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Results for “Vitamin A Deficiency”

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At least 19 recordsLinked to original sources
PubMed1979

Relevance of a borderline vitamin deficiency in relation to the question of vitamin requirement.

A definition is given for the terms of latent and borderline vitamin deficiency, and the vitamin requirement and optimal vitamin supply, respectively, are discussed in relation to these two terms. The upper limit of the latent vitamin deficiency status can be used to define the optimal intake of vitamins, whereas the lower limit indicates the minimum requirement. The impact on health of a latent vitamin deficiency lies in the risk of falling into a manifest vitamin deficiency during sudden stress, whereas, in borderline vitamin deficiency status, some health functions are affected so that a problem of public health may arise and countermeasures should be taken.

Adolescent↗
PubMed1977

Influence of norethindrone on drug-metabolizing enzymes of female rat liver in various B-vitamin deficiency states.

Ingestion of high levels of thiamin significantly decreased the activity of cytochrome P-450, NADPH cytochrome c reductase, and the metabolism of aniline and ethylmorphine. Apparent VmaxS for ethylmorphine N-demethylase and aniline hydroxylase were decreased by high levels of riboflavin even though NADPH cytochrome c reductase was elevated. High levels of dietary pyridoxine significantly decreased only the Vmax for aniline hydroxylase. Generally, norethindrone produces either no change or slight depression of cytochrome P-450 regardless or diet, whereas the administration of norethindrone produced no change or an increase in activity of c reductase and ethylmorphine N-demethylase. Norethindrone induces aniline hydroxylase in animals fed all diets except those deficient in thiamin and riboflavin. The activities of the four parameters of the drug metabolizing system measured in these studies as well as the effects of norethindrone are clearly affected by the dietary status of the animal.

Aniline Hydroxylase↗
PubMedDate not supplied

Changes in the levels of certain vitamins from B group under conditions of vitamin deficiency.

In experiments on rabbits the levels of vitamins B1, B2, B6, PP and pantothenic acid were determined to establish the grade and the sequence of their disappearance from the blood and liver in states of exogenous and endogenous vitamin deficiency. The experiments were carried out in which vitamin deficiency was produced by removing vitamins from the diet or by giving the rabbits antibiotics of different activity spectrum when the animals were kept on a diet without vitamins. Determinations of vitamin levels were performed using microbiological methods. It was found that the time after which changes in vitamin levels developed as well as the intensity of changes differ, depending on the experimental model used, but the sequence of vitamin disappearance from the organism is always the same. The first to disappear were vitamins B1, followed by vitamin B6 and pantothenic acid.

Animals↗
PubMed1979

Drugs and vitamin deficiency.

During the past 10 to 20 years it has become increasingly clear that a certain number of drugs may lead to increased vitamin requirements. However, it is unusual for symptomatic avitaminosis to develop, and then only when circumstances are present which in themselves increase the risk of vitamin deficiency. Therapeutic doses of drugs will interfere with the vitamin status only to a restricted degree, provided they are administered for brief periods and to patients receiving a normal supply of vitamins. Most cases of vitamin deficiency have in fact been described in connection with drugs usually taken for a longer period of time by patients who were already in negative vitamin balance as a result of disease or marginal supply of the necessary vitamins. This review describes some of the more important articles covering this topic.

Ascorbic Acid Deficiency↗
PubMed1979

[Visual disorders, functional defects and vitamin deficiencies].

The comparison between complaints, functional defects and vitamin deficiencies is reported for several professional groups characterized by different work conditions. Results suggest that complaints are an useful indicator of visual load and that retinal sensitivity to the light is especially tried. Longitudinal studies are required to verify whether some functional alterations on the aging process of the eye can be aggravated by a visual overload. Visual complaints, functional defects and vitamin deficiencies as indicators of visual load.

Adult↗
PubMedDate not supplied

Behavioral consequences of dietary vitamin deficiency in young and middle-aged rats.

The behavioral correlates of vitamin A and B 6 dietary deficiency in young adult rats (Experiment 1) and middle-aged, retired breeder rats (Experiment 2) were examined. Male and female rats received either vitamin A deficient, vitamin B6 deficient, or normal control diets for two and a half months. Body weight, eating, and drinking of water and adulterated fluids were monitored. Pyridoxine deficiency generally had greater effects on consummatory behavior and weight gain than vitamin A deficiency, but this effect was influenced by the rats' age and sex. Wheel running, (Experiment 1), increased above control levels in both the vitamin delete groups. Vitamin A and B 6 deplete diets may affect behavior before an animal displays classical physical signs. Furthermore, such behavioral changes are not restricted to young, rapidly growing male rats; instead, their character is influenced by both the sex and age of the animal.

Age Factors↗
PubMed1978

Detection and incidence of B and C vitamin deficiency in alcohol-related illness.

The activity of the red blood cell enzymes transketolase, glutathione reductase, and aspartate transaminase, and their activation by the coenzymes thiamine, riboflavin, and pyridoxine, the pyruvate tolerance test, the leucocyte vitamin C concentration, and the activity in serum of gamma-glutamyl transferase were measured in a series of 35 patients with alcohol-related illness. The incidence of thiamine deficiency was 31% as assessed by the activation of transketolase, and 55% as assessed by the pyruvate tolerance test. The incidence of riboflavin deficiency was 23% and of ascorbic acid deficiency 91%. No cases of pyridoxine deficiency were detected. The pyruvate tolerance test was found to be a more sensitive test of thiamine deficiency than the transketolase activation, and the activation of red blood cell aspartate transaminase was found to be a poor indicator of pyridoxine deficiency. There was a poor correlation of the gamma-glutamyl transferase activity with the degree of vitamin deficiency, suggesting that alcohol exposure is only partly responsible for the observed vitamin deficiency.

Adult↗
PubMed1976

The influence of vitamin E deficiency and combined deficiency in vitamin E and polyunsaturated fatty acids on the biosynthesis and degradation of rat central nervous system myelin.

The ability to incorporate intracranially injected 14C-labelled leucine into central nervous system (CNS) myelin was studied in developing rats fed a control diet, a diet deficient in vitamin E and a diet deficient both in vitamin E and polyunsaturated fatty acids. The turnover of radioactivity incorporated into myelin and the distribution of radioactivity between the individual proteins of rat CNS myelin at various stages of the deficiency state was studied. Impaired myelin formation was found in cases of both types of deficiency. The level of incorporated radioactivity was raised by both types of deficiency throughout the experimental period. The mean half life of myelin radioactivity was found higher in combined deficient animals as compared to control and vitamin-E-deficient rats. The distribution of radioactivity between myelinproteins, separated by polyacrylamide gel electrophoresis, appeared identical in the three experimental groups.

Age Factors↗
PubMed1976

The effect of certain vitamin deficiencies on hepatic drug metabolism.

There is increasing evidence that the liver microsomal drug metabolizing system is affected by various vitamins such as ascorbic acid, riboflavin, and alpha-tocopherol. In regard to ascorbic acid deficiency there is a decrease in the quantity of hepatic microsomal electron transport components such as cytochrome P-450 and NADPH-cytochrome P-450 reductase, as well as decreases in a variety of drug enzyme reactions such as N-demethylation, O-demethylation, and steroid hydroxylation. In addition, young animals given high supplements of vitamin C have increased quantities of electron transport components and overall drug metabolism activities. Kinetic studies indicate no change in the apparent Km of N-demethylase, O-demethylase or hydroxylase for drug substrates in animals depleted or given high amounts of the vitamin. However, there are qualitative changes in both type I and II substrate-cytochrome P-450 binding. Ascorbic acid is not involved in microsomal lipid peroxidation or in any qualitative or quantitative change in phosphatidylcholine. Replenishing vitamin C-deficient animals with ascorbic acid required 3 to 7 days for the electron transport components and drug metabolism activities to return to normal levels. Induction with phenobarbital and 3-methylcholanthrene is not impaired in the deficient animal since drug metabolism activities are induced to the same extent as normal controls; however, the administration of delta-aminolevulinic acid, a precursor of heme synthesis, to deficient animals caused an increase in the quantity of cytochrome P-450. The effects of riboflavin deficiency on electron transport components and drug metabolism activities have been noted only in adult animals after prolonged periods of deficiency. Decreases in drug metabolism activities occur with both type I (aminopyrine and ethylmorphine) and type II (aniline) substrates. As was found with ascorbic acid deficiency, drug enzyme induction occurred to the same extent with phenobarbital in deficient and normal animals. In addition, it required from 10 to 15 days for the drug metabolism activities to return to normal levels when deficient animals were replenished with riboflavin. The effect of vitamin E on drug metabolism is specific in N-demethylase activities decrease while O-demethylase activities are not affected in the deficient state. This vitamin differs from ascorbic acid and riboflavin in that several laboratories have reported no quantitative decrease in cytochrome P-450, although there are some reports that it and delta-aminolevulinic acid dehydratase are lowered quantity of cytochrome in E-deficient animals. The effect of vitamin E, if any, on the P-450 is unresolved; an important question that requires further clarification. As with ascorbic acid there is no difference in the apparent Km of N-demethylase enzymes for varous substrates and the protective effect of vitamin E does not appear to be one of an antioxidant inhibiting microsomal lipid peroxidation.

Animals↗