Ординатура / Офтальмология / Английские материалы / Handbook of Nutrition and Ophthalmology_Semba_2007
.pdfChapter 7 / Amblyopia and B Deficiency |
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309.Figure from Dirección Nacional de Estadísticas, Ministerio de Salud Pública, Cuba.
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313.Mas Bermejo P, Rodriguez R, Barcelo C, et al. Neuropatía epidémica en Cuba: un análisis epidemiológico. Ministerio de Salud Pública, La Habana: 1993; pp. 1–14.
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316.Lincoff NS, Odel JG, Hirano M. Letter from Havana: ‘Outbreak’ of optic and peripheral neuropathy in Cuba? JAMA 1993;270:511–518.
317.Santiesteban R, Luis S, Marquez M, et al. Aspectos neuro-oftalmológicos de la neuropatía epidémica en Cuba: Estudio de 602 pacientes. Instituto de Neurología y Neurocirurgía, La Habana: 1993; pp. 1–22.
318.Borrajero I, Pérez JL, Domínguez C, et al. Epidemic neuropathy in Cuba: morphological characterization of peripheral nerve lesions in sural nerve biopsies. J Neurol Sci 1994;127:68–76.
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320.Ascherio A. Antimetabolites and an optic neuropathy epidemic in Cuba [letter]. Am J Clin Nutr 1997; 65:1092.
321.Johns DR, Neufeld MJ, Hedges TR III. Mitochondrial DNA mutations in Cuban optic and peripheral neuropathy. J Neuro-Ophthalmol 1994;14:135–140.
322.Johns DR, Sadun AA. Cuban epidemic optic neuropathy: mitochondrial DNA analysis. J Neuro-Ophthal- mol 1994;14:130–134.
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323.Newman NJ, Torroni A, Brown MD, et al. Epidemic neuropathy in Cuba not associated with mitochondrial DNA mutations found in Leber’s hereditary optic neuropathy patients. Am J Ophthalmol 1994; 118:158–168.
324.Román GC. On politics and health: an epidemic of neurologic disease in Cuba. Ann Intern Med 1995; 122:530–533.
325.Bates CJ. Intake and status in healthy Havana men, 2 years after the Cuban epidemic neuropathy. Br J Nutr 2001;85:641–642.
326.Macias-Matos C, Rodriguez-Ojea A, Chi N, Jimenez S, Zulueta D, Bates CJ. Biochemical evidence of thiamine depletion during the Cuban neuropathy epidemic, 1992–1993. Am J Clin Nutr 1996;64: 347–353.
327.Bowman BA, Bern C, Philen RM. Nothing’s simple about malnutrition: complexities raised by epidemic neuropathy in Cuba. Am J Clin Nutr 1996;64:383–384.
328.Arnaud J, Fleites-Mestre P, Chassagne M, et al. Vitamin B intake and status in healthy Havanan men, 2 years after the Cuban neuropathy epidemic. Br J Nutr 2001;85:741–748.
329.Arnaud J, Fleites P, Chassagne M, et al. Seasonal variations of antioxidant imbalance in Cuban healthy men. Eur J Clin Nutr 2001;55:29–38.
330.Barnouin J, Cristiá RP, Chassagne M, et al. Vitamin and nutritional status in Cuban smokers and nonsmokers in the context of an emerging epidemic neuropathy. Int J Vitam Nutr Res 2000;70:126–138.
331.Ordúñez-Garcia PO, Nieto FJ, Espinosa-Brito AD, Caballero B. Cuban epidemic optic neuropathy, 1991 to 1994: history repeats itself a century after the “Amblyopia of the Blockade.” Am J Pub Health 1996;86:738–743.
332.Perez-Stable E. Epidemic neuropathy in Cuba [letter]. Ann Intern Med 1995;123:734.
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334.Román GC. Epidemic neuropathy in Cuba: reply [letter]. Ann Intern Med 1995;123:734.
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336.Cullom ME, Heher KL, Miller NR, Savino PJ, Johns DR. Leber’s hereditary optic neuropathy masquerading as tobacco-alcohol amblyopia. Arch Ophthalmol 1993;111;1482–1485.
337.Kerrison JB. Optic neuropathies caused by toxins and adverse drug reactions. Ophthalmol Clin North Am 2004;17:481–488.
338.Blyth AW. The composition of cows’ milk in health and disease. J Chem Soc 1879;35:530–539.
339.McCollum EV, Kennedy C. The dietary factors operating in the production of polyneuritis. J Biol Chem 1916;24:491–502.
340.Emmett AD, Luros GO. Water soluble vitamins. I. Are the antineuritic and the growth-promoting watersoluble B vitamines the same? J Biol Chem 1920;43:265–287.
341.Smith MI, Hedrick EG. Some nutrition experiments with brewers’ yeast with especial reference to its value in supplementing certain deficiencies in experimental rations. US Public Health Rep 1926;41: 201–207.
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344.Kuhn R, György P, Wagner-Jauregg T. Über Ovoflavin, den Farbstoff des Eiklars. Berichte der Deutschen Chemischen Gesellschaft 1933;66:576–580.
345.Booher LE. The concentration and probable chemical nature of vitamin G. J Biol Chem 1933;102: 39–46.
346.Kuhn R, Reinemund K, Kaltschmitt H, Ströbele R, Trischmann H. Synthetisches 6,7-Dimethyl-9-d- riboflavin. Naturwissenschaften 1935;23:260.
347.Karrer P, Schöpp K, Benz F. Synthesen von Flavinen IV. Helv Chim Acta 1935;18:426–429.
348.Spoerl E, Huhle M, Seiler T. Induction of cross-links in corneal tissue. Exp Eye Res 1998;66:97–103.
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350.Bates CJ. Bioavailability of riboflavin. Eur J Clin Nutr 1997;51(suppl 1):S38–S42.
351.Zempleni J, Galloway JR, McCormick DB. Pharmacokinetics of orally and intravenously administered riboflavin in healthy humans. Am J Clin Nutr 1996;63:54–66.
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352.Jusko WJ, Levy G. Absorption, protein binding and elimination of riboflavin. In: Rivlin RS (ed). Riboflavin. New York, Plenum: 1975; pp. 99–152.
353.Merrill AH Jr, Lambeth JD, Edmondson DE, McCormick DB. Formation and mode of action of flavoproteins. Annu Rev Nutr 1981;1:281–317.
354.Jamieson CP, Obeid OA, Powell-Tuck J. The thiamin, riboflavin and pyridoxine status of patients on emergency admission to hospital. Clin Nutr 1999;18:87–91.
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357.Bates CJ, Prentice AM, Watkinson M, et al. Efficacy of a food supplement in correcting riboflavin deficiency in pregnant Gambian women. Hum Nutr Clin Nutr 1984;38C:363–374.
358.Ajayi OA. Biochemical ariboflavinosis among Nigerian rural school children. Hum Nutr Clin Nutr 1984; 38:383–389.
359.Ajayi OA, James OA. Effect of riboflavin supplementation on riboflavin nutriture of a secondary school population in Nigeria. Am J Clin Nutr 1984;39:787–791.
360.Wacker J, Fruhauf J, Schulz M, Chiwora FM, Volz J, Becker K. Riboflavin deficiency and preeclampsia. Obstet Gynecol 2000;96:38–44.
361.Lo CS. Riboflavin status of adolescents in southern China: average intake of riboflavin and clinical findings. Med J Aust 1984;141:635–637.
362.Cunha DF, Cunha SF, Unamuno MR, Vannucchi H. Serum levels assessment of vitamin A, E, C, B2 and carotenoids in malnourished and non-malnourished hospitalized elderly patients. Clin Nutr 2001; 20:167–170.
363.Rosado JL, Bourges H, Saint-Martin B. Deficiencia de vitaminas y minerales en México. Una revisión crítica del estado de la información: II. Deficiencia de vitaminas. Salud Publica Mex 1995;37:452–461.
364.Boisvert WA, Castañeda C, Mendoza I, et al. Prevalence of riboflavin deficiency among Guatemalan elderly people and its relationship to milk intake. Am J Clin Nutr 1993;58:85–90.
365.Vudhivai N, Ali A, Pongpaew P, et al. Vitamin B1, B2, and B6 status of vegetarians. J Med Assoc Thai 1991;74:465–470.
367.Cole HS, Lopez R, Cooperman JM. Riboflavin deficiency in children with diabetes mellitus. Acta Diabetol Lat 1976;13:25–29.
368.Rivlin RS. Riboflavin and cancer. In: Rivlin RS (ed). Riboflavin. New York, Plenum: 1975; pp. 369–391.
369.Steier M, Lopez R, Cooperman JM. Riboflavin deficiency in infants and children with heart disease. Am Heart J 1976;92:139–143.
370.Goldsmith GA. Riboflavin deficiency. In: Rivlin RS (ed). Riboflavin. New York, Plenum: 1975; pp. 221–244.
371.Sebrell WH, Butler RE. Riboflavin deficiency in man. A preliminary note. Publ Health Rep 1938;53: 2282–2284.
372.Powell SR, Schwab IR. Nutritional disorders affecting the peripheral cornea. Int Ophthalmol Clin 1986; 26:137–146.
373.Sydenstricker VP. Clinical manifestations of ariboflavinosis. Am J Pub Health 1941;31:344–350.
374.Sebrell WH. Identification of riboflavin deficiency in human subjects. Fed Proc 1979;38:2694–2495.
375.Zilstorff-Pedersen K. To tilfælde af ariboflavinosis. Helbredt ved behandling med store doser riboflavin. Ugesk Laeger 1927;114:393–395.
376.Sydenstricker VP, Sebrell WH, Cleckley HM, Kruse HD. The ocular manifestations of ariboflavinosis: a progress note. J Am Med Assoc 1940;114:2437–2445.
377.Kruse HD, Sydenstricker VP, Sebrell WH, Cleckley HM. Ocular manifestations of ariboflavinosis. Pub Health Rep 1940;55:157–169.
378.Sydenstricker VP, Kelly AR, Weaver JW. Ariboflavinosis, with special reference to the ocular manifestations. South Med J 1941;34:165–170.
379.Rof Carballo J, Grande Covián F. Arriboflavinosis e invasión capilar de la córnea. Invasión capilar y su relación con el contenido en riboflavina de la dieta. Rev Clin Espan 1944;13:315–321.
380.Rof Carballo J, Grande Covean F. Arriboflavinosis e invasión capilar de la córnea. Pruebas terapéuticas. Rev Clin Espan 1944;13:380–387.
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381.Bassi G, Jona S. Sulle manifestazioni oculari dell’alattoflavinosi umana. Boll d’Ocul 1945;24:3–18.
382.Stern HJ. Acute ocular manifestations of ariboflavinosis. Ophthalmologica 1947;114:103–106.
383.Jackson CRS. Riboflavin deficiency with ocular signs: report of a case. Br J Ophthalmol 1950;34:259– 260.
384.Bellomio S. Contributo clinico alla conoscenza della alattoflavinosi oculare. Boll Ocul 1955;34:157– 170.
385.Raymond LF. Reversible chronic recurrent keratitis with vascularization due to ariboflavinosis. J Med Soc New Jersey 1955;52:315–316.
386.Lundh B, Frandsen H. Riboflavin and ariboflavinosis, with special reference to eye changes. Acta Ophthalmol 1941;19:331–345.
387.Spies TD, Perry DJ, Cogswell RC, Frommeyer WB. Ocular disturbances in riboflavin deficiency. J Lab Clin Med 1945;30:751–765.
388.Chen TT. Angular blepharitis in ariboflavinosis—a not well known clinical manifestation of riboflavin deficiency. Chinese Med J 1948;66:1–4.
389.Stern JJ. The ocular manifestations of riboflavin deficiency. Am J Ophthalmol 1950;33:1127–1136.
390.Aykroyd WR, Verma OP. Superficial keratitis due to riboflavin deficiency. Indian Med Gaz 1942;77: 1–5.
391.Verma OP. Further experience in the treatment of superficial keratitis with riboflavin. Indian Med Gaz 1942;77:471–472.
392.Gregory MK. The ocular criteria of deficiency of riboflavin. Br Med J 1943;2:134–135.
393.Vail D, Ascher KW. Corneal-vascularization problems. Am J Ophthalmol 1943;26:1025–1044.
394.Mann I. Ariboflavinosis. Am J Ophthalmol 1945;28:243–247.
395.Scarborough H. Circumcorneal injection as a sign of riboflavin deficiency in man, with an account of three cases of ariboflavinosis. Br Med J 1942;2:601–604.
396.Sandstead HR. Superficial vascularization of the cornea. The result of riboflavin therapy. Pub Health Rep 1942;57:1821–1825.
397.Youmans JB, Patton EW, Robinson WD, Kern R. An analysis of corneal vascularization as found in a survey of nutrition. Tran Assoc Am Physicians 1942;57:49–54.
398.Tisdall FF, McCreary JF, Pearce H. The effect of riboflavin on corneal vascularization and symptoms of eye fatigue in R.C.A.F. personnel. Canad Med Assoc J 1943;49:5–13.
399.Lyle TK, Macrae TF, Gardiner PA. Corneal vascularisation in nutritional deficiency. Lancet 1944;1: 393–395.
400.Borsook H, Alpert E, Keighley GL. Nutritional status of aircraft workers in southern California. II. Clinical and laboratory findings. Milbank Mem Fund Quart Bull 1943;21:115–157.
401.Scott JG. Corneal vascularity as a sign of ariboflavinosis. J Roy Army Med Corps 1944;82:133–135.
402.Kodicek JH, Yudkin J. Slit-lamp microscope in nutrition surveys. Lancet 1942;2:753–756.
403.Venkataswamy G. Ocular manifestations of vitamin B-complex deficiency. Br J Ophthalmol 1967;51: 749–754.
404.Hou HC. Riboflavin deficiency among Chinese. I. Ocular manifestations. Chinese Med J 1940;58:616– 628.
405.Stern HJ. Conditioned corneal vascularity in riboflavin deficiency: report of a case. Arch Ophthalmol 1949;42:438–442.
406.Landau J, Stern HJ. Flare-up of trachomatous pannus due to ariboflavinosis. Am J Ophthalmol 1948;31: 952–954.
407.Takami Y, Gong H, Amemiya T. Riboflavin deficiency induces ocular surface damage. Ophthalmic Res 2004;36:156–165.
408.Wagener HP. Nutritional diseases and the eye. The rôle of vitamin B. Am J Med Sci 1936;192:296– 300.
409.Johnson LV, Eckardt RE. Rosacea keratitis and conditions with vascularization of cornea treated with riboflavin. Arch Ophthalmol 1940;23:899–907.
410.Cosgrove KW, Day PL. The use of riboflavin in the treatment of corneal diseases. Am J Ophthalmol 1942;25:544–551.
411.Fish WM. Acne rosacea keratitis and riboflavine (vitamin B2). Br J Ophthalmol 1943;27:107–109.
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412.Pirie A. The relation of riboflavin to the eye. A review article. Br J Ophthalmol 1943;27:291–301.
413.Stern HJ, Landau J. Eczematous keratitis and ariboflavinosis. Am J Ophthalmol 1948;31:1619–1623.
414.Corkey JA. Riboflavin in marginal keratitis. Trans Ophthalmol Soc UK 1952;72:291–303.
415.Machella TE, McDonald PR. Studies of the B vitamins in the human subject. VI. Failure of riboflavin therapy in patients with the accepted picture of riboflavin deficiency. Am J Med Sci 1943;205:214–223.
416.Day PL, Langston WC, O’Brien CS. Cataract and other ocular changes in vitamin G deficiency: an experimental study on albino rats. Am J Ophthalmol 1931;14:1005–1009.
417.Bessey OA, Wolbach SB. Vascularization of the cornea of the rat in riboflavin deficiency, with a note on corneal vascularization in vitamin A deficiency. J Exp Med 1939;69:1–12.
418.Cochran W, DeVaughn NM, Allen L. Corneal vascularization in ariboflavinosis. South Med J 1942;35: 888–889.
419.Wiesinger H , Kaunitz H, Slanetz CA. Hornhautveränderungen bei Ratten im Riboflavinomangel. Oph- thal-mologica 1955;129:389–395.
420.Fromer CH, Klintworth GK. An evaluation of the role of leukocytes in the pathogenesis of experimentally induced corneal vascularization. Am J Pathol 1975;79:537–550.
421.Lowry OH, Bessey OA. The effects of light, trauma, riboflavin, and ariboflavinosis on the production of corneal vascularity and on healing of corneal lesions. J Nutr 1945;30:285–292.
422.Williams RD, Mason HL, Cusick PL, Wilder RM. Observations on induced riboflavin deficiency and the riboflavin requirement of man. J Nutr 1943;25:361–377.
423.Keys A, Henschel A, Taylor HL, Mickelsen O, Brozek J. Experimental studies on man with a restricted intake of the B vitamins. Am J Physiol 1945;144:5–45.
424.Boehrer JJ, Stanford CE, Ryan E. Experimental riboflavin deficiency in man. Am J Med Sci 1943;205: 544–549.
425.Sebrell WH, Butler RE, Wooley JG, Isbell H. Human riboflavin requirement established by urinary excretion of subjects on controlled intake. Pub Health Report 1941;56:510–519.
426.Lane M, Mengel CE, Doherty DJ. Rapid induction of isolated riboflavin deficiency in man. J Clin Invest 1960;39:1004.
427.Lane M, Alfrey CP, Mengel CE, Doherty MA, Doherty J. The rapid induction of human riboflavin deficiency with galactoflavin. J Clin Invest 1964;43:357–373.
428.Lane M, Brindley CO. Laboratory and clinical studies with the riboflavin antagonist, galactoflavin. Proc Soc Exp Biol Med 1964;116:57–61.
429.Gordon OE. Riboflavin and the cornea. Quart Bull Northwestern Univ Med School 1952;26:120–123.
430.Langston WC, Day PL, Cosgrove KW. Cataract in the albino mouse resulting from a deficiency of vitamin G (B2). Arch Ophthalmol 1933;10:508–514.
431.Day PL, Langston WC. Further experiments with cataract in albino rats resulting from the withdrawal of vitamin G (B2) from the diet. J Nutr 1934;7:97–106.
432.O’Brien CS. Experimental cataract in vitamin G deficiency. Arch Ophthalmol 1932;8:880–887.
433.Yudkin AM. Ocular disturbances produced in experimental animals by dietary changes: clinical implications. J Am Med Assoc 1933;101:921–926.
434.Langston WC, Day PL. Nutritional cataract in the Norway rat (Mus norvegicus). South Med J 1933;26: 128–129.
435.Langston WC, Day PL. The arrest of nutritional cataract in the albino rat by the use of vitamin G (B2). South Med J 1934;27:170–176.
436.Day PL, Darby WJ, Langston WC. The identity of flavin with the cataract-preventive factor. J Nutr 1937;13:389–399.
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438.Baum HM, Michaelree JF, Brown EB. The quantitative relationship of riboflavin to cataract formation in rats. Science 1942;95:24–25.
439.Bowles LL, Allen L, Sydenstricker VP, Hock CW, Hall WK. The development and demonstration of corneal vascularization in rats deficient in vitamin A and in riboflavin. J Nutr 1946;32:19–31.
440.Kaunitz H, Wiesinger H, Blodi FC, Johnson RE, Slanetz CA. Relation of protein and fat intake to growth and corneal vascularization in galactoflavin-produced ariboflavinosis. J Nutr 1954;52:467–482.
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Chapter 8 / Zinc and Eye Health |
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8Zinc and Eye Health
1.INTRODUCTION
Zinc plays an essential role in growth, neurodevelopment, immunity, reproduction, and
a wide range of physiological processes, including metabolism of nucleic acids, protein, and lipids, synthesis of hormones, and apoptosis. Zinc deficiency is common in developing countries worldwide (1), and zinc supplementation studies suggest that zinc deficiency may be widespread in North America among infants, children, and pregnant women (2). Acrodermatitis enteropathica, an inborn error of zinc metabolism, is characterized by compromised immunity and skin and ocular findings. Zinc deficiency can also occur in Crohn disease and among individuals receiving total parenteral nutrition without sufficient zinc. The retina and choroid contain the highest concentrations of zinc of any tissue in the human body. Zinc plays an important role in eye health, and recent investigations have demonstrated a causal link between zinc status and age-related macular degeneration. The role of zinc in age-related maculopathy and age-related macular degeneration are presented in greater detail in Chapter 4, under Subheading 5.4.
2. HISTORICAL BACKGROUND
Zinc was used empirically as both an oral and topical therapeutic agent for a variety of human illnesses in the nineteenth century (3). In 1854, zinc was detected in the ashes of vegetables by the German botanist Alexander Braun (1805–1877) (4). Zinc was first recognized to be an essential factor for plant growth by the French plant physiologist, Jules Raulin (1836–1896). Raulin studied the type of nutrients, especially minerals, that were needed for the growth of Aspergillus niger, and concluded that zinc was essential for growth (5). In 1877, zinc was described in human muscle and liver (6) and in plants
(7), and subsequent investigations revealed the presence of zinc in a wide variety of plants and animals (8). Birckner, after finding high zinc concentrations in egg yolk and human milk, argued on teleological grounds that this element “exerts an important nutritive function, the nature of which is not at present understood” (9). In the 1920s, efforts were made to establish an essential role for zinc in animal models. Despite problems with producing control diets and low zinc diets, these studies suggested that growth and survival of experimental animals was improved by zinc (10–13). With experimental advances, zinc deficiency was convincingly produced in rats (14,15). Further studies showed that hormone production and alanine metabolism were impaired during zinc deficiency (16,17) and that accompanying pathology included atrophy of the thymus, corneal vascularization, and hyperkeratosis and parakeratosis of the skin and esophagus (18). Enzymes such
From: Nutrition and Health: Handbook of Nutrition and Ophthalmology
By: R. D. Semba © Humana Press Inc., Totowa, NJ
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as carbonic anhydrase and kidney phosphatase were found to contain zinc, suggesting an important basic role for zinc (19,20).
Although zinc was considered by many to be an essential mineral by the late 1930s (21–23), many thought that zinc deficiency could not be a practical problem in human nutrition because of the widespread occurrence of zinc in nature (24). Variations in the zinc concentrations in blood, colostrum, milk, and tissues of humans were known, but no characteristic manifestations of a suspected zinc deficiency were identified (25). William Eggleton showed that the average amount of zinc ingested in a well balanced diet was about 12 mg per day (26). Low concentrations of blood, hair, and fingernail zinc were described among patients with beriberi and pellagra in China (27,28). Metabolic studies of zinc absorption and excretion were used to establish the daily requirements for zinc (28–30). Zinc deficiency in pigs, or parakeratosis, was described in 1955 (31). Human zinc deficiency was described in the 1960s when a syndrome of dwarfism, delayed sexual maturation, and iron deficiency anemia was found in young men who practiced geophagia and had low dietary intakes of zinc (32). Growth and sexual maturation occurred with zinc supplementation, showing that zinc was a limiting essential nutrient (33,34). Zinc supplementation increased sexual maturation faster than a well-balanced diet (35). In 1974, the Food and Nutrition Board of the National Research Council of the National Academy of Sciences established the recommended dietary allowance for zinc. The history of human zinc deficiency has been summarized elsewhere (36).
3. BIOCHEMISTRY OF ZINC
Zinc, a small ion with atomic number of 30 and atomic weight of 65.37, occurs in a divalent state (Zn++) in living organisms and is a strong Lewis acid, or electron acceptor. Zinc is the most abundant intracellular trace element (37). In biological systems, zinc does not exhibit direct redox chemistry. It has a high affinity for electrons and typically binds to proteins, amino acids, peptides, and nucleotides, with an affinity for thiol groups, hydroxy groups, and electron-rich ligands.
4. DIETARY SOURCES OF ZINC
Animal proteins constitute the richest dietary source of zinc, and foods that are especially rich in zinc include shellfish, red meat, liver, kidney, and chicken (38). Whole grains, pork, eggs, dairy products, nuts, beans, lentils, chickpeas, and peas contain moderate concentrations of zinc. Poor sources of zinc include fish, fruits, vegetables, butter, and fats. White breads contain little zinc, as milling removes the zinc-rich bran and germ portions of grains. Drinking water is a minor source of zinc in most populations. The zinc content of some common foods is shown in Table 1 (38). Dietary intakes of zinc can vary greatly, depending on other factors in the diet which may inhibit or enhance zinc absorption. In many populations in developing countries, the consumption of meat and animal products is low and intake and dietary fiber is high, a principle factor contributing to zinc deficiency.
The absorption and availability of dietary zinc can be greatly reduced by substances in plant foods such as phytates (inositol hexaphosphate), fiber, oxalate, tannin, and lignins (39–41). Zinc forms insoluble complexes with phytate, and these complexes reduces the bioavailability of dietary zinc (42). Phytates and other factors are found in high concentrations in whole grains, legumes, leafy vegetables, soy products and formula (43,44), coffee,
Chapter 8 / Zinc and Eye Health |
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Table 1
Approximate Zinc Content of Selected Foods
|
Zinc |
Food |
(mg/100 mg) |
|
|
Oysters, raw |
16.40 |
Beef liver, pan fried |
5.45 |
Beef kidney, simmered |
4.22 |
Sirloin, lean, roasted |
3.54 |
Cheese, cheddar |
3.11 |
Chicken, dark meat, roasted |
2.80 |
Clams, raw |
1.35 |
Chicken, light meat, roasted |
1.23 |
Shrimp, raw |
1.09 |
Salmon, raw |
0.58 |
Spinach, boiled |
0.57 |
Butter |
0.01 |
|
|
From ref. 38.
and tea. Zinc absorption studies have shown, for example, that little zinc is absorbed after ingestion of a beef taco because the phytates in the corn tortilla reduce the availability of zinc in the beef (41). Other factors that may interfere with zinc absorption include iron, especially when the iron:zinc ratio exceeds 2:1, and calcium, as found in dairy products. Soaking and fermentation of plant foods can reduce the content of phytic acid (45).
5. ABSORPTION, METABOLISM, AND STORAGE OF ZINC
Zinc is absorbed in the small intestine, primarily the duodenum and jejunum (46). The small intestine plays a central role in zinc metabolism and homeostasis, as the absorption of zinc depends on both zinc status and the dietary intake of zinc. Low zinc intake increases the efficiency of absorption of zinc. Zinc is absorbed by passive diffusion down a concentration gradient and also through an active, energy-dependent carrier-mediated process (47,48). The absorption of dietary zinc can range from 1% to 80%, and zinc absorption is increased during pregnancy and lactation (49). Diarrheal disease may interfere with the absorption of zinc and contribute to accelerated fecal losses of zinc. In the enterocytes, metallothionein and cysteine-rich intestinal protein play a role in transmucosal transport of zinc (50,51). Zinc released into the mesenteric capillaries and the portal circulation is bound to albumin and most is taken up by the liver (52). In the plasma, about 60% of zinc is bound to albumin, about 40% is bound to α2-macroglobulin, and a small fraction is bound to amino acids (53,54). Plasma zinc represents about 0.1% of total body zinc. In adults, the total body zinc content is estimated to be about 1.5 g in women and 2.5 g in men. The total body zinc content of adults may be maintained with the absorption of about 5 mg/d of zinc (55).
There is no specific storage organ for zinc in the body. Most of the zinc in the body is found in skeletal muscle and bone and is largely unavailable for other nutritional functions in the body. Zinc is found in high concentrations in the pancreas and gonads. The highest concentrations of zinc in the human body are found in the choroid and the retina
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Table 2
Zinc Concentrations in Human Tissues
|
Zinc |
Tissue |
(μg/g dry weight) |
|
|
Choroid |
472 |
Retina |
464 |
Ciliary body |
227 |
Optic nerve |
170 |
Hair |
150 |
Pancreas |
135 |
Bone |
100 |
Liver |
58 |
Kidney |
55 |
Skeletal muscle |
51 |
Cornea |
41 |
Skin |
32 |
Heart |
23 |
Lens |
21 |
Plasma |
1 |
|
|
Based on refs. 37,54,56.
(Table 2) (56). There appear to be two major zinc pools in the body, one with a short halflife and another with a long half-life. The liver, pancreas, kidney, and spleen have more rapid turnover of zinc than bone, muscle, and central nervous system. Zinc is excreted mostly in the feces from pancreatic, biliary, gastric, and intestinal excretion. Lesser amounts of zinc are excreted in the urine, sweat, and through turnover of skin, hair, nails, and through menstrual blood loss, human milk, and semen. About 2–3 mg of zinc are excreted per day in human milk during the first several weeks postpartum, decreasing to 1 mg/d by 2–3 mo postpartum and declining dramatically beyond this period (57).
6. FUNCTIONS OF ZINC
6.1. General Functions
Zinc is essential for immunity, growth, neurological transmission, and reproduction (58). Zinc is involved in the function of more than 300 zinc metalloenzymes that are involved in a wide range of structural, catalytic, and regulatory processes (59). Zinc is an essential component in at least one enzyme in every class of enzyme (60), including oxidoreductases, hydrolases, lyases, and transferases. Zinc plays an important structural role in zinc fingers, protein complexes which form a tetrahedral complex with zinc and provide structural stability for small polypeptides (61). The region of the protein containing the zinc binding domain is essential for binding to DNA and initiation of transcription. An estimated 1% of the human genome codes for zinc finger proteins (62). Zinc has been hypothesized to play a role in the stability of membranes because of its ability to stabilize thiol groups and phospholipids and to quench free radicals (63). Zinc plays an essential role in the function of polymorphonuclear leukocytes, natural killer cells, T and B lymphocytes, and the generation of antibody responses (64). In biological systems,