beta-carotene and Hemorrhage

To review the association between major causes of maternal mortality and vitamin A, trying to determine if these associations are causal in nature, and to highlight possible biological pathways that may explain vitamin A effects.. Literature review, observational studies and clinical trials. The strength of association was determined by applying Bradford Hill criteria of causality.. In a vitamin A deficient population, vitamin A is essential for adequate treatment of anaemia. While vitamin A does not seem to be capable of preventing uterine atony, obstetric or surgical trauma, which are important causes of haemorrhage, it might be capable of preventing or decreasing coagulopathy. Possible effects on the placenta as regards implantation, site and size are not clear. As regards pregnancy-related infections, vitamin A supplementation can improve wound healing by decreasing fibrosis and increasing transforming growth factor-beta (TFG-beta). It can increase resistance to infection by increasing mucosal integrity, increasing surface immunoglobulin A (sIgA) and enhancing adequate neutrophil function. If infection occurs, vitamin A can act as an immune enhancer, increasing the adequacy of natural killer (NK) cells and increasing antibody production. beta-carotene in its provitamin form can act as an antioxidant by decreasing endothelial cell damage (the pathognomonic feature of pre-eclampsia) and promote the vasodilator effect of nitric oxide that might bring about a better outcome of toxaemia in pregnancy. It is unlikely that vitamin A or beta-carotene has an effect on obstructed labour.. Plausible biomedical pathways can only be constructed for obstetric haemorrhage, anaemia in pregnancy, hypertension in pregnancy and pregnancy-related infections. A 40% reduction in the maternal mortality ratio, as observed in Nepal, is unlikely to be solely explained through the aforementioned pathways.

Topics: Anemia; beta Carotene; Cause of Death; Dietary Supplements; Dystocia; Female; Hemorrhage; Humans; Hypertension; Maternal Mortality; Pregnancy; Pregnancy Complications; Pregnancy Complications, Infectious; Vitamin A; Vitamin A Deficiency

Some studies have indicated that the injury induced by the hepato- and pneumotoxin monocrotaline (MCT) is in part mediated by oxidation. Because beta-carotene is a potent antioxidant, we hypothesized that it would protect the lung and liver parenchyma against MCT-induced injury. Twenty rats were assigned randomly to four groups. All rats were fed a standard AIN93G diet with or without beta-carotene. After 1 week on the purified diets, half of the rats fed the control (standard) diet and half of the rats fed the beta-carotene-supplemented diet were injected subcutaneously with 60 mg MCT/kg body weight or its vehicle (water). All rats were sacrificed at 4 weeks. Histological examination showed that beta-carotene alone did not affect lung or liver structure. On the other hand, lungs of MCT-treated rats had severe focal pneumonia, extensive deposition of collagen in the septa, marked inflammation of the small arteries and arterioles, and arterialization of the small venules. Livers of MCT-treated rats showed some fatty infiltration and diffuse hemorrhages, more prominent sometimes in the centrilobular area and sometimes in the periportal region. Concomitant treatment with beta-carotene protected the lung parenchyma from the inflammatory reaction and the septal fibrosis, but did not prevent cardiac right ventricular hypertrophy and only slightly reduced the thickening of the wall of small arteries and arterioles. Incidence of steatosis and hemorrhages was decreased in the liver. These results indicate that MCT-induced pulmonary vascular remodeling occurs in the absence of inflammatory cell infiltration. Furthermore, beta-carotene prevented inflammation and protected the lung and liver parenchyma of MCT-treated rats.

Topics: Animals; Antidotes; Antioxidants; beta Carotene; Chemical and Drug Induced Liver Injury; Collagen; Diet; Fatty Liver; Hemorrhage; Hypertrophy, Right Ventricular; Liver; Lung; Lung Diseases; Male; Monocrotaline; Poisons; Rats; Rats, Sprague-Dawley

Antioxidants occasionally have become prooxidants when a large amount was ingested. The haemorrhagic toxicity of butylated hydroxytoluene, a synthetic antioxidant, may involve such a mechanism. This study investigated whether haemorrhage is induced by overdoses of tocopherols, beta-carotene, ubiquinone or L-ascorbic acid, which are representative biological antioxidants. Male Jcl:SD rats (six rats/group) were fed d-alpha, d-beta, d-gamma or d-delta-tocopherols, ubiquinone Q-10, beta-carotene or retinol acetate at a level of 0.5%, or L-ascorbic acid at 5% in the diet for 7 days. Only two rats given retinol acetate died with lung haemorrhages. Haemorrhages were observed in five or six, six, one, one, one or one of six surviving rats given d-alpha, d-beta or d-gamma-tocopherols, ubiquinone Q-10, beta-carotene or retinol acetate, respectively (except for a retinol group in which four rats survived). Major haemorrhages were noted in the epididymis. In the alpha-, beta- and gamma-tocopherol, ubiquinone Q-10, beta-carotene or retinol acetate-treated groups, prothrombin and kaoline-activated partial thromboplastin time indices were 26-28, 37, 59, 42, 63 and 65% or 27-28, 35, 65, 38, 59 and 28%, respectively, of the control values. Only the prothrombin index was significantly decreased to 67% in delta-tocopherol-administered rates, whereas controls and those receiving L-ascorbic acid showed no signs of bleeding or coagulation defect. The same tendency was also seen in the decreasing effect on vitamin K-dependent blood coagulation factors. These results suggest that the four naturally occurring tocopherols have a tendency to cause haemorrhage in the order of alpha > beta > gamma > delta, and ubiquinone Q-10 and beta-carotene als0o have relatively strong and weak haemorrhagic effects, respectively, with regard to prothrombin and partial thromboplastin time indices.

Topics: Adjuvants, Immunologic; Analysis of Variance; Animals; Anticarcinogenic Agents; Antineoplastic Agents; Ascorbic Acid; beta Carotene; Blood Coagulation; Carotenoids; Diterpenes; Epididymis; Exophthalmos; Eye; Hemorrhage; Male; Prothrombin Time; Rats; Rats, Sprague-Dawley; Retinyl Esters; Stereoisomerism; Thromboplastin; Ubiquinone; Vitamin A; Vitamin E