text:
Mouth breathing
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Mouth breathing
Classification and external resources
ICD-10
R06.5
ICD-9-CM
784.9
MeSH
D009058
[edit on Wikidata]
Mouth breathing (also termed open-mouth breathing or a mouth breathing habit) is breathing through the mouth rather than the nose.[1]
Human infants are sometimes considered obligate nasal breathers, but generally speaking healthy humans may breathe through their nose, their mouth, or both. During rest, breathing through the nose is common for most individuals. Breathing through both nose and mouth during exercise is also normal, a behavioral adaptation to increase air intake and hence supply more oxygen to the muscles. Mouth breathing may be called abnormal when an individual breathes through the mouth even during rest. Some sources use the term "mouth breathing habit" but this incorrectly implies that the individual is fully capable of normal nasal breathing, and is breathing through their mouth out of preference. However, in about 85% of cases, mouth breathing represents an involuntary, subconscious adaptation to reduced patency of the nasal airway, and mouth breathing is a requirement simply in order to get enough air. Chronic mouth breathing in children may have implications on dental and facial growth.[2] It also may cause gingivitis (inflamed gums) and halitosis (bad breath), especially upon waking if mouth breathing occurs during sleeping.
In the United States, the term "mouth-breather" is sometimes utilized as an insult to imply low intelligence.[3]
Causes[edit]
An antrochoanal polyp, one possible cause of nasal obstruction and adaptive mouth breathing.
Mouth breathing has been classified according to etiology into three groups: obstructive, habitual and anatomic.[4]:281
The nasal airway may be compromised partially (where there is increased resistance to the flow of air due to narrowing of the lumen at some point in the upper respiratory tract) or completely obstructed. Such individuals may find it difficult or impossible to breathe through their nose alone. In about 85% of cases, mouth breathing is an adaptation to nasal obstruction.[1] Specific causes of nasal obstruction which have been linked to mouth breathing include antrochoanal polyps.[5]:350
"Pregnancy rhinitis" may lead to nasal obstruction and mouth breathing. This tends to occur in the third trimester of pregnancy.[6]:435
Some individuals breathe through their mouth through force of habit, perhaps due to a previous cause of nasal obstruction that is now corrected.[4]:281
In other cases, the upper lip may be short, and the lips do not meet at rest ("lip incompetence").[4]:281
Potential effects[edit]
Gingivitis,[6]:85 gingival enlargement,[6]:85 and increased levels of dental plaque[6]:108 are common in persons who chronically breathe through their mouth. The usual effect on the gums is sharply confined to the anterior maxillary region, especially the incisors (the upper teeth at the front). The appearance is erythematous (red), edematous (swollen) and shiny. This region receives the greatest exposure to airflow during mouth breathing, and it is thought that the inflammation and irritation is related to surface dehydration, but in animal experimentation, repeated air drying of the gums did not create such an appearance.[6]:85
It has been suggested that chronic mouth breathing in children can lead to the development of a long, narrow face, sometimes termed "long face syndrome", or specifically "adenoid facies" when the mouth breathing is related to adenoid hypertrophy. Malocclusion of the teeth (e.g., "crowded teeth") is also suggested to result from chronic mouth breathing in children. Conversely, it has been suggested that a long thin face type, with corresponding thin nasopharyngeal airway, predisposes to nasal obstruction and mouthbreathing,[1] i.e., a long thin face may cause mouth breathing rather than the other way around. Facial form is also strongly influenced by genetic factors.
The following other conditions are also associated with mouth breathing: cheilitis glandularis,[5]:490 Down syndrome,[7]:365 anterior open bite,[6]:225 tongue thrusting habit,[6]:225 cerebral palsy,[8]:422 sleep apnea, and snoring.
References[edit]
^ Jump up to: a b c Rao A, ed. (2012). Principles and Practice of Pedodontics (3rd ed.). New Delhi: Jaypee Brothers Medical Pub. pp. 169, 170. ISBN 9789350258910.
Jump up ^ https://www.sciencedaily.com/releases/2010/04/100406125714.htm
Jump up ^ Dalzell T, Victor T, eds. (2008). The concise new Partridge dictionary of slang and unconventional English (8th ed.). London: Routledge. p. 443. ISBN 9780203962114.
^ Jump up to: a b c Phulari BS, ed. (2011). Orthodontics : principles and practice. New Delhi: Jaypee Bros. Medical Publishers. ISBN 9789350252420.
^ Jump up to: a b Barnes L, ed. (2009). Surgical pathology of the head and neck (3rd ed.). New York: Informa healthcare. ISBN 9781420091632.
^ Jump up to: a b c d e f g Newman MG, Takei HH, Klokkevold PR, Carranza FA, eds. (2012). Carranza's clinical periodontology (11th ed.). St. Louis, Mo.: Elsevier/Saunders. ISBN 978-1-4377-0416-7.
Jump up ^ Regezi JA, Sciubba JJ, Jordan RK (2011). Oral pathology : clinical pathologic correlations (6th ed.). St. Louis, Mo.: Elsevier/Saunders. ISBN 978-1455702626.
Jump up ^ Cawson RA, Odell EW (2008). Cawson's essentials of oral pathology and oral medicine (8th ed.). Edinburgh: Churchill Livingstone. ISBN 9780702040016.
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Vitamin A
From Wikipedia, the free encyclopedia
Jump to: navigation, search
This article is about the family of vitamers. For the form usually used as a supplement, see Retinol.
Chemical structure of retinol, one of the major forms of vitamin A
Vitamin A is a group of unsaturated nutritional organic compounds that includes retinol, retinal, retinoic acid, and several provitamin A carotenoids (most notably beta-carotene).[1][2] Vitamin A has multiple functions: it is important for growth and development, for the maintenance of the immune system and good vision.[3][4] Vitamin A is needed by the retina of the eye in the form of retinal, which combines with protein opsin to form rhodopsin, the light-absorbing molecule[5] necessary for both low-light (scotopic vision) and color vision.[6] Vitamin A also functions in a very different role as retinoic acid (an irreversibly oxidized form of retinol), which is an important hormone-like growth factor for epithelial and other cells.[4][7]
In foods of animal origin, the major form of vitamin A is an ester, primarily retinyl palmitate, which is converted to retinol (chemically an alcohol) in the small intestine. The retinol form functions as a storage form of the vitamin, and can be converted to and from its visually active aldehyde form, retinal.
All forms of vitamin A have a beta-ionone ring to which an isoprenoid chain is attached, called a retinyl group.[1] Both structural features are essential for vitamin activity.[8] The orange pigment of carrots (beta-carotene) can be represented as two connected retinyl groups, which are used in the body to contribute to vitamin A levels. Alpha-carotene and gamma-carotene also have a single retinyl group, which give them some vitamin activity. None of the other carotenes have vitamin activity. The carotenoid beta-cryptoxanthin possesses an ionone group and has vitamin activity in humans.
Vitamin A can be found in two principal forms in foods:
Retinol, the form of vitamin A absorbed when eating animal food sources, is a yellow, fat-soluble substance. Since the pure alcohol form is unstable, the vitamin is found in tissues in a form of retinyl ester. It is also commercially produced and administered as esters such as retinyl acetate or palmitate.[9]
The carotenes alpha-carotene, beta-carotene, gamma-carotene; and the xanthophyll beta-cryptoxanthin (all of which contain beta-ionone rings), but no other carotenoids, function as provitamin A in herbivores and omnivore animals, which possess the enzyme beta-carotene 15,15'-dioxygenase which cleaves beta-carotene in the intestinal mucosa and converts it to retinol.[10] In general, carnivores are poor converters of ionone-containing carotenoids, and pure carnivores such as cats and ferrets lack beta-carotene 15,15'-dioxygenase and cannot convert any carotenoids to retinal (resulting in none of the carotenoids being forms of vitamin A for these species).
Contents
[hide]
1 Medical use
1.1 Deficiency
1.2 Vitamin A supplementation
2 Side effects
3 History
4 Equivalencies of retinoids and carotenoids (IU)
5 Dietary recommendations
6 Sources
7 Metabolic functions
7.1 Vision
7.2 Gene transcription
7.3 Dermatology
7.4 Retinal/retinol versus retinoic acid
8 Vitamin A and derivatives in medical use
9 References
10 Further reading
11 External links
Medical use[edit]
Deficiency[edit]
Main article: Vitamin A deficiency
Vitamin A deficiency is estimated to affect approximately one third of children under the age of five around the world.[11] It is estimated to claim the lives of 670,000 children under five annually.[12] Approximately 250,000–500,000 children in developing countries become blind each year owing to vitamin A deficiency, with the highest prevalence in Southeast Asia and Africa.[13] Vitamin A deficiency is "the leading cause of preventable childhood blindness," according to UNICEF.[14][15] It also increases the risk of death from common childhood conditions such as diarrhea. UNICEF regards addressing vitamin A deficiency as critical to reducing child mortality, the fourth of the United Nations' Millennium Development Goals.[14]
Vitamin A deficiency can occur as either a primary or a secondary deficiency. A primary vitamin A deficiency occurs among children and adults who do not consume an adequate intake of provitamin A carotenoids from fruits and vegetables or preformed vitamin A from animal and dairy products. Early weaning from breastmilk can also increase the risk of vitamin A deficiency.
Secondary vitamin A deficiency is associated with chronic malabsorption of lipids, impaired bile production and release, and chronic exposure to oxidants, such as cigarette smoke, and chronic alcoholism. Vitamin A is a fat-soluble vitamin and depends on micellar solubilization for dispersion into the small intestine, which results in poor use of vitamin A from low-fat diets. Zinc deficiency can also impair absorption, transport, and metabolism of vitamin A because it is essential for the synthesis of the vitamin A transport proteins and as the cofactor in conversion of retinol to retinal. In malnourished populations, common low intakes of vitamin A and zinc increase the severity of vitamin A deficiency and lead physiological signs and symptoms of deficiency.[16] A study in Burkina Faso showed major reduction of malaria morbidity with combined vitamin A and zinc supplementation in young children.[17]
Due to the unique function of retinal as a visual chromophore, one of the earliest and specific manifestations of vitamin A deficiency is impaired vision, particularly in reduced light – night blindness. Persistent deficiency gives rise to a series of changes, the most devastating of which occur in the eyes. Some other ocular changes are referred to as xerophthalmia. First there is dryness of the conjunctiva (xerosis) as the normal lacrimal and mucus-secreting epithelium is replaced by a keratinized epithelium. This is followed by the build-up of keratin debris in small opaque plaques (Bitot's spots) and, eventually, erosion of the roughened corneal surface with softening and destruction of the cornea (keratomalacia) and leading to total blindness.[18] Other changes include impaired immunity (increased risk of ear infections, urinary tract infections, Meningococcal disease), hyperkeratosis (white lumps at hair follicles), keratosis pilaris and squamous metaplasia of the epithelium lining the upper respiratory passages and urinary bladder to a keratinized epithelium. In relation to dentistry, a deficiency in vitamin A may lead to enamel hypoplasia.
Adequate supply, but not excess vitamin A, is especially important for pregnant and breastfeeding women for normal fetal development and in breastmilk. Deficiencies cannot be compensated by postnatal supplementation.[19][20] Excess vitamin A, which is most common with high dose vitamin supplements, can cause birth defects and therefore should not exceed recommended daily values.[21]
Vitamin A metabolic inhibition as a result of alcohol consumption during pregnancy is the elucidated mechanism for fetal alcohol syndrome and is characterized by teratogenicity closely matching maternal vitamin A deficiency.[22]
Vitamin A supplementation[edit]
Global efforts to support national governments in addressing vitamin A deficiency are led by the Global Alliance for Vitamin A (GAVA), which is an informal partnership between A2Z, the Canadian International Development Agency, Helen Keller International, the Micronutrient Initiative, UNICEF, USAID, and the World Bank. Joint GAVA activity is coordinated by the Micronutrient Initiative.
While strategies include intake of vitamin A through a combination of breast feeding and dietary intake, delivery of oral high-dose supplements remain the principal strategy for minimizing deficiency.[23] A meta-analysis of 43 studies showed that vitamin A supplementation of children under five who are at risk of deficiency reduces mortality by up to 24%.[24] About 75% of the vitamin A required for supplementation activity by developing countries is supplied by the Micronutrient Initiative with support from the Canadian International Development Agency.[25] Food fortification approaches are becoming increasingly feasible[26] but cannot yet ensure coverage levels.[23]
The World Health Organization estimates that Vitamin A supplementation has averted 1.25 million deaths due to vitamin A deficiency in 40 countries since 1998.[27] In 2008 it was estimated that an annual investment of US$60 million in vitamin A and zinc supplementation combined would yield benefits of more than US$1 billion per year, with every dollar spent generating benefits of more than US$17.[28] These combined interventions were ranked by the Copenhagen Consensus 2008 as the world’s best development investment.[28]
Observational studies of pregnant women in sub-Saharan Africa have shown that low serum vitamin A levels are associated with an increased risk of mother-to-child transmission (MTCT) of HIV. Vitamin A is cheap and easily provided through existing health services in low-income settings. It is thus important to determine the effect of routine supplementation of H levels,[29][30] and because low blood vitamin A levels have been associated with rapid HIV infection and deaths,[31][32] To identify randomised controlled trials comparing vitamin A supplementation with placebo in known HIV-infected pregnant women, authors searched the Cochrane Library, PubMed, EMBASE, AIDSearch and GATEWAY; checked reference lis,.[33][34] Authoritative reviews of more recent and better-designed studies have found no relationship between the level of serum maternal and/or infant vitamin A and the likelihood of vertical (MTCT) HIV transmission.[35] of HIV,[35][36] our trials which enrolled 3033 HIV-infected pregnant women met inclusion criteria. Authors found significant statistical heterogeneity between the three trials with information on MTCT of HIV. Overall, there was no evidence of an effect of antenatal vitamin A supplementation on the risk of MTCT of HIV. However, antenatal vitamin A supplementation significantly improved birth weight, but there was no evidence of an effect on preterm births, stillbirths, deaths by 24 months.[36] Evidence is also lacking on whether vitamin A supplementation for infants up to six months of age reduces infant mortality or morbidity in low- and middle-income countries.[37]
A 2012 systematic review found no evidence that beta-carotene or vitamin A supplements increase longevity in healthy people or in people with various diseases (gastrointestinal, cardiovascular, neurological, ocular, dermatological, rheumatoid, endocrinological, and others).[38]
Side effects[edit]
Main article: Hypervitaminosis A
Since vitamin A is fat-soluble, disposing of any excesses taken in through diet takes much longer than with water-soluble B vitamins and vitamin C. This allows for toxic levels of vitamin A to accumulate. These toxicities only occur with preformed (retinoid) vitamin A (such as from liver). The carotenoid forms (such as beta-carotene as found in carrots), give no such symptoms, but excessive dietary intake of beta-carotene can lead to carotenodermia, a harmless but cosmetically displeasing orange-yellow discoloration of the skin.[39][40][41]
In general, acute toxicity occurs at doses of 25,000 IU/kg of body weight, with chronic toxicity occurring at 4,000 IU/kg of body weight daily for 6–15 months.[42] However, liver toxicities can occur at levels as low as 15,000 IU (4500 micrograms) per day to 1.4 million IU per day, with an average daily toxic dose of 120,000 IU, particularly with excessive consumption of alcohol.[citation needed] In people with renal failure, 4000 IU can cause substantial damage. Signs of toxicity may occur with long-term consumption of vitamin A at doses of 25,000-33,000 IU per day.[1]
Excessive vitamin A consumption can lead to nausea, irritability, anorexia (reduced appetite), vomiting, blurry vision, headaches, hair loss, muscle and abdominal pain and weakness, drowsiness, and altered mental status. In chronic cases, hair loss, dry skin, drying of the mucous membranes, fever, insomnia, fatigue, weight loss, bone fractures, anemia, and diarrhea can all be evident on top of the symptoms associated with less serious toxicity.[43] Some of these symptoms are also common to acne treatment with Isotretinoin. Chronically high doses of vitamin A, and also pharmaceutical retinoids such as 13-cis retinoic acid, can produce the syndrome of pseudotumor cerebri.[44] This syndrome includes headache, blurring of vision and confusion, associated with increased intracerebral pressure. Symptoms begin to resolve when intake of the offending substance is stopped.[45]
Chronic intake of 1500 RAE of preformed vitamin A may be associated with osteoporosis and hip fractures because it suppresses bone building while simultaneously stimulating bone breakdown,[46] although other reviews have disputed this effect, indicating further evidence is needed.[1]
A 2012 systematic review found that beta-carotene and higher doses of supplemental vitamin A increased mortality in healthy people and people with various diseases.[38] The findings of the review extend evidence that antioxidants may not have long-term benefits.
History[edit]
The discovery of vitamin A may have stemmed from research dating back to 1816, when physiologist François Magendie observed that dogs deprived of nutrition developed corneal ulcers and had a high mortality rate.[47] In 1912, Frederick Gowland Hopkins demonstrated that unknown accessory factors found in milk, other than carbohydrates, proteins, and fats were necessary for growth in rats. Hopkins received a Nobel Prize for this discovery in 1929.[47][48] By 1913, one of these substances was independently discovered by Elmer McCollum and Marguerite Davis at the University of Wisconsin–Madison, and Lafayette Mendel and Thomas Burr Osborne at Yale University who studied the role of fats in the diet. McCollum and Davis ultimately received credit because they submitted their paper three weeks before Mendel and Osborne. Both papers appeared in the same issue of the Journal of Biological Chemistry in 1913.[49] The "accessory factors" were termed "fat soluble" in 1918 and later "vitamin A" in 1920. In 1919, Harry Steenbock (University of Wisconsin–Madison) proposed a relationship between yellow plant pigments (beta-carotene) and vitamin A. In 1931, Swiss chemist Paul Karrer described the chemical structure of vitamin A.[47] Vitamin A was first synthesized in 1947 by two Dutch chemists, David Adriaan van Dorp and Jozef Ferdinand Arens.
Equivalencies of retinoids and carotenoids (IU)[edit]
As some carotenoids can be converted into vitamin A, attempts have been made to determine how much of them in the diet is equivalent to a particular amount of retinol, so that comparisons can be made of the benefit of different foods. The situation can be confusing because the accepted equivalences have changed. For many years, a system of equivalencies in which an international unit (IU) was equal to 0.3 μg of retinol, 0.6 μg of β-carotene, or 1.2 μg of other provitamin-A carotenoids was used.[50] Later, a unit called retinol equivalent (RE) was introduced. Prior to 2001, one RE corresponded to 1 μg retinol, 2 μg β-carotene dissolved in oil (it is only partly dissolved in most supplement pills, due to very poor solubility in any medium), 6 μg β-carotene in normal food (because it is not absorbed as well as when in oils), and 12 μg of either α-carotene, γ-carotene, or β-cryptoxanthin in food.
Newer research has shown that the absorption of provitamin-A carotenoids is only half as much as previously thought. As a result, in 2001 the US Institute of Medicine recommended a new unit, the retinol activity equivalent (RAE). Each μg RAE corresponds to 1 μg retinol, 2 μg of β-carotene in oil, 12 μg of "dietary" beta-carotene, or 24 μg of the three other dietary provitamin-A carotenoids.[51]
Substance and its chemical environment
Micrograms of retinol equivalent
per microgram of the substance
retinol 1
beta-carotene, dissolved in oil 1/2
beta-carotene, common dietary 1/12
alpha-carotene, common dietary 1/24
gamma-carotene, common dietary 1/24
beta-cryptoxanthin, common dietary 1/24
Because the conversion of retinol from provitamin carotenoids by the human body is actively regulated by the amount of retinol available to the body, the conversions apply strictly only for vitamin A-deficient humans. The absorption of provitamins depends greatly on the amount of lipids ingested with the provitamin; lipids increase the uptake of the provitamin.[52]
The conclusion that can be drawn from the newer research is that fruits and vegetables are not as useful for obtaining vitamin A as was thought; in other words, the IUs that these foods were reported to contain were worth much less than the same number of IUs of fat-dissolved oils and (to some extent) supplements. This is important for vegetarians, as night blindness is prevalent in countries where little meat or vitamin A-fortified foods are available.
A sample vegan diet for one day that provides sufficient vitamin A has been published by the Food and Nutrition Board (page 120[51]). On the other hand, reference values for retinol or its equivalents, provided by the National Academy of Sciences, have decreased. The RDA (for men) established in 1968 was 5000 IU (1500 μg retinol). In 1974 the RDA was revised to 1000 RE (1000 μg retinol). As of 2001 the RDA for adult males is now 900 RAE (900 μg or 3000 IU retinol). This is equivalent to 1800 μg of β-carotene supplement (3000 IU) or 10800 μg of β-carotene in food (18000 IU).
Dietary recommendations[edit]
The U.S. Institute of Medicine (IOM) updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for vitamin A in 2001. For infants up to 12 months there was not sufficient information to establish a RDA, so Adequate Intake (AI) shown instead. As for safety the IOM sets Tolerable upper intake levels (ULs) for vitamins and minerals when evidence is sufficient. Collectively the EARs, RDAs, AIs and ULs are referred to as Dietary Reference Intakes (DRIs). The calculation of retinol activity equivalents (RAE) is each μg RAE corresponds to 1 μg retinol, 2 μg of β-carotene in oil, 12 μg of "dietary" beta-carotene, or 24 μg of the three other dietary provitamin-A carotenoids.[51]
Life stage group
U.S. RDAs or
Adequate intakes (AI)
Retinol activity equivalents μg/day
Upper limits (UL*)
μg/day
Infants
0–6 months
7–12 months

400 (AI)
500 (AI)
600
600
Children
1–3 years
4–8 years

300
400
600
900
Males
9–13 years
14–18 years
19 – >70 years

600
900
900
1700
2800
3000
Females
9–13 years
14–18 years
19 – >70 years

600
700
700
1700
2800
3000
Pregnancy
<19 years
19 – >50 years

750
770
2800
3000
Lactation
<19 years
19 – >50 years

1200
1300
2800
3000
ULs are for natural and synthetic retinol ester forms of vitamin A. Beta-carotene and other provitamin A carotenoids from foods and dietary supplements are not added when calculating total vitamin A intake for safety assessments, although they are included as RAEs for RDA and AI calculations.[1][51]
For U.S. food and dietary supplement labeling purposes the amount in a serving is expressed as a percent of Daily Value (%DV). For vitamin A labeling purposes 100% of the Daily Value was set at 5,000 IU, but as of May 27, 2016 it has been revised to 900 μg RAE.[53] A table of the pre-change adult Daily Values is provided at Reference Daily Intake. Food and supplement companies have until July 28, 2018 to comply with the change.
The European Food Safety Authority (EFSA) refers to the collective set of information as Dietary Reference Values, with Population Reference Intake (PRI) instead of RDA, and Average Requirement instead of EAR. AI and UL defined the same as in United States. For women and men ages 15 and older the PRIs are set at 650 and 750 μg/day, respectively. PRI for pregnancy is 700 μg/day, for lactation 1300/day. For children ages 1–14 years the PRIs increase with age from 250 to 600 μg/day. These PRIs are similar to the U.S. RDAs.[54] The European Food Safety Authority reviewed the same safety question as the United States and set a UL at 3000 μg/day.[55]
Sources[edit]
carrots
Vitamin A is found in many foods:[56]
cod liver oil (30000 μg 3333%)
liver (turkey) (8058 μg 895%)
liver (beef, pork, fish) (6500 μg 722%)
liver (chicken) (3296 μg 366%)
capsicum, red (2081 μg 231%)
sweet potato (961 μg 107%)
carrot (835 μg 93%)
broccoli leaf (800 μg 89%)
butter (684 μg 76%)
kale (681 μg 76%)
collard greens (frozen then boiled) (575 μg 64%)
Butternut squash (532 μg 67%)
dandelion greens (508 μg 56%)
spinach (469 μg 52%)
pumpkin (426 μg 43%)
collard greens (333 μg 37%)
cheddar cheese (265 μg 29%)
cantaloupe melon (169 μg 19%)
egg (140 μg 16%)
apricot (96 μg 11%)
papaya (55 μg 6%)
tomatoes (42 μg 5%)
mango (38 μg 4%)
pea (38 μg 4%)
broccoli florets (31 μg 3%)
milk (28 μg 3%)
bell pepper, green (18 μg 2%)
spirulina (3 μg 0.3%)
Bracketed values are retinol activity equivalences (RAEs) and percentage of the adult male RDA, per 100 grams of the foodstuff (average). Conversion of carotene to retinol varies from person to person and bioavailability of carotene in food varies.[57][58]
Metabolic functions[edit]
Vitamin A plays a role in a variety of functions throughout the body,[3] such as:
Vision
Gene transcription
Immune function
Embryonic development and reproduction
Bone metabolism
Haematopoiesis
Skin and cellular health
Teeth
Mucous membrane
Vision[edit]
The role of vitamin A in the visual cycle is specifically related to the retinal form. Within the eye, 11-cis-retinal is bound to the protein "opsin" to form rhodopsin in rods[5] and iodopsin (cones) at conserved lysine residues. As light enters the eye, the 11-cis-retinal is isomerized to the all-"trans" form. The all-"trans" retinal dissociates from the opsin in a series of steps called photo-bleaching. This isomerization induces a nervous signal along the optic nerve to the visual center of the brain. After separating from opsin, the all-"trans"-retinal is recycled and converted back to the 11-"cis"-retinal form by a series of enzymatic reactions. In addition, some of the all-"trans" retinal may be converted to all-"trans" retinol form and then transported with an interphotoreceptor retinol-binding protein (IRBP) to the pigment epithelial cells. Further esterification into all-"trans" retinyl esters allow for storage of all-trans-retinol within the pigment epithelial cells to be reused when needed.[16] The final stage is conversion of 11-cis-retinal will rebind to opsin to reform rhodopsin (visual purple) in the retina. Rhodopsin is needed to see in low light (contrast) as well as for night vision. Kühne showed that rhodopsin in the retina is only regenerated when the retina is attached to retinal pigmented epithelium,[5] which provides retinal. It is for this reason that a deficiency in vitamin A will inhibit the reformation of rhodopsin and lead to one of the first symptoms, night blindness.[59]
Gene transcription[edit]
Main article: Gene transcription
Vitamin A, in the retinoic acid form, plays an important role in gene transcription. Once retinol has been taken up by a cell, it can be oxidized to retinal (retinaldehyde) by retinol dehydrogenases and then retinaldehyde can be oxidized to retinoic acid by retinaldehyde dehydrogenases.[21] The conversion of retinaldehyde to retinoic acid is an irreversible step, meaning that the production of retinoic acid is tightly regulated, due to its activity as a ligand for nuclear receptors.[16] The physiological form of retinoic acid (all-trans-retinoic acid) regulates gene transcription by binding to nuclear receptors known as retinoic acid receptors (RARs) which are bound to DNA as heterodimers with retinoid "X" receptors (RXRs). RAR and RXR must dimerize before they can bind to the DNA. RAR will form a heterodimer with RXR (RAR-RXR), but it does not readily form a homodimer (RAR-RAR). RXR, on the other hand, may form a homodimer (RXR-RXR) and will form heterodimers with many other nuclear receptors as well, including the thyroid hormone receptor (RXR-TR), the Vitamin D3 receptor (RXR-VDR), the peroxisome proliferator-activated receptor (RXR-PPAR) and the liver "X" receptor (RXR-LXR).[60] The RAR-RXR heterodimer recognizes retinoic acid response elements (RAREs) on the DNA whereas the RXR-RXR homodimer recognizes retinoid "X" response elements (RXREs) on the DNA; although several RAREs near target genes have been shown to control physiological processes,[21] this has not been demonstrated for RXREs. The heterodimers of RXR with nuclear receptors other than RAR (i.e. TR, VDR, PPAR, LXR) bind to various distinct response elements on the DNA to control processes not regulated by vitamin A.[16] Upon binding of retinoic acid to the RAR component of the RAR-RXR heterodimer, the receptors undergo a conformational change that causes co-repressors to dissociate from the receptors. Coactivators can then bind to the receptor complex, which may help to loosen the chromatin structure from the histones or may interact with the transcriptional machinery.[60] This response can upregulate (or downregulate) the expression of target genes, including Hox genes as well as the genes that encode for the receptors themselves (i.e. RAR-beta in mammals).[16]
Dermatology[edit]
Vitamin A, and more specifically, retinoic acid, appears to maintain normal skin health by switching on genes and differentiating keratinocytes (immature skin cells) into mature epidermal cells.[61] Exact mechanisms behind pharmacological retinoid therapy agents in the treatment of dermatological diseases are being researched. For the treatment of acne, the most prescribed retinoid drug is 13-cis retinoic acid (isotretinoin). It reduces the size and secretion of the sebaceous glands. Although it is known that 40 mg of isotretinoin will break down to an equivalent of 10 mg of ATRA — the mechanism of action of the drug (original brand name Accutane) remains unknown and is a matter of some controversy. Isotretinoin reduces bacterial numbers in both the ducts and skin surface. This is thought to be a result of the reduction in sebum, a nutrient source for the bacteria. Isotretinoin reduces inflammation via inhibition of chemotactic responses of monocytes and neutrophils.[16] Isotretinoin also has been shown to initiate remodeling of the sebaceous glands; triggering changes in gene expression that selectively induce apoptosis.[62] Isotretinoin is a teratogen with a number of potential side-effects. Consequently, its use requires medical supervision.
Retinal/retinol versus retinoic acid[edit]
Vitamin A deprived rats can be kept in good general health with supplementation of retinoic acid. This reverses the growth-stunting effects of vitamin A deficiency, as well as early stages of xerophthalmia. However, such rats show infertility (in both male and females) and continued degeneration of the retina, showing that these functions require retinal or retinol, which are interconvertible but which cannot be recovered from the oxidized retinoic acid. The requirement of retinol to rescue reproduction in vitamin A deficient rats is now known to be due to a requirement for local synthesis of retinoic acid from retinol in testis and embryos.[63][64]
Vitamin A and derivatives in medical use[edit]
Retinyl palmitate has been used in skin creams, where it is broken down to retinol and ostensibly metabolised to retinoic acid, which has potent biological activity, as described above.
The retinoids (for example, 13-cis-retinoic acid) constitute a class of chemical compounds chemically related to retinoic acid, and are used in medicine to modulate gene functions in place of this compound. Like retinoic acid, the related compounds do not have full vitamin A activity, but do have powerful effects on gene expression and epithelial cell differentiation.[65]
Pharmaceutics utilizing mega doses of naturally occurring retinoic acid derivatives are currently in use for cancer, HIV, and dermatological purposes.[66] At high doses, side-effects are similar to vitamin A toxicity.
References[edit]
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Further reading[edit]
Litwack, Gerald (2007). Vitamin A. Vitamins and Hormones. 75. San Diego, CA: Elsevier Academic Press. ISBN 978-0-12-709875-3.
UNICEF, Vitamin A Supplementation: A Decade of Progress, UNICEF, New York, 2007.
Flour Fortification Initiative, GAIN, Micronutrient Initiative, USAID, The World Bank, UNICEF, Investing in the Future: A United Call to Action on Vitamin and Mineral Deficiencies, 2009.
External links[edit]
Vitamin A at the US National Library of Medicine Medical Subject Headings (MeSH)
World Health Organization Database on Vitamin A Deficiency
[show]
v
t
e
Vitamins (A11)
Fat soluble
A
α-Carotene
β-Carotene
Retinol#
Tretinoin
D
D2
Ergosterol
Ergocalciferol#
D3
7-Dehydrocholesterol
Previtamin D3
Cholecalciferol#
25-hydroxycholecalciferol
Calcitriol (1,25-dihydroxycholecalciferol)
Calcitroic acid
D4
Dihydroergocalciferol
D5
D analogues
Alfacalcidol
Dihydrotachysterol
Calcipotriol
Tacalcitol
Paricalcitol
E
Tocopherol
Alpha
Beta
Gamma
Delta
Tocotrienol
Alpha
Beta
Gamma
Delta
Tocofersolan
K
Naphthoquinone
Phylloquinone (K1)
Menaquinones (K2)
Menadione (K3)‡
Menadiol (K4)
Water soluble
B
B1
Thiamine#
B1 analogues
Acefurtiamine
Allithiamine
Fursultiamine
Octotiamine
Prosultiamine
Sulbutiamine
B2
Riboflavin#
B3
Niacin
Nicotinamide#
B5
Pantothenic acid
Dexpanthenol
Pantethine
B6
Pyridoxine#, Pyridoxal phosphate
Pyridoxamine
Pyritinol
B7
Biotin
B9
Folic acid
Dihydrofolic acid
Folinic acid
Levomefolic acid
B12
Adenosylcobalamin
Cyanocobalamin
Hydroxocobalamin
Methylcobalamin
Choline
C
Ascorbic acid#
Dehydroascorbic acid
Combinations
Multivitamins
#WHO-EM
‡Withdrawn from market
Clinical trials:
†Phase III
§Never to phase III
[show]
v
t
e
Antioxidants
Food antioxidants
6-Hydroxymelatonin
Acetyl-L-carnitine (ALCAR)
Alpha-lipoic acid (ALA)
Ascorbic acid (vitamin C)
Carotenoids (vitamin A)
Curcumin
Edaravone
Polyphenols
Glutathione
Hydroxytyrosol
L-carnitine
Ladostigil
Melatonin
Mofegiline
N-Acetylcysteine (NAC)
N-Acetylserotonin (NAS)
Oleocanthal
Oleuropein
Rasagiline
Resveratrol
Selegiline
Selenium
Tocopherols (vitamin E)
Tocotrienols (vitamin E)
Tyrosol
Ubiquinone (coenzyme Q)
Uric acid
Fuel antioxidants
Butylated hydroxytoluene
2,6-Di-tert-butylphenol
1,2-Diaminopropane
2,4-Dimethyl-6-tert-butylphenol
Ethylenediamine
Measurements
Folin method
ORAC
TEAC
FRAP
[show]
v
t
e
Retinoid receptor modulators
RAR
Agonists: 9CDHRA
9-cis-Retinoic acid (alitretinoin)
AC-261066
AC-55649
Acitretin
Adapalene
all-trans-Retinoic acid (tretinoin)
AM-580
BMS-493
BMS-753
BMS-961
CD-1530
CD-2314
CD-437
Ch-55
EC 23
Etretinate
Fenretinide
Isotretinoin
Palovarotene
Retinoic acid
Retinol (vitamin A)
Tamibarotene
Tazarotene
Tazarotenic acid
TTNPB
Antagonists: BMS-195614
BMS-493
CD-2665
ER-50891
LE-135
MM-11253
Retinoic acid metabolism inhibitors: Liarozole
RXR
Agonists: 9CDHRA
9-cis-Retinoic acid (alitretinoin)
all-trans-Retinoic acid (tretinoin)
Bexarotene
CD 3254
Docosahexaenoic acid
Fluorobexarotene
Isotretinoin
LG-100268
LG-101506
LG-100754
Retinoic acid
Retinol (vitamin A)
SR-11237
Antagonists: HX-531
HX-630
LG-100754
PA-452
UVI-3003
HX-603
LE135 (RAR beta selective)
LE-540
CD3254
PA-451
PA-452
Rhein
HX-711
6-(N-ethyl-N-(5-isobutoxy-4-isopropyl-2-(E)-styrylphenyl)amino)nicotinic acid
See also
Receptor/signaling modulators
Nuclear receptor modulators
Authority control
NDL: 00576536
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Vitamin A – Bosnian
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Vitamin A – Serbo-Croatian
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