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PubMed2000

Plasma and breast milk vitamin A as indicators of vitamin A status in pregnant women.

Breast milk vitamin A is not well characterized as an indicator of vitamin A status in women with infections. A controlled trial of vitamin A, 3 mg retinol equivalent/day, was conducted among 697 pregnant women with human immunodeficiency virus (HIV) infection in Malawi which allowed comparison of plasma versus breast milk vitamin A as indicators of vitamin A status. Retinol concentrations were measured in plasma at baseline (18-28 weeks) and 38 weeks gestation and breast milk at 6 weeks post-partum. Plasma alpha 1-acid glycoprotein (AGP) and C-reactive protein (CRP) were measured at baseline. Plasma retinol (geometric mean, SD) at 38 weeks was 0.72 (0.44, 1.18) and 0.61 (0.38, 0.98) mumol/L (P < 0.0002) and breast milk retinol was 1.32 (0.71, 2.43) and 0.95 (0.49, 1.82) mumol/L (P < 0.0001) in vitamin A and placebo groups, respectively. Women with elevated acute phase protein (AGP > 1 gm/L and/or CRP > 5 mg/L) at baseline who received vitamin A had significantly higher plasma and breast milk vitamin A at follow-up compared with placebo. Elevated acute phase proteins did not distinguish women with low body stores of vitamin A. Breast milk retinol appears to be a better indicator of vitamin A status than plasma retinol in women with infections.

Adult↗
PubMed2006

Vitamin D fortification as public health policy: significant improvement in vitamin D status in young Finnish men.

BACKGROUND: Vitamin D insufficiency is common in northern countries during wintertime. In Finland, after the recommendation by the Ministry of Social Affairs and Health, vitamin D has been added to liquid milk products and margarines from February 2003. OBJECTIVE: We determined the effects of national policy on vitamin D fortification on vitamin D status among young Finnish men. DESIGN: A comparison before and after intervention with study population of 196 young Finnish men (18-28 years) was carried out. Serum 25-hydroxyvitamin D3 (25-OHD3) concentrations were determined with the OCTEIA enzymeimmunoassay by IDS (Immunodiagnostic Systems Limited, Bolden, UK) in January 2003 (n = 96) and in January 2004 (n = 100), nearly 1 year after national vitamin D fortification had started. RESULTS: The mean serum 25-OHD3 concentrations during the wintertime increased by 50% after implementation of the vitamin D fortification of dairy products. Correspondingly, the prevalence of vitamin D insufficiency (serum 25-OHD3 < 40 nmol/l) was decreased by 50% from 78% in January 2003 to 35% in January 2004. CONCLUSIONS: Our results demonstrate that national vitamin D fortification substantially improved the vitamin D status of young Finnish men. Still, a third remained vitamin D insufficient.

Adolescent↗
PubMed2003

National immunisation days and vitamin A distribution in Mali: has the vitamin A status of pre-school children improved?

OBJECTIVES: The impact on vitamin A status of the distribution of vitamin A during national immunisation days (NIDs) has not been well established despite strong promotion by international agencies and donors. Using a pre-post design, the change in prevalence of vitamin A deficiency was examined in pre-school children in Mali. DESIGN: Two cross-sectional surveys were conducted in Mopti region, the first in March 1997 before this strategy was adopted and the second in March 1999, four-and-a-half months after a mass distribution of vitamin A during NIDs. SUBJECTS AND SETTING: We compared the vitamin A status of children aged 12 to 66 months targeted in 1999 by NIDs with the status of children in the same age group in 1997. Infectious events of the previous two weeks were concurrently recorded. Within the 1999 sample, the status of recipient and non-recipient children was also compared. RESULTS: In 1997, the prevalence of xerophthalmia (defined by the presence of night blindness and/or Bitot spots) was 6.9% (95% confidence interval (CI) 5.1-9.2) and the modified retinol dose response (MRDR) test proved abnormal in 77.8% of 12-66-month-old children (95% CI 68.27-85.17). In 1999 this picture had improved significantly, both for xerophthalmia prevalence, 3.3% (95% CI 2.1-5.2), and abnormal MRDR test response, 63.1% (95% CI 54.25-71.23). The infectious morbidity rates between 1997 and 1999 tended to decrease. No significant improvement was found among children older than those targeted by NIDs. In 1999, children who received vitamin A had a lower risk for xerophthalmia (3.0% for recipients vs. 8.7% for non-recipients) and experienced fewer infectious events. CONCLUSIONS: The clinical and biological vitamin A status of pre-school children improved between 1997 and 1999. Mass distribution of vitamin A appears to reduce the occurrence of xerophthalmia and would seem to be associated with a decrease in other related illnesses. Vitamin A supplementation during NIDs should be given a high priority when vitamin A deficiency remains a public health problem.

Anthropometry↗
PubMed1976

Effects of zinc and vitamin A deficient diets on the hepatic mobilization and urinary excretion of vitamin A in rats.

Weanling rats were fed diets deficient in zinc (ZD), vitamin A (AD), or both (ZAD) for 3 weeks. Each then received 20 mug of 11,12-3H-retinyl acetate. Plasma retinol was monitored for radioactivity for 5 hours and urine for 6 days. Rats were killed and measurements made of plasma and liver vitamin A and plasma zinc. Plasma vitamin A was depressed but growth was not affected in AD rats compared to pair-fed controls. Radioactivity appeared most rapidly in the plasma retinol fractions of the two vitamin A-depleted groups (AD and ZAD) and was excreted most rapidly in the urine of these same groups. Zinc-deficient diets (ZD and ZAD) caused depressed plasma levels of zinc and vitamin A and growth retardation greater than in pair-fed controls. However zinc deficiency had no effect on mobilization of newly-ingested vitamin A or urinary excretion of labeled metabolites. Liver stores of vitamin A were lower for ZD rats than for controls. The data indicate that zinc deficiency is not a limiting factor in hepatic vitamin A release except as it influences growth and body demand for the vitamin. The data also suggest that newly-absorbed vitamin A is mobilized and utilized in preference to that previously stored in the liver.

Animals↗
PubMed1977

Sparing effect of folic acid deficiency on the development of vitamin B12 deficiency in baboons fed a vitamin B12 deficient diet.

The effect of a vitamin B12 and folic acid deficient diet on juvenile and adolescent baboons (Papio cynocephalus anubis) was studied. The baboons developed clinical and hematological signs characteristics of folacin deficiency, although they were less severe in juvenile baboons. The signs disappeared when folic acid was replaced in the diet. The serum vitamin B12 levels increased in all baboons fed the vitamin B12 and folic acid deficient diet. When folic acid was added to the diet, the levels gradually decreased in adolescent baboons, liver vitamin B12 levels decreased to a lesser extent when fed a vitamin B12 and folic acid deficient diet than when fed a vitamin B12 deficient diet. In juvenile baboons fed a vitamin B12 and folic acid deficient diet, for 7 months and a vitamin B12 deficient diet for a further 11 months, liver vitamin B12 levels did not decrease at any time but were similar to those in baboons fed a vitamin B12 and folic acid supplemented diet.

Aging↗
PubMed1993

Vitamin E is protective against iron toxicity and iron-induced hepatic vitamin E depletion in mice.

This study examined the effect of excess dietary iron on liver function, iron and vitamin E status and the protective activity of vitamin E. Consumption of excess dietary iron (3000, 5000, 8000 mg iron/kg/diet) compared with consumption of the control diet (120 mg iron/kg diet) by weanling male CD-1 mice for 7 wk resulted in accumulation of iron in liver, increased relative liver weights and a reduction in hepatic vitamin E stores. The concentration of vitamin E in the liver was negatively correlated with dietary iron concentration (r = 0.998). Weekly administration of vitamin E (20 mg/kg, subcutaneously) prevented iron-induced liver damage without altering hepatic iron stores. Pretreatment of adult male CD-1 mice with a single subcutaneous dose of vitamin E (20 mg/kg body wt) 24 h prior to a lethal dose of iron (60 mg/kg, intraperitoneally) resulted in 100% protection. A similar dose of vitamin E given 5, 30 or 60 min (intravenously) after iron intoxication enhanced survival to 90, 70 and 80%, respectively, compared with the untreated control group. Vitamin E treatment 30 min after iron intoxication reduced mortality by 75% compared with intravenous treatment with 10 mg/kg of deferoxamine (Desferal). Data in this study indicate that vitamin E may be a useful antidote for iron toxicoses and that iron-induced depletion of vitamin E may play a role in the pathogenesis of iron toxicity.

Animals↗
PubMed1996

Acute respiratory infections prevent improvement of vitamin A status in young infants supplemented with vitamin A.

At immunization contact, 165 infants 2.5 mo old were randomly assigned to receive either 15 mg vitamin A (retinyl palmitate) or placebo. Three doses were given at monthly intervals with each diphtheria, pertussis, tetanus and oral polio (DPT/OPV) immunization dose. The diarrhea and acute respiratory infection (ARI) morbidity was similar in the vitamin A and placebo groups. However, the duration (days per child-year, mean +/- SD) of ARI was less in the vitamin A group compared with placebo group (27.6 +/- 17.1 vs. 40.8 +/- 22.7; P = 0.005). Fasting retinol concentrations were measured at entry and in 61 infants, the relative dose response (RDR) test was done 1 mo after the third dose of vitamin A. Eighty-five percent of the infants had serum retinol concentration < 0.70 mol/L at entry. After 3 mo the serum retinol levels improved significantly in both groups, and in the vitamin A-supplemented group the serum retinol concentration was significantly better than that in the placebo group (P= 0.02). However, 61% of the infants remained deficient despite vitamin A supplementation. Among vitamin A-supplemented infants only, diarrhea and ARI morbidity during the 3-mo period were compared in children with normal versus children with abnormal RDR at the end of the supplementation period. The ARI episodes were more frequent in the supplemented infants who remained vitamin A deficient at the end of the 3 mo (P = 0.027). Also, the cumulative duration (days, mean +/- SD) of fever and cough was 5.0 +/- 2.8 in the normal versus 11.2 +/- 6.0 in the deficient group (P = 0.04). The results of this study suggest that a large proportion of infants remain vitamin A deficient even after large dose vitamin A supplementation because of frequent respiratory infections, particularly those accompanied by fever.

Acute Disease↗
PubMed1999

Vitamin A antagonizes the action of vitamin D in rats.

Interactions between vitamin A and vitamin D have been suggested for several decades but have not been established. In particular, vitamin A has been proposed to intensify the severity of the bone mineralization disease, rickets and inhibit the ability of vitamin D to cure this disease. To investigate this hypothesis, weanling Holtzman rats were fed a 1.2% calcium, 0.1% phosphorus diet and 15.5 ng ergocalciferol (vitamin D(2)) every 3 d for 21 d in the presence of increasing amounts of retinyl acetate (0 microg to 8621 microg/d). The increasing amounts of retinyl acetate produced a progressive and significant decrease in total bone ash (P < 0.001) and an increase in epiphyseal plate width (P < 0.001). The same experiment conducted with increasing amounts of vitamin D(2) (0 to 645 ng/d) indicated that the antagonism by retinyl acetate could be demonstrated at all vitamin D(2) dosages. To further investigate this antagonistic relationship, weanling Holtzman rats were fed a 0. 47% calcium, 0.3% phosphorus diet and 15.5 ng vitamin D(2) every 3 d for 33 d in the presence of increasing retinyl acetate (0 to 3448 microg/d). In the absence of retinyl acetate, these rats maintained a normal serum calcium level (2.34 mmol/L). Increasing retinyl acetate, however, eliminated the ability of vitamin D(2) to elevate the level of serum calcium (1.35 mmol/L). These results illustrated in vivo antagonism of vitamin D(2) action on intestine and bone by retinyl acetate.

Animals↗
PubMed1990

Synchronization of the seminiferous epithelium after vitamin A replacement in vitamin A-deficient mice.

The effect of vitamin A deficiency and vitamin A replacement on spermatogenesis was studied in mice. Breeding pairs of Cpb-N mice were given a vitamin A-deficient diet for at least 4 wk. The born male mice received the same diet and developed signs of vitamin A deficiency at the age of 14-16 wk. At that time, only Sertoli cells and A spermatogonia were present in the seminiferous epithelium. These spermatogonia were topographically arranged as single and paired cells and as clones of 4, 8 and more cells. A few mitoses of single, paired, and clones of 4 A spermatogonia were found, which were randomly distributed over the seminiferous epithelium. When vitamin A-deficient mice were treated with retinol-acetate combined with a normal vitamin A-containing diet, spermatogenesis restarted again synchronously. Only a few successive stages of the cycle of the seminiferous epithelium were present up to at least 43 days after vitamin A replacement. After 20 days, 98.3% of the seminiferous tubules were synchronized, showing pachytene spermatocytes as the most advanced cell type, mostly being in epithelium stages IX-XII. After 35 and 43 days, spermatogenesis was complete in 99.6% of the tubular cross sections, and most tubular cross sections were in stages IV-VII of the cycle of the seminiferous epithelium. The degree of synchronization was comparable or even higher than found in rats. The rate of development of the spermatogenic cells between 8 and 43 days after vitamin A replacement seemed to be similar to that in normal mice. Assuming that the rate of development of the spermatogenic cells is also normal during the first 8 days after vitamin A replacement, it can be deduced that the preleptotene spermatocytes, present after 8 days, were A spermatogonia in the beginning of stage VIII at the moment of vitamin A replacement. These results indicate that the mouse can be used as a model to study epithelial stage-dependent processes in the testis.

Animals↗
PubMed2004

Protective effects of vitamin A and vitamin E succinate against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced body wasting, hepatomegaly, thymic atrophy, production of reactive oxygen species and DNA damage in C57BL/6J mice.

The protective effect of vitamin A and vitamin E succinate against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced acute toxicity and measures of oxidative stress was studied. Ten mice were treated with either vitamin A (50 mg/kg every other day for eight days) or vitamin E succiante (150 mg/kg/day followed by a dose of 40 mg/kg/day for five additional days). Half of each of the above groups of animals received TCDD on day 4. Five mice received corn oil or TCDD alone. After five days of TCDD treatment, antioxidant combination treatment with vitamin A and TCDD or vitamin E succinate and TCDD resulted in a significant reduction in indicators of acute toxicity including the decrease in total body and thymus weight as compared to TCDD alone (P<0.05). The combination treatment produced also a significant reduction in the increase in liver weight as compared to TCDD only (P<0.05). Following one day of treatment with 50 microg TCDD/kg, vitamin A and vitamin E succinate produced a significant decrease in the production of superoxide anion by peritoneal lavage cells (P<0.05) and in DNA-single strand breaks in the same cells (P<0.05) as assessed by the reduction of cytochrome c and the alkaline elution technique, respectively. A significant decrease in DNA-single strand breaks in peritoneal lavage cells was observed following 5 days treatment with 50 microg TCDD/kg (P<0.05). The results indicate a potential role for oxidative stress in the acute toxicity of TCDD and a protective effect for vitamin A and vitamin E succinate in the overall toxicity of TCDD including measures of oxidative stress.

Animals↗
PubMed1980

Lack of effect of the vitamin D status on the concentration of the vitamin D-binding protein in rat serum.

The influence of the vitamin D status on the concentration of the serum vitamin D-binding protein was studied. In normal rats the serum vitamin D-binding protein increases gradually from birth to adulthood; after puberty a higher concentration is found in male rats than in female rats. Rats fed a vitamin D-deficient diet containing a sufficient amount of calcium and phosphorus were found to have a normal DBP (binding protein for vitamin D and its hydroxylated metabolites) pattern indistinguishable from that of rats receiving the same diet but supplemented with a weekly injection of 500 microgram vitamin D3. Rats fed a vitamin D-deficient, low calcium, low phosphorus diet developed severe hypocalcemia and growth retardation, but their DBP pattern was not significantly different from that of rats fed the same diet but supplemented with a weekly injection of 500 microgram vitamin D3. The concentration of the transport protein for vitamin D was thus unrelated to the vitamin D status of the rat.

Aging↗
PubMed1998

Distinct, tissue-specific regulation of vitamin D receptor in the intestine, kidney, and skin by dietary calcium and vitamin D.

We studied the effects of vitamin D deficiency and its correction by vitamin D or calcium-lactose supplementation on vitamin D receptor (VDR) expression in skin keratinocytes, kidney, and duodenum of adult rats. VDR messenger RNA (mRNA) was assayed by Northern blot, and VDR protein was determined immunocytochemically. In addition, four subpopulations of keratinocytes were isolated, characterized for their stages of differentiation, and analyzed for VDR expression. Vitamin D deficiency decreased VDR mRNA in all three tissues. Treatment with vitamin D or calcium-lactose reestablished the VDR mRNA content of the epidermis, but not that of the kidneys, and only the calcium-lactose diet increased duodenal VDR mRNA. The regulation of VDR mRNA in the epidermis was independent of cell differentiation, whereas VDR protein varied with differentiation. The VDR-positive cells in the control rats were at early and advanced states of differentiation. The expression of VDR was decreased by vitamin D deficiency and returned to control values after vitamin D or calcium supplementation. Vitamin D treatment, but not calcium, induced VDR expression in the normally immature population. Vitamin D and calcium, therefore, have distinct, tissue-specific effects on VDR. In epidermis, the posttranscriptional regulation of VDR expression is linked to cell differentiation. Calcium may be a key factor for VDR transcription, whereas both vitamin D and calcium seem to contribute to its posttranscriptional regulation.

Animals↗
PubMed1993

Vitamin D hydroxylases and their regulation in a naturally vitamin D-deficient subterranean mammal, the naked mole rat (Heterocephalus glaber).

The vitamin D hormone 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is generated by a series of hydroxylation steps in the liver and kidneys. We investigated whether naturally vitamin D-deficient subterranean mammals (naked mole rats, Heterocephalus glaber) employ the same enzymatic pathways, and whether these are regulated in a similar manner to that established for other mammals. Vitamin D3-25-hydroxylase in the liver and both 25-hydroxyvitamin D3-1-hydroxylase and 25-hydroxyvitamin D3-24 hydroxylase (1-OHase and 24-OHase) in the kidney were detectable in mole rats. As expected for vitamin D-deficient mammals, the 1-OHase activity predominated over the 24-OHase. After mole rats received a supraphysiological supplement of vitamin D3, 1-OHase activity was suppressed and 24-OHase activity was enhanced. Irrespective of vitamin D status, forskolin (a protein kinase A activator) and dibutyryl cyclic AMP did not alter the activity of either 1-OHase or 24-OHase. These findings suggest that the response of renal hydroxylases to parathyroid hormone was blunted. Phorbol esters, 12-O-tetradecanoylphorbol 13-acetate (TPA) and 1-oleoyl-2-acetylglycerol (OAG) (protein kinase C activators), suppressed 1-OHase activity. 24-OHase activity was induced by TPA but not by OAG. These effects were similar to those illicited by vitamin D3 supplementation but were additive in that they increased the responses shown in vitamin D-replete mole rats. These data confirm that naturally vitamin D-deficient mole rats can convert vitamin D3 to the hormone, 1,25(OH)2D3.(ABSTRACT TRUNCATED AT 250 WORDS)

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1992

Interactions of vitamin D with sodium zeolite A in rats from low and adequate vitamin D colonies.

Weanling rats (21 days old) from either a low vitamin D colony or an adequate vitamin D colony fed either a vitamin D adequate or a vitamin D deprived AIN-76A purified diet were used as a model to investigate interactions of vitamin D status with dietary sodium zeolite A (100 mg/kg body wt/day). Rats with adequate or replete vitamin D status had greater overall body weight gain, dry tibia weights and femur densities and ash weights than rats fed a vitamin D deprived diet. Addition of sodium zeolite A to the diets did not have an effect on plasma calcium, body weight gain or on femur density, ash and percent ash. Dietary sodium zeolite A increased total tibia fat in rats fed the vitamin D adequate diet and decreased total tibia fat in rats fed the vitamin D deprived diet. This effect of sodium zeolite A appeared to be beneficial to bone status in the groups fed adequate vitamin D, since these treatment groups had higher, although not significant, dry tibia weights with and without fat.

Aluminum Silicates↗
PubMed1965

LIVER VITAMIN A STORAGE IN FATTENING CATTLE FOLLOWING INTRARUMINAL OR INTRAMUSCULAR INJECTION OF VITAMIN A.

The effect of intramuscular or intraruminal injection of 1 million I.U. of an emulsifiable vitamin A preparation upon liver vitamin A stores in fattening steers was investigated. Pre-injection liver stores were 52 mcg vitamin A/gm fresh liver. At 7 days post-injection, these stores had increased to an average of 88 mcg vitamin A/gm fresh liver. Thereafter, the liver vitamin A stores declined until at 73 days post-injection they were approximately 28 mcg vitamin A/gm fresh liver. During depletion the pre-injection liver vitamin A levels were reached between 30-35 days post-injection. The method of administration had little effect on repletion of liver vitamin A stores; however, the steers injected intramuscularly showed a slightly slower depletion of liver vitamin A, than those injected intraruminally. Very little difference was observed in average daily weight gains between the two methods of vitamin A administration.

Animals↗
PubMed1990

Effects of chronic haloperidol on vitamin E levels and monoamine metabolism in rats fed normal and vitamin E deficient diets.

Experiments were conducted to study the effects of chronic haloperidol treatment on brain catechols and indoles in rats fed vitamin E deficient diets. Rats were fed basal diet or vitamin E deficient diet and injected with saline or haloperidol (1 mg/kg/day x 28 days i.p.). Tissue levels of catechols, indoles and vitamin E were measured using HPLC-EC techniques. Chronic haloperidol reduced striatal vitamin E levels. Activity in the striatal dopaminergic systems was also reduced, as, shown by reduced 3,4-dihydrophenylanine (DOPA), homovanillic acid (HVA), 3-methoxytyramine (3-MT), and dopamine (DA) levels. In addition, serotonergic activity was reduced, as indicated by lowered 5-hydroxytryptophan (5-HTP), 5-hydroxyindoleacetic acid (5-HIAA), and 5-hydroxytryptamine (5-HT) levels. In the substantia nigra, only 5-HIAA levels were reduced by treatment with haloperidol. These effects of haloperidol on monoamine metabolism were noted in both the vitamin E deficient and basal diet treated rats. However, vitamin E deficiency alone resulted in reduced DOPA and dopamine in the striatum. The vitamin E deficient diets resulted in markedly lowered vitamin E levels in the striatum and substantia nigra. All of these effects were more profound in rats that had been maintained on a vitamin E deficient diet for 7 weeks than those that were so treated for 5 weeks. These results suggest that alterations in dopamine metabolism and endogenous antioxidant systems may interact. Neuroleptics such as haloperidol that acutely accelerate dopamine synthesis and metabolism may cause peroxidative stress as indicated by depletions of vitamin E. Such depletions are capable of reducing dopamine levels and synthesis. The possibility that this and the effect of chronic haloperidol are mediated by peroxidative damage to dopamine neurons must be considered.

Animals↗
PubMed1988

Vitamin K1 (phylloquinone) and vitamin K2 (menaquinone) status in newborns during the first week of life.

Since 1961 the Committee on Nutrition of the American Academy of Pediatrics has recommended that prophylactic vitamin K be administered parenterally to all newborn infants, although the exact requirement for vitamin K in the newborn infant is unknown. There is little information about the vitamin K1 (phylloquinone, present in green vegetables) and vitamin K2 (menaquinones, synthesized by intestinal flora) status of newborn infants. In this study during the first week of life vitamin K status was assessed by measuring serum concentrations of phylloquinone in 23 mother-infant pairs at the time of birth. Maternal phylloquinone concentration (1.7 +/- 1.0 ng/mL, mean +/- SD) was significantly higher (P less than .02) than cord serum concentration (1.1 +/- 0.6 ng/mL). All infants were then given a standard 1-mg injection of vitamin K1. Ten infants were fed formula (containing 58 ng/mL of vitamin K1) and 13 were exclusively breast-fed. On day 5 of life, serum concentrations of vitamin K1 did not differ between breast-fed (21.0 +/- 12.4 ng/mL) and formula-fed (27.5 +/- 9.7 ng/mL) infants, reflecting the large amounts of parenteral vitamin K1 at birth. During the first week of life, formula-fed infants had much higher fecal concentrations of vitamin K1 (due to large oral intake) and more significant quantities (greater than or equal to 200 pmol/g of dry weight) of fecal menaquinones (reflecting differences in bacterial flora) than did breast-fed infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Bottle Feeding↗
PubMed1981

Effect of vitamin E administration on photoreceptor outer segment and retinal pigment epithelium of vitamin E deficient rats.

The photoreceptor outer segment and retinal pigment epithelium of vitamin E deficient rats given vitamin E were studied by electron microscopy. In rats fed a vitamin E deficient diet for more than 12 months, the photoreceptor outer segment did not regenerate after the administration of 400 mg of vitamin E. The retinal pigment epithelium was filled with lipofuscin granules and contained cytoplasmic organelles such as mitochondria, ribosomes and Golgi apparatus. The microvilli of the retinal pigment epithelium were long and in contact with the outer nuclear layer cells. The photoreceptor inner segment and nucleus had almost disappeared. In rats given 400 mg of vitamin E after vitamin E deficiency for 6 months, the photoreceptor outer segment showed no vesiculation and were increased in number. However, some retinal pigment epithelial cells still contained many lipofuscin granules. In conclusion, the photoreceptor outer segment and retinal pigment epithelium can be repaired in mild vitamin E deficiency by vitamin E administration, but vitamin E cannot reproduce the photoreceptor cells in nuclei of which have been broken by severe vitamin E deficiency.

Animals↗