Effects of vitamin A deficiency on cell proliferation and morphology of trachea of the hamster

Abstract. Regulation by vitamin A of cell proliferation and differentiation of epithelial tissues is well-established. Deficiency of vitamin A in experimental animals leads to the development of hyperplasia and squamous metaplasia. The objective of the present study was to examine, for young hamsters, the effects of variable levels of the vitamin in the liver and trachea, on cell proliferation and morphology of tracheal epithelium and on body weights. Newly born litters were maintained on vitamin A-supplemented and vitamin A-deficient diets, and various parameters were examined at different ages. Retinol and retinyl palmitate levels were determined by high performance liquid chromatography. For animals on the supplemented diet, concentrations of liver retinyl palmitate and retinol increased progressively with age, reaching highest levels of approximately 84 and 1 -9 μg/g liver, respectively, at 28 d. In contrast, in animals on the vitamin A-deficient diet, the retinyl palmitate and retinol levels decreased progressively, reaching the lowest levels of approximately 0–32 and 0–09 μg/g, respectively. No significant reduction in retinol was observed in the trachea of animals maintained on the deficient diet for at least 20 d; their tracheas were depleted of retinol at 28 d. No vitamin A-associated differences were, however, observed in the labelling indices, growth fraction or in the morphology of the tracheal epithelium. Both the control and vitamin A-deficient animals gained weight progressively until 36 d of age, although the weight of animals in the latter group remained below those in the former group. These results show that mild-to-severe deficiency of vitamin A had no effects on cell proliferation or tracheal morphology of the hamster. The hyperplasia and squamous metaplasia in the trachea occurs only at an extreme vitamin A-deficiency when the tissue levels of the vitamin are depleted.     

Effects of vitamin A deficiency on cell proliferation and morphology of trachea of the hamster

Regulation by vitamin A of cell proliferation and differentiation of epithelial tissues is well-established. Deficiency of vitamin A in experimental animals leads to the development of hyperplasia and squamous metaplasia. The objective of the present study was to examine, for young hamsters, the effects of variable levels of the vitamin in the liver and trachea, on cell proliferation and morphology of tracheal epithelium and on body weights. Newly born litters were maintained on vitamin A-supplemented and vitamin A-deficient diets, and various parameters were examined at different ages. Retinol and retinyl palmitate levels were determined by high performance liquid chromatography. For animals on the supplemented diet, concentrations of liver retinyl palmitate and retinol increased progressively with age, reaching highest levels of approximately 84 and 1.9 micrograms g liver, respectively, at 28 d. In contrast, in animals on the vitamin A-deficient diet, the retinyl palmitate and retinol levels decreased progressively, reaching the lowest levels of approximately 0.32 and 0.09 micrograms/g, respectively. No significant reduction in retinol was observed in the trachea of animals maintained on the deficient diet for at least 20 d: their tracheas were depleted of retinol at 28 d. No vitamin A-associated differences were, however, observed in the labelling indices, growth fraction or in the morphology of the tracheal epithelium. Both the control and vitamin A-deficient animals gained weight progressively until 36 d of age, although the weight of animals in the latter group remained below those in the former group. These results show that mild-to-severe deficiency of vitamin A had no effects on cell proliferation or tracheal morphology of the hamster. The hyperplasia and squamous metaplasia in the trachea occurs only at an extreme vitamin A-deficiency when the tissue levels of the vitamin are depleted.     

Metabolism of a physiological amount of all-trans-retinol in the vitamin A-deficient rat

Because only retinol and not all-trans-retinoic acid (atRA) can satisfy all of the functions of vitamin A, we have investigated the retinol metabolites in tissues of vitamin A-deficient (VAD) rats responding to a radioactive dose of [20-(3)H]all-trans-retinol. As expected, atRA is the major vitamin A metabolite present in the target tissues of VAD rats given a physiological dose (1 microg) of [20-(3)H]all-trans-retinol (atROL). Both atROL and atRA were detected by high-performance liquid chromatographic (HPLC) analysis of the radioactivity extracted from the liver, kidney, small intestine, lung, spleen, bone, skin, or testis of these animals. Novel retinol metabolites were observed in the aqueous extracts from the testis, lung, and skin. However, these metabolites were detected in very small amounts and were not characterized further. Importantly, neither 9-cis-retinoic acid (9cRA), 9-cis-retinol (9cROL), nor 13-cis-retinoic acid (13cRA) was present in detectable amounts. The amounts of atRA varied in each tissue, ranging from 0.29 +/- 0.05 fmol of RA/g of tissue in the femurs to 12.9 +/- 4.3 fmol of RA/g of tissue in the kidneys. The absence of 9cRA in vivo was not due to degradation of this retinoid during the extraction procedure or HPLC analysis of the extracted radioactivity. As atROL completely fulfills all of the physiological roles of vitamin A, and 9cRA is not detected in any of the tissues analyzed, these results suggest that 9cRA may have no physiological relevance in the rat.     

Free Radical-Induced Liver Injury. I. Effects of Dietary Vitamin E Deficiency on Triacylglycerol Level and its Fatty Acid Profile in Rat Liver

Effects of dietary vitamin E deficiency on the fatty acid compositions of total lipids and phospholipids were studied in several tissues of rats fed a vitamin E-deficient diet for 4, 6, and 9 months. No significant differences were observed between the vitamin E deficiency and controls except in the fatty acid profiles of liver total lipids. Triacylglycerol (TAG) accumulation was found in the liver of rats fed a vitamin E-deficient diet. The levels of TAG-palmitate and -oleate increased particularly in the liver from such animals. The fatty acid compositions of hepatic phospholipids were not affected by the diet. Increased TAG observed in the liver of rats fed a vitamin E-deficient diet was restored to normal when the diet was supplemented with 20 mg α-tocopheryl acetate/kg diet. These findings indicate that dietary vitamin E deficiency causes TAG accumulation in the liver and that the antioxidant, vitamin E, is capable of preventing free radical-induced liver injury.     

Venlafaxine Modulates Depression-Induced Oxidative Stress in Brain and Medulla of Rat

Venlafaxine is an approved antidepressant that is an inhibitor of both serotonin and norepinephrine transporters. Medical treatment with oral venlafaxine can be beneficial to depression due to reducing free radical production in the brain and medulla of depression- induced rats because oxidative stress may a play role in some depression. We investigated the effect of venlafaxine administration and experimental depression on lipid peroxidation and antioxidant levels in cortex brain, medulla and erythrocytes of rats. Thirty male wistar rats were used and were randomly divided into three groups. Venlafaxine (20 mg/kg) was orally supplemented to depression-induced rats constituting the first group for four week. Second group was depression-induced group although third group was used as control. Depressions in the first and second groups were induced on day zero of the study by chronic mild stress. Brain, medulla and erythrocytes samples were taken from all animals on day 28. Depression resulted in significant decrease in the glutathione peroxidase (GSH-Px) activity and vitamin C concentrations of cortex brain, glutathione (GSH) value of medulla although their levels were increased by venlafaxine administration to the animals of depression group. The lipid peroxidation levels in the three tissues and nitric oxide value in cortex brain elevated although their levels were decreased by venlafaxine administration. There were no significant changes in cortex brain vitamin A, erythrocytes vitamin C, GSH-Px and GSH, medulla vitamin A, GSH and GSH-Px values. In conclusion, cortex brain within the three tissues was most affected by oxidative stress although there was the beneficial effect of venlafaxine in the brain of depression-induced rats on investigated antioxidant defenses in the rat model. The treatment of depression by venlafaxine may also play a role in preventing oxidative stress. Abstract of the paper was submitted in 1st Ion Channels and Oxidative Stress Congress, 14–16 September 2006, Isparta, Turkey.     

Metabolism of [11-3H]retinyl acetate in liver tissues of vitamin A-sufficient, -deficient and retinoic acid-supplemented rats

A study was conducted on the incorporation of [11-3H]retinyl acetate into various retinyl esters in liver tissues of rats either vitamin A-sufficient, vitamin A-deficient or vitamin A-deficient and maintained on retinoic acid. Further, the metabolism of [11-3H]retinyl acetate to polar metabolites in liver tissues of these three groups of animals was investigated. Retinol metabolites were analyzed by high-performance liquid chromatography. In vitamin A-sufficient rat liver, the incorporation of radioactivity into retinyl palmitate and stearate was observed at 0.25 h after the injection of the label. The label was further detected in retinyl laurate, myristate, palmitoleate, linoleate, pentadecanoate and heptadecanoate 3 h after the injection. The specific radioactivities (dpm/nmol) of all retinyl esters increased with time. However, the rate of increase in the specific radioactivity of retinyl laurate was found to be significantly higher (66-fold) than that of retinyl palmitate 24 h after the injection of the label. 7 days after the injection of the label, the specific radioactivity between different retinyl esters were found to be similar, indicating that newly dosed labelled vitamin A had now mixed uniformly with the endogenous pool of vitamin A in the liver. The esterification of labelled retinol was not detected in liver tissues of vitamin A-deficient or retinoic acid-supplemented rats at any of the time point studied. Among the polar metabolites analyzed, the formation of [3H]retinoic acid from [3H]retinyl acetate was found only in vitamin A-deficient rat liver 24 h after the injection of the label. A new polar metabolite of retinol (RM) was detected in liver of the three groups of animals. The formation of 3H-labelled metabolite RM from [3H]retinyl acetate was not detected until 7 days after the injection of the label in the vitamin A-sufficient rat liver, suggesting that metabolite RM could be derived from a more stable pool of vitamin A.     

Biosynthetic studies on mannolipids and mannoproteins of normal and vitamin A-depleted hamster livers.

The incorporation of [1-14C]mannose into hamster liver glycolipids and glycoproteins was studied in normal and vitamin A-depleted hamsters. Severly (25% weight loss) and mildly (no weight loss) deficient animals were compared to vitamin A-fed controls. The incorporation of [14C]mannose into glycolipids and glycoproteins decreased in mild and severe vitamin A deficiency by 63-90% compared to vitamin A-fed animals. These results were essentially the same whether expressed per g of wet liver, per DNA or per protein. The size of the pools of mannose, glucose and galactose and their specific radioactivity in liver were determined by gas-liquid chromatography of the boronates of the hexitols (Eisenberg, Jr, F. (1972) Methods Enzymol. XXVIIIB, 168-178) in normal and vitamin A-deficient conditions. It was found that the amount of free hexoses per g of liver was very similar in normal and vitamin A-deficient conditions. The specific radioactivities for mannose and glucose were greater in vitamin A deficiency, thus excluding the possibility that the observed severe decrease in glycopeptide and glycolipid synthesis is a reflection of a similar decrease in the specific radioactivity of the precursor pools. Quantitation of mannose in glycoprotein showed a 79% decrease in vitamin A deficiency. Specific radioactivity of mannose in glycoproteins, 20 min after injection of the label, was 187 dpm/mug of mannose in the normal and 48 kpm/mug of mannose in the vitamin A-deficient livers. It is concluded that vitamin A is necessary for the biosynthesis of liver mannose-containing glycoproteins and glycolipids.     

Serum vitamin A and vitamin E concentrations after parenteral vitamin A administration in sheep

Twenty primiparous dairy sheep of the Mytilene breed, which were fed with a ration deficient in vitamin A and carotenes, were divided into 2 groups of 10 animals each after a 2-month adaptation period. The animals of group A were administered vitamin A palmitate by intramuscular injection (3500 IU/kg bodyweight), while the animals of group B were used as controls and received only the vehicle of the preparation without vitamin A. Serum vitamin A concentrations increased significantly in the animals of group A compared to the animals of group B (P < 0.01) from the first 24 h post-injection and remained significantly high for 8 days, and at 10 days post-injection they reached the pre-injection levels. The serum vitamin E concentration declined significantly (P < 0.05) in the animals of group A compared to the animals of group B for 8 days, when they reached the pre-injection levels. No changes in serum vitamins A and E levels in the animals of the 2 groups were observed 20 days after the injection of vitamin A.     

Dietary vitamins A and E influence retinyl ester composition and content of the retinal pigment epithelium

Experiments were conducted to determine the influence of dietary levels of vitamin A and alpha-tocopherol on the amounts and composition of retinyl esters in the retinal pigment epithelium of light-adapted albino rats. Groups of rats were fed diets containing alpha-tocopherol and either no retinyl palmitate, adequate retinyl palmitate, or excessive retinyl palmitate. Other groups of rats received diets lacking alpha-tocopherol and containing the same three levels of retinyl palmitate. Retinoic acid was added to diets lacking retinyl palmitate. After 27 weeks, the animals were light-adapted to achieve essentially total visual pigment bleaches, and the neural retinas and retinal pigment epithelium-eyecups were then dissected from each eye for vitamin A ester determinations. Almost all of the retinyl esters were found in the retinal pigment epithelium-eyecup portions of the eyes, mainly as retinyl palmitate and retinyl stearate. Maintaining rats on a vitamin A-deficient, retinoic acid-containing diet led to significant reductions in retinal pigment epithelial retinyl ester levels in rats fed both the vitamin E-supplemented and vitamin E-deficient diets; contrary to expectations, the effect of dietary vitamin A deficiency was more pronounced in the vitamin E-supplemented rats. Vitamin A deficiency in retinoic acid-maintained animals also led to significant reductions in retinyl palmitate-to-stearate ester ratios in the retinal pigment epithelia of both vitamin E-supplemented and vitamin E-deficient rats. Excessive dietary intake of vitamin A had little, if any, effect on retinal pigment epithelial retinyl ester content or composition. Vitamin E deficiency resulted in significant increases in retinal pigment epithelial retinyl palmitate content and in palmitate-to-stearate ester ratios in rats fed all three levels of vitamin A, but had little effect on retinal pigment epithelial retinyl stearate content. In other tissues, vitamin E deficiency has been shown to lower vitamin A levels, and it is widely accepted that this effect is due to autoxidative destruction of vitamin A. The increase in retinal pigment epithelial vitamin A ester levels in response to vitamin E deficiency indicates that vitamin E does not regulate vitamin A levels in this tissue primarily by acting as an antioxidant, but rather may act as an inhibitor of vitamin A uptake and/or storage. The effect of vitamin E on pigment epithelial vitamin A levels may be mediated by the vitamin E-induced change in retinyl palmitate-to-stearate ratios.     

1,25-dihydroxyvitamin D3 receptor is upregulated in aortic smooth muscle cells during hypervitaminosis D

Several studies have demonstrated that excess of vitamin D3 is toxic particularly to vascular tissues. A notable pathological feature is arterial calcification. The nature of the toxic metabolite in hypervitaminosis D and the pathogenesis of arterial calcification are not clearly understood. The present study was undertaken to explore whether arterial calcification is a sequel of increased calcium uptake by arterial smooth muscle mediated by up regulation of vitamin D receptor in the cells in response to elevated circulating levels of vitamin D3 in serum. The experimental study was performed in 20 New Zealand white female rabbits aged 6 months. Animals in the test group were injected 10,000 IU of cholecalciferol intramuscularly twice a week for one month. Six control animals were given intra-muscular injections of plain cottonseed oil. Animals were sacrificed and aortas were examined for pathological lesions, 1,25-dihyroxyvitamin D3 (1,25(OH)2 D3) receptor levels and 45Ca uptake in smooth muscle cells. Serum samples collected at intervals were assayed for levels of 25-OH-D3 and calcium. The results showed that in animals given injections of cholecalciferol, serum levels of 25-OH-D3 were elevated. In four of these animals calcification and aneurysmal changes were seen in the aorta. Histological lesions comprised of fragmentation of elastic fibers as well as extensive loss of elastic layers. 1,25(OH)2 D3 receptor levels were up regulated and 45Ca uptake enhanced in aortas of animals which were given excessive vitamin D3. The evidences gathered suggest that excess vitamin D is arteriotoxic and that the vitamin induces arterial calcification through up regulation of 1,25(OH)2D3 receptor and increased calcium uptake in smooth muscle cells of the arteries.     

Garlic and vitamin E provides antioxidant defence in tissues of female rats treated with nicotine

Nicotine is known to induce oxidative stress in rat tissues and the antioxidant properties of garlic have been reported. This study was designed to determine if the peroxidative damage caused by nicotine administration can be effectively prevented with garlic juice, and vitamin E, a known antioxidant.Four groups of six rats each were divided into: Group I: (control) received 0.2ml of 0.9% normal saline, group II (received nicotine 0.6mg/kg b.w subcutaneously), group III (received nicotine 0.6mg/kg b.w + garlic juice 100mg/kg b.w orally), and group IV (received nicotine 0.6mg/kg b.w + Vitamin E 100mg/kg b.w orally). All animals were treated for 21 days. The pituitary gland, ovary, uterus, heart, liver and kidney of the animals were harvested, weighed and homogenized. Malondialdehyde (MDA), superoxide dismutase (SOD) and reduced glutathione (GSH) were then measured.Concentration of MDA was significantly increased in tissues of nicotine treated rats when compared with the control. In group III and IV, MDA levels were significantly reduced when compared with nicotine group. The activities of SOD and GSH significantly decreased in group II (nicotine only) rat tissues, while it was significantly increased in group III and IV rat tissues. The study showed that garlic juice extract (100mg/kg b.w) and vitamin E (100mg/kg b.w) administration prevented oxidative damage in rat tissues treated with nicotine. The study also showed that vitamin E has a more potent antioxidant activity than garlic juice in preventing nicotine induced oxidative damage in rat. Keywords: Nicotine, Vitamin E, Garlic, antioxidant.     

STUDY OF VITAMIN A SUPPLEMENTATION IN CAPTIVE NORTHERN FUR SEALS (CALLORHINUS URSINUS) AND ITS EFFECT ON SERUM VITAMIN E

Two experiments were conducted to determine the effect of vitamin A supplementation on serum vitamin E in adult female northern fur seals ( Callorhinus ursinus ). In the first experiment five animals received, in addition to their routine dietary multivitamin supplement, a high-level vitamin A supplement (53 μmol retinyl palmitate/d) for 30 d. Five seals consuming their routine dietary supplement served as controls. Serum vitamin E decreased significantly in animals receiving high-level vitamin A supplements. At the end of 30 d serum vitamin E averaged 18.6 μg/mL in the control animals and 13.4 μg/mL in the animals receiving the high-Ieve1 vitamin A supplement. In experiment 2 ten animals received the high level vitamin A supplement for 60 d. After 30 d, serum vitamin E levels were reduced, but by 60 d had returned to baseline levels. However, the ratio of serum vitamin E to phospholipid, another index of vitamin E status, remained decreased. Although the exact mechanism of interaction is unknown, this study shows that when providing vitamin supplements for captive pinnipeds, vitamin interactions must be considered. The vitamin A supplementation currently used by some institutions seems unnecessary and may have detrimental effects on vitamin E status.     

Gamma-tocopherol supplementation inhibits protein nitration and ascorbate oxidation in rats with inflammation

Gamma-tocopherol (gammaT) complements alpha-tocopherol (alphaT) by trapping reactive nitrogen oxides to form a stable adduct, 5-nitro-gammaT [Christen et al., PNAS 94:3217-3222; 1997]. This observation led to the current investigation in which we studied the effects of gammaT supplementation on plasma and tissue vitamin C, vitamin E, and protein nitration before and after zymosan-induced acute peritonitis. Male Fischer 344 rats were fed for 4 weeks with either a normal chow diet with basal 32 mg alphaT/kg, or the same diet supplemented with approximately 90 mg d-gammaT/kg. Supplementation resulted in significantly higher levels of gammaT in plasma, liver, and kidney of control animals without affecting alphaT, total alphaT+gammaT or vitamin C. Intraperitoneal injection of zymosan caused a marked increase in 3-nitrotyrosine and a profound decline in vitamin C in all tissues examined. Supplementation with gammaT significantly inhibited protein nitration and ascorbate oxidation in the kidney, as indicated by the 29% and 56% reduction of kidney 3-nitrotyrosine and dehydroascorbate, respectively. Supplementation significantly attenuated inflammation-induced loss of vitamin C in the plasma (38%) and kidney (20%). Zymosan-treated animals had significantly higher plasma and tissue gammaT than nontreated pair-fed controls, and the elevation of gammaT was strongly accentuated by the supplementation. In contrast, alphaT did not significantly change in response to zymosan treatment. In untreated control animals, gammaT supplementation lowered basal levels of 3-nitrotyrosine in the kidney and buffered the starvation-induced changes in vitamin C in all tissues examined. Our study provides the first in vivo evidence that in rats with high basal amounts of alphaT, a moderate gammaT supplementation attenuates inflammation-mediated damage, and spares vitamin C during starvation-induced stress without affecting alphaT.     

Dietary vitamin E affects α-TTP mRNA levels in different tissues of the Tan sheep

The α-tocopherol transfer protein (α-TTP) is a ~ 32 kDa cytosolic protein that plays an important role in the efficient circulation of plasma α-tocopherol in the body, a factor with great relevance in reproduction. The α-TTP gene has been studied in a number of tissues; however, its expression and function in some ovine tissues remain unclear. A previous study from our laboratory has demonstrated α-TTP expression in sheep liver. In the present study we determined whether α-TTP is expressed in non-liver tissues and investigated the effects of dietary vitamin E on the α-TTP mRNA levels. Thirty-five male Tan sheep with similar body weight were randomly allocated into five groups and supplemented 0, 20, 100, 200 and 2000 IU sheep^− 1 day^− 1 vitamin E, for four months, respectively. At the end of the study, the animals were slaughtered and tissue samples from the heart, spleen, lung, kidney, longissimus dorsi muscle and gluteus muscle were immediately collected. We found that the α-TTP gene is expressed in sheep tissues other than the liver. Moreover, dietary vitamin E levels had influenced the expression levels of α-TTP gene in these tissues in a tissue-specific way. The technique of immunohistochemistry was used to detect α-TTP in tissues of the heart, spleen, lung, and kidney and we found that α-TTP was mainly located in the cytoplasm while no α-TTP immunoreactivity was detected in the cytoplasm of longissimus dorsi and gluteus muscle samples. Importantly, our findings lay the foundation for additional experiments focusing on the absorption and metabolism of vitamin E in tissues other than the liver.     

Influence of high vitamin E dosages on retinol and carotinoid concentration in body tissues and eggs of laying hens

The aim of the study was to contribute to the discussion of overdosing vitamin E in laying hens. A total of 45 laying hens, divided into 5 groups were fed diets supplemented with either 0; 100; 1000; 10 000 or 20 000 mg dl‐α‐tocopheryl acetate/kg diet over a period of 10 weeks. Concentrations of vitamins A and E were measured in plasma, various tissues and egg yolk. Furthermore egg yolk colour and some carotinoids were measured in egg yolks. None of the vitamin E doses significantly influenced performance of the hens. As expected, vitamin E concentration in plasma, all tissue samples and egg yolk was significantly increased with increasing tocopherol content in the diet. The egg yolk showed the highest vitamin E concentration, followed by liver and muscles. Feeding 1000 mg α‐tocopheryl acetate per kg diet resulted in an increase of vitamin A concentration in the liver. Very high doses (10 000 and 20 000 mg/kg diet) significantly decreased retinol concentration in the liver and egg yolk, as well as carotinoid concentration in the egg yolk. The lower carotinoid concentration in egg yolk resulted in a decreased intensity of egg yolk colour. A prooxidative and/or competitive effect of very high doses of vitamin E with other fat soluble substances has been discussed.     

Vitamin E Concentrations in the Brains and Some Selected Peripheral Tissues of Selenium-Deficient and Vitamin E-Deficient Mice

Abstract: Weanling male CD-1 mice were fed control, vitamin E-deficient or selenium-deficient diets for periods of 12 to 20 weeks. α-Tocopherol concentrations in plasma, liver, and testes, as well as in three specific areas in the brain (cerebral hemisphere, cerebellum, and medulla plus pons) were determined by high performance liquid chromatography. Significant concentrations of α-tocopherol were found in all brain samples from vitamin E-deficient animals long after the peripheral tissues were depleted, indicating that brain is more resistant to vitamin E deficiency than peripheral tissues. Cerebellar concentrations of α-tocopherol were consistently lower than those of cerebral hemisphere and medulla-pons. Further more, the cerebellar α-tocopherol concentration sustained a larger decline than the other two brain areas within 6 weeks of vitamin E deficiency treatment. These and other data suggest that cerebellum may be more susceptible to damage from vitamin E deficiency than other parts of the brain. Selenium deficiency did not affect brain a-tocopherol concentrations during the 12 weeks of the study.     

饲料硒和维生素E对大鼠机体抗氧化能力的影响

 用克山病病区粮配成基础低硒饲料,补充硒和/或维生素E组成四种不同水平的饲料,饲喂雄性断乳大鼠,观察其对机体抗氧化能力的影响。评价指标是用抗坏血酸诱发的红细胞溶血率、被O~-_2(超氧阴离子)氧化的血红蛋白量和组织中的TBA值。动物饲养13周后,自尾静脉取血,测定溶血率和血红蛋白被氧化的百分率,和全血SeGSHPx(含硒谷胱甘肽过氧化物酶)活力。15周后将动物断头杀死,立即取出心脏和肝脏测定SeGSHPx活力和TBA值。结果表明在克山病病区粮的饲料中补充硒或维生素E,或者二者同时补充均明显提高组织中的SeGSHPx活力和降低组织中的TBA值。不论在硒缺乏时或硒充足时,饲料中补充维生素E显著降低抗坏血酸诱发的红细胞溶血率,对O~-_2氧化血红蛋白无保护作用。在维生素E缺乏时,仅补充硒对溶血无作用。不论饲料中维生素E缺乏或者充足,补充硒对O~-_1氧化血红蛋白均有显著保护作用。     

Blood vitamin values of common marmosets (Callithrix jacchus)

The blood vitamin analyses of the common marmoset (Callithrix jacchus) were determined to provide baseline reference values for the normal animal. Ascorbic acid, riboflavin (erythrocyte glutathione reductase) [ECR], measurement, thiamin (erythrocyte transketolase) measurement and vitamin A (retinol) were determined for Texas A&M colony-born animals and those obtained from the wild. The analyses were completed on the animals, three times each, for a total of 93 analyses, which included 51 colony-born and 60 wild-born marmosets. A mean value of 0.98 mg/dl for ascorbic acid was found for the colony with a range from 0.06 to 4.1 mg/dl. The normal range for the marmosets appeared to be 0.5 to 1.5 mg/dl. The mean activity coefficient (AC) for the marmosets was 1.0 indicating that the animals had adequate riboflavin in the diet. The mean transketolase activities were (ribose remaining ?30.1 IU/L) and (sedoheptulose appearance ?7.9 IU/L). The mean and range for serum vitamin A (retinol) were 20.4 mg/dl and 6.96–57.44 mg/dl, respectively. None of the animals (colony-born or wild-born) exhibited any clinical signs of vitamin deficiencies as a result of being maintained in an indoor-outdoor environment over a three-year period.