one week interruption. In the experiment were assessed daily physical examination and blood pressure (plethysmography). At sacrifice, blood was collected for measurement of serum malondialdehyde, liver and carotid arteries for histological examination. Results: temporary change in color of the fur, decreased significantly (p<0.0001) blood pressure (20mg supplementation âcaroteno) and serum levels of malondialdehyde (p<0.05) and increased amount of elastic fibers in the carotid wall of SHR and SHR-sp. Conclusion: supplementation of supraphysiological âcaroteno caused no toxic effects, showed positive response in the modulation of blood pressure and lower serum malondialdehyde. No significant morphological changes were found in both groups, except an increase in the number of elastic fibers in the muscle layer carotid suggesting elastosis in SHR and SHR-sp. .

Objetivo: investigar o efeito da administração suprafisiológica de bcaroteno sobre parâmetros biológicos, laboratoriais e histológicos dos ratos espontaneamente hipertensos com tendência ao acidente vascular encefálico (SHR-sp). Métodos: utilizaram-se 36 ratos machos, distribuídos em três grupos, contendo cada um dos 12 ratos das linhagens Wistar, SHR e SHR-sp, subdivididos em seis animais controle e seis animais tratados com doses suprafisiológicas de âcaroteno por dois períodos de dez semanas, intercalados por uma semana de interrupção. No experimento foram avaliados diariamente o exame físico e a pressão arterial. Foi coletado sangue para dosagem sérica de malondialdeído; o fígado e as artérias carótidas para exame histológico. Resultados: alteração provisória na coloração dos pelos, diminuição significativa (p<0,0001) da pressão arterial (suplementação de 20mg de bcaroteno) e dos níveis séricos de malondialdeído (p<0,05) e aumento da quantidade de fibras elásticas na parede carotídea dos ratos SHR e SHR-sp. Conclusão: A suplementação suprafisiológica de bcaroteno não causou efeitos tóxicos, apresentou resposta positiva na modulação da pressão arterial e diminuição na concentração sérica de malondialdeído. Não foram encontradas alterações morfológicas significativas nos grupos estudados, exceto um aumento no número de fibras elásticas da camada muscular carotídea sugerindo elastose nos ratos SHR e SHR-sp. .

Efeito do betacaroteno sobre o estresse oxidativo e a expressão de conexina 43 cardíaca / Effect of beta-carotene on oxidative stress and expression of cardiac connexin 43

FUNDAMENTO: Estudos de intervenção mostraram aumento da mortalidade em pacientes que receberam betacaroteno. Contudo, não são conhecidos os mecanismos envolvidos nesse fenômeno. OBJETIVO: Avaliar a influência do betacaroteno sobre o estresse oxidativo e a expressão de conexina 43 em coração de ratos. MÉTODOS: Ratos Wistar, pesando aproximadamente 100 g, foram alocados em dois grupos: Grupo Controle (n = 30), que recebeu a dieta usada de rotina em nosso laboratório, e Grupo Betacaroteno (n = 28), que recebeu betacaroteno (na forma de cristal, adicionado e misturado à dieta) na dose de 500 mg de betacaroteno/kg de dieta. Os animais receberam tratamento até que atingissem entre 200 e 250 g, quando eram sacrificados. Foram coletados sangue, fígado e coração para realização de Western blotting e imunoistoquímica para conexina 43; foram realizados estudos morfométricos, dosagens de betacaroteno por cromatografia líquida de alta eficiência bem como de glutationa reduzida, glutationa oxidada e hidroperóxidos de lipídeos por análises bioquímicas. RESULTADOS: O betacaroteno foi detectado apenas no fígado dos animais do Grupo Betacaroteno (288 ± 94,7 µg/kg). Os níveis de glutationa reduzida/glutationa oxidada foram maiores no fígado e no coração dos animais do Grupo Betacaroteno (fígado - Grupo Controle: 42,60 ± 1,62; fígado - Grupo Betacaroteno: 57,40 ± 5,90; p = 0,04; coração: - Grupo Controle: 117,40 ± 1,01; coração - Grupo Betacaroteno: 121,81 ± 1,32 nmol/mg proteína; p = 0,03). O conteúdo de conexina 43 total foi maior no Grupo Betacaroteno. CONCLUSÃO: O betacaroteno apresentou efeito benéfico, caracterizado pelo aumento da comunicação intercelular e melhora do sistema de defesa antioxidante. Nesse modelo, os mecanismos não explicam a maior mortalidade observada com a suplementação de betacaroteno em estudos clínicos. (Arq Bras Cardiol. 2013; [online].ahead print, PP.0-0).

BACKGROUND: Intervention studies have shown an increased mortality in patients who received beta-carotene. However, the mechanisms involved in this phenomenon are still unknown. OBJECTIVE: Evaluate the influence of beta-carotene on oxidative stress and the expression of connexin 43 in rat hearts. METHODS: Wistar rats, weighing approximately 100 g, were allocated in two groups: Control Group (n=30), that received the diet routinely used in our laboratory, and Beta-Carotene Group (n = 28), which received beta-carotene (in crystal form, added and mixed to the diet) at a dose of 500 mg of beta-carotene/kg of diet. The animals received the treatment until they reached 200-250g, when they were sacrificed. Samples of blood, liver and heart were collected to perform Western blotting and immunohistochemistry for connexin 43; morphometric studies, dosages of beta-carotene by high-performance liquid chromatography as well as reduced glutathione, oxidized glutathione and lipids hydroperoxides were performed by biochemical analysis. RESULTS: Beta-carotene was detected only in the liver of Beta-Carotene Group animals (288 ± 94.7 µg/kg). Levels of reduced/oxidized glutathione were higher in the liver and heart of Beta-Carotene Group animals (liver - Control Group: 42.60 ± 1.62; liver - Beta-Carotene Group: 57.40 ± 5.90; p = 0.04; heart: - Control Group: 117.40 ± 1.01; heart - Beta-Carotene Group: 121.81 ± 1.32 nmol/mg protein; p = 0.03). The content of total connexin 43 was larger in Beta-Carotene Group. CONCLUSION: Beta-carotene demonstrated a positive effect, characterized by the increase of intercellular communication and improvement of anti-oxidizing defense system. In this model, mechanism does not explain the increased mortality rate observed with the beta-carotene supplementation in clinical studies. (Arq Bras Cardiol. 2013; [online].ahead print, PP.0-0).

Papel da lipoperoxidação na intensificação da remodelação causada pelo betacaroteno após o infarto / Rol de la lipoperoxidación en la intensificación de la remodelación ocasionada por el betacaroteno tras infarto / Role of lipoperoxidation in the remodeling intensification induced by beta-carotene after infarction

FUNDAMENTO: Os mecanismos envolvidos na maior remodelação causada pelo betacaroteno após o infarto são desconhecidos. OBJETIVO: Analisar o papel da lipoperoxidação na remodelação ventricular após o infarto do miocárdio, em ratos suplementados com betacaroteno. MÉTODOS: Ratos foram infartados e distribuídos em dois grupos: C (controle) e BC (500mg/kg/dieta). Após seis meses, foram realizados ecocardiograma e avaliação bioquímica. Utilizamos o teste t, com significância de 5 por cento. RESULTADOS: Os animais do grupo BC apresentaram maiores médias das áreas diastólicas (C = 1,57 ± 0,4 mm²/g, BC = 2,09 ± 0,3 mm²/g; p < 0,001) e sistólicas (C = 1,05 ± 0,3 mm²/g, BC = 1,61 ± 0,3 mm²/g; p < 0,001) do VE, ajustadas ao peso corporal do rato. A função sistólica do VE, avaliada pela fração de variação de área, foi menor nos animais suplementados com betacaroteno (C = 31,9 ± 9,3 por cento, BC = 23,6 ± 5,1 por cento; p = 0,006). Os animais suplementados com betacaroteno apresentaram valores maiores da relação E/A (C = 2,7 ± 2,5, BC = 5,1 ± 2,8; p = 0,036). Não foram encontradas diferenças entre os grupos em relação aos níveis cardíacos de GSH (C = 21 ± 8 nmol/mg de proteína, BC = 37 ±15 nmol/mg de proteína; p = 0,086), GSSG (C = 0,4 (0,3-0,5) nmol/g de proteína, BC = 0,8 (0,4-1,0; p = 0,19) de proteína; p = 0,246) e lipoperóxidos (C = 0,4 ± 0,2 nmol/mg de tecido, BC = 0,2 ± 0,1 nmol/mg de tecido; p = 0,086). CONCLUSÃO: A maior remodelação em animais infartados e suplementados com betacaroteno não depende da lipoperoxidação.

BACKGROUND: The mechanisms involved in the biggest remodeling caused by the post-infarct beta-carotene are unknown. OBJECTIVE: To analyze the role of lipoperoxidation in the ventricular remodeling after infarct of the myocardium in rats supplemented with beta-carotene. METHODS: Rats were infarcted and divided into two groups: C (control) and BC (500mg/kg/regimen). After six months, echocardiogram and biochemical evaluation were performed. The t test was used, with 5 percent significance. RESULTS: The animals from BC group presented highest means of the diastolic (C = 1.57 ± 0.4 mm²/g, BC = 2.09 ± 0.3 mm²/g; p < 0.001) and systolic (C = 1.05 ± 0.3 mm²/g, BC = 1.61 ± 0.3 mm²/g; p < 0.001) areas of LV, which were adapted according to the rat's body weight. The systolic function of LV, evaluated by the area variation fraction, was lower in the animals supplemented with beta-carotene (C = 31.9 ± 9.3 percent, BC = 23.6 ± 5.1 percent; p = 0.006). The animals supplemented with beta-carotene presented higher values of the E/A relation (C = 2.7 ± 2.5, BC = 5.1 ± 2.8; p = 0.036). No differences were found between the groups concerning the cardiac levels of the GSH (C = 21 ± 8 nmol/mg of protein, BC = 37 ± 15 nmol/mg of protein; p = 0.086), GSSG (C = 0.4 (0.3-0.5) nmol/g of protein, BC = 0.8 (0.4-1.0; p = 0.19) of protein; p = 0.246) and lipoperoxides (C = 0.4 ± 0.2 nmol/mg of tissue, BC = 0.2 ± 0.1 nmol/mg of tissue; p = 0.086). CONCLUSION: The highest remodeling in infarcted rats supplemented with beta-carotene does not depend on the lipoperoxidation.

FUNDAMENTO: Los mecanismos implicados en la mayor remodelación ocasionada por betacaroteno tras el infarto son desconocidos. OBJETIVO: Analizar el rol que juega la lipoperoxidación en la remodelación ventricular tras el infarto de miocardio, en ratas suplementadas con betacaroteno. MÉTODOS: Se había inducido a un infarto a las ratas y se las distribuyó en grupos: C (control) y BC (500mg/kg/dieta). Tras seis meses, se realizaron ecocardiograma y evaluación bioquímica. Utilizamos la prueba t, con significancia del 5 por ciento. RESULTADOS: Los animales del grupo BC presentaron mayores promedios de las áreas diastólicas (C = 1,57 ± 0,4 mm²/g, BC = 2,09 ± 0,3 mm²/g; p < 0,001) y sistólicas (C = 1,05 ± 0,3 mm²/g, BC = 1,61 ± 0,3 mm²/g; p < 0,001) del VI, ajustadas al peso corporal de la rata. La función sistólica del VI, evaluada por la fracción de variación de área, fue menor en los animales suplementados con betacaroteno (C = 31,9 ± 9,3 por ciento, BC = 23,6 ± 5,1 por ciento; p = 0,006). Los animales suplementados con betacaroteno presentaron valores mayores de la relación E/A (C = 2,7 ± 2,5, BC = 5,1 ± 2,8; p = 0,036). No se encontraron diferencias entre los grupos con relación a los niveles cardiacos de GSH (C = 21 ± 8 nmol/mg de proteína, BC = 37 ±15 nmol/mg de proteína; p = 0,086), GSSG (C = 0,4 (0,3-0,5) nmol/g de proteína, BC = 0,8 (0,4-1,0; p = 0,19) de proteína; p = 0,246) y lipoperóxidos (C = 0,4 ± 0,2 nmol/mg de tejido, BC = 0,2 ± 0,1 nmol/mg de tejido; p = 0,086). CONCLUSIÓN: La mayor remodelación en animales infartados y suplementados con betacaroteno no depende de la lipoperoxidación.

Efeitos do betacaroteno e do tabagismo sobre a remodelação cardíaca pós-infarto do miocárdio / Effects of beta-carotene and smoking on heart remodeling after myocardial infarction

OBJETIVO: Analisar os efeitos do betacaroteno no processo de remodelação ventricular após o infarto agudo do miocárdio (IAM), em ratos expostos à fumaça do cigarro. MÉTODOS: Após o IAM, os animais foram divididos em quatro grupos: 1) grupo C, 24 animais que receberam dieta-padrão; 2) grupo BC, 26 animais que receberam betacaroteno; 3) grupo EFC, 26 animais que receberam dieta-padrão e foram expostos à fumaça de cigarro; e 4) grupo BC+EFC, 20 animais que receberam betacaroteno e foram expostos à fumaça de cigarro. Após seis meses, foi realizado estudo morfofuncional. Utilizou-se significância de 5 por cento. RESULTADOS: Em relação às áreas diastólicas (AD) e sistólicas (AS), os valores do grupo BC foram maiores que os do grupo C. Considerando a AD/peso corporal (PC) e AS/PC, os valores do grupo BC+EFC foram maiores que os valores de C. Em relação à fração de variação de área, foram observadas diferenças significativas entre EFC (valores menores) e C (valores maiores) e entre BC (valores menores) e C (valores maiores). Não foram observadas diferenças entre os grupos em relação ao tamanho do infarto. O grupo EFC apresentou valores maiores da área seccional dos miócitos (ASM) que os animais-controle. Em adição, o grupo BC+EFC apresentou maiores valores de ASM que BC, EFC e C. CONCLUSÃO: Após o infarto do miocárdio, o tabagismo e o betacaroteno promoveram intensificação do processo de remodelação cardíaca; houve potencialização dos efeitos deletérios no processo de remodelação com os dois tratamentos em conjunto.

OBJECTIVE: To analyze the effects of beta-carotene on the ventricular remodeling process following myocardial infarction (MI) in rats exposed to cigarette smoke. METHODS: After acute myocardial infarction (AMI), the animals were divided into four groups: 1) Group C, 24 animals that were given standard diet; 2) Group BC, 26 animals that were given beta-carotene; 3) Group ECS, 26 animals that were given standard diet and were exposed to cigarette smoke; and 4) Group BC+ECS, 20 animals that were given beta-carotene and were exposed to cigarette smoke. After six months, a morphofunctional study was performed. We used a 5 percent significance level. RESULTS: As regards diastolic areas (DA) and systolic areas (SA), the values for the BC group were higher than those for the C group. If DA/body weight (BW) and SA/BW are considered, the values for group BC+ECS were higher than the values for group C. As regards the fractional area change, we observed significant differences between ECS (lower values) and C (higher values) and between BC (lower values) and C (higher values). Differences between groups regarding infarction size were not observed. The ECS group presented higher values for myocyte cross-section area (MCA) than control animals. Additionally, the BC+ECS group presented higher MCA values than the BC, ECS and C groups. CONCLUSION: After myocardial infarction, smoking and beta-carotene intensified the heart remodeling process; harmful effects of the remodeling process were heightened when the two treatments were used in conjunction.

effects of beta-carotene and vitamin E on erythrocytes lipid peroxidation in beta-thalassemia patients

Thalassemia is the most common hereditary disease in the world. Thalassemic erythrocytes are exposed to higher oxidative stress and lipid peroxidation. The aim of this study was to investigate the effects of beta-carotene and vitamin E on erythrocytes lipid peroxidation in beta-thalassemia patients. A prospective double-blind, placebo-controlled study of the effect of beta-carotene and vitamin E on lipid peroxidation in erythrocytes membranes was performed on 120 beta-thalassemia major patients in four groups. The patients were supplemented for 4 weeks as follows: group 1 with beta-carotene [13 mg/day], group 2 with vitamin E [550 mg/day], group 3 with beta-carotene plus vitamin E and group 4 with placebo. We prepared all capsules for 4 roups in the same shape and color. Measurements of serum beta-carotene and vitamin E were performed by high performance liquid chromatography. After preparation of ghost cells from blood specimens, malondialdehyde [MDA] was determined as index of lipid peroxidation in erythrocytes membranes before and after treatment. The levels of serum beta-carotene and vitamin E were significantly lower and MDA concentrations in erythrocytes membranes were significantly higher in beta-thalassemia patients compared to controls [P < 0.001]. In groups that treated with vitamin supplements for 4-weeks, lipid peroxidation rates were significantly reduced after treatment [P<0.001], but in placebo group there was not significant difference [P > 0.05]. Our findings provide evidence that an oral treatment with beta-carotene and vitamin E can significantly reduce lipid peroxidation of erythrocytes membranes and could be useful in management of beta-thalassemia major patients

influence of lipid composition and beta-carotene on lipid peroxidation in liposomes

Oxidative damage to membrane lipid is one of the prime events occurring in aging and other undesirable physiological processes. In this study experiments were performed on liposomes [prepared either from crude erythrocyte phospholipids or purified egg yolk phosphatidylcholine] as models of lipid bilayer portion of biomembranes. The effects of beta-carotene, and phospholipid composition on peroxidation process, initiated by Fe[2+], were studied. It was found that beta-carotene does not show any noticeable antioxidant effect on the peroxidation process initiated by Fe[2+] in liposomes prepared from erythrocyte phosphatides, whereas it effectively suppressed the same process in egg yolk phosphatidylcholine [EYPC]. It is concluded that the anti-/pro-oxidant activity of beta-carotene is also dependent on the membrane lipid composition and this may provide an explanation about the conflicting reports on its role in ordinary or promoted oxidation experiments

beta-Carotene inhibits inflammatory gene expression in lipopolysaccharide-stimulated macro phages by suppressing redox-based NF-kappaB activation

beta-Carotene has shown antioxidant and antiinflammatory activities; however, its molecular mechanism has not been clearly defined. We examined in vitro and in vivo regulatory function of beta-carotene on the production of nitric oxide (NO) and PGE2 as well as expression of inducible NO synthase (iNOS), cyclooxygenase-2, TNF-alpha, and IL-1beta. beta-Carotene inhibited the expression and production of these inflammatory mediators in both LPSstimulated RAW264.7 cells and primary macrophages in a dose-dependent fashion as well as in LPS-administrated mice. Furthermore, this compound suppressed NF-kappaB activation and iNOS promoter activity in RAW264.7 cells stimulated with LPS. beta-Carotene blocked nuclear translocation of NF-kappaB p65 subunit, which correlated with its inhibitory effect on IkappaBalpha phosphorylation and degradation. This compound directly blocked the intracellular accumulation of reactive oxygen species in RAW264.7 cells stimulated with LPS as both the NADPH oxidase inhibitor diphenylene iodonium and antioxidant pyrrolidine dithiocarbamate did. The inhibition of NADPH oxidase also inhibited NO production, iNOS expression, and iNOS promoter activity. These results suggest that beta-carotene possesses anti-inflammatory activity by functioning as a potential inhibitor for redox-based NF-kappaB activation, probably due to its antioxidant activity.

Pre-administration of beta-carotene protects tissue glutathione and lipid peroxidation status following exposure to gamma radiation.

The present study has been aimed to investigate the protective effect of beta-carotene against radiation-induced oxidative stress in mice tissues using lipid peroxidation and glutathione (GSH) as end points. Fourteen days oral priming administration of beta-carotene (35 mg/kg body weight) followed by an acute dose of gamma radiation (5 Gy) inhibited the augmented level of thiobarbituric acid reactive substance (TBARS) and a statistically significant protection against GSH depletion. Results evaluated from this study clearly indicate the antioxidative property of beta-carotene against gamma radiation, which is suggestive of free radical scavenging and singlet oxygen quenching.

Carcinogenic effect of nicotine on normal mammary ductal epithelial cells and the protective role of beta-carotene.

A number of carcinogens like polycyclic hydrocarbons and aromatic amines have been incriminated to induce mammary carcinomas in vitro and in vivo. Studies have supported an inter-relationship between tobacco consumption and breast cancer. Because nicotine is the major alkaloid present in tobacco this study was conducted to find the direct in vitro effect of nicotine on normal mammary ductal epithelial cells. It was seen in the present work that nicotine causes a statistically significant increase in the proliferative rate and ER (estrogen receptor) expression as compared to the control group. This change was more pronounced with a lower concentration of nicotine (650 microg/ml). Colony efficiency also showed a similar trend. Beta carotene was added in the present work to study its anti oxidant effect on nicotine induced changes. Beta carotene significantly decreased the proliferation rate induced by 650 microg/ml nicotine. It also prevented the cytotoxic effect of higher dose of nicotine, however, it failed to alter significantly the ER expression induced by lower concentration of nicotine though it showed decreasing trend.

Effect of melatonin and beta-carotene on indomethacin induced gastric mucosal injury.

The study was conducted to examine the role of free radicals in Indomethacin induced gastric mucosal injury and to evaluate the gastroprotective effects of melatonin and beta-carotene. Gastric mucosal injury was produced in rats by administering indomethacin 30 mg/kg subcutaneously. Melatonin was administered in three different doses of 5, 10 and 20 mg/kg, 30 minutes prior to the administration of indomethacin. Beta-carotene was administered as a single dose of 100 mg/kg. Following parameters were calculated: ulcer index, lipid peroxidation and antioxidant defense enzymes i.e. superoxide dismutase, glutathione peroxidase and catalase. Indomethacin caused gastric mucosal injury in the form of haemorrhages, increased the lipid peroxidation and decreased the levels of the antioxidant defense enzymes. Melatonin (20 mg/kg) and beta-carotene decreased the ulcer index and lipid peroxidation, and reduced the decrease in antioxidant enzyme levels. These findings suggest the melatonin and beta-carotene show protective effect against indomethacin induced gastric injury and this effect is mediated by scavenging of oxygen derived free radicals.

Antioxidantes: mitos y realidades / Antioxidants: myths and reallity

La homeostasis de los seres vivos aeróbicos se ve constantemente amenazada por la formación de moléculas químicamente inestables y altamente reactivas llamadas radicales libres. Estos pueden generarse por agresores metabólicos endógenos (metabolismo celular) o exógenos, como el tabaco, el ozono y la radiación ultravioleta. Se les relaciona con una serie de condiciones patológicas, como la carcinogénesis, la aterosclerosis y el envejecimiento tisular. Los antioxidantes son sustancias que al interactuar con estos radicales libres previenen o demoran su acción deletérea. En la dieta se encuentran diversos compuestos que pueden contribuir a la modulación interna de los antioxidantes, apartándolos en forma directa o como cofactores. Es importante conocer estos antioxidantes dietarios, saber sus requerimientos mínimos y los potenciales riesgos por uso inapropiado

Effect of betacarotene on protein glycosylation in alloxan induced diabetic rats.

Free radicals are increasingly formed in diabetes mellitus by the auto oxidation of glucose and glycosylated proteins. Oxidative stress and proteinglycosylation are closely related processes and have been shown to contribute to the development of complications in diabetes mellitus. The extent of protein glycosylation was assessed in alloxan induced diabetic rats after being treated with 50 mg of betacarotene for 40 days. The level of fructosamine and glycosylated haemoglobin was comparison with non treated diabetic rats. The results indicate the beneficial role of betacarotene in reducing diabetic complications like glycosylation in experimental diabetic rats.

Transplacental inhibitory effect of carrot juice on the clastogenicity of cyclophosphamide in mice

Genetic damage during the prenatal period can provoke important neoplastic alterations and other diseases in postnatal life. Beta-carotene (ßC) is considered to be one of the most important anticarcinogens in the diet and can protect mammalian cells against genotoxic events. As carrots are important dietary source of ßC, we decided to test the effect of fresh carrot juice (CaJ) on cyclophosphamide (CP)-induced genotoxicity in maternal and fetal erythropoietic tissues. The treatment with CaJ started on the 7th day of the pregnancy of BALB/c female mice. We observed, on the 16th gestational day, that this treatment did not modify the spontaneous frequency of micronucleated polychromatic erythrocytes (mPCE) in the bone marrow of the females nor in the livers of their fetuses. The mPCE frequency observed 24 h after an intraperitoneal injection of CP (40 mg/kg) on the 15th day was significantly lower in CaJ-pretreated pregnant female bone marrow and in the liver of their fetuses than those observed in the group treated with CP only. These results demonstrate the presence of natural anticlastogens in carrots.

Antioxidant activity of the microalga Spirulina maxima

Spirulina maxima, which is used as a food additive, is a microalga rich in protein and other essential nutrients. Spirullina contains phenolic acids, tocopherols and Beta-carotene which are known to exhibit antioxidant properties. The aim of the present study was to evaluate the antioxidant capacity of a Spirulina extract. The antioxidant activity of a methanolic extract of Spirulina was determined in vitro and in vivo. The in vitro antioxidant capacity was tested on a brain homogenate incubated with and without the extract at 37 degrees Celsius. The IC(50) (concentration which causes a 50 per cent reduction of oxidation) of the extract in this system was 0.18 mg/ml. The in vivo antioxidant capacity was evaluated in plasma and liver of animals recceiving a daily dose of 5 mg for 2 and 7 weeks Plasma antioxidant capacity was measured in brain homogenate incubated for 1 h at 37 degrees Celsius. The production of oxidized compounds in liver after 2 h of incubation at 37 degrees Celsius was measured in terms of thiobarbituric acid reactant substances (TBARS) in control and experimental groups. Upon treatment, the antioxidant capacity of plasma was 71 per cent for the experimental group and 54 per cent for the control group. Data from liver spontaneous peroxidation studies were not significantly different between groups. The amounts of phenolic acids, alpha-tocopherol and Beta-carotene were determined in Spirulina extracts. The results obtained indicate that Spirulina provides some antioxidant protection for both in vitro and in vitro and vivo systems.